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Guttermouth

Guttermouth is an American punk rock band formed in 1989 in Huntington Beach, California. They have released nine full-length studio albums and two live albums and have toured extensively, including performances on the Vans Warped Tour. They are infamous for their outrageous lyrics and behavior which are deliberately explicit, offensive and intended to shock, though usually in a humorous and sarcastic manner. This behavior has sometimes resulted in high-profile problems for the band, such as being banned from performing in Canada for eighteen months and leaving the 2004 Warped Tour amidst controversy over their political views and attitudes towards other performers.

Formation
The members of Guttermouth began playing music in various parts of Orange County, California in the early 1980s. Singer Mark Adkins performed in the La Habra punk rock band Republic in 1982 with guitarist and classmate Scott Sheldon. Adkins has remained the sole permanent member of Guttermouth over all its iterations; some of the songs written by Sheldon and Adkins at this time would later be used in Guttermouth and would remain in their live set throughout their career. Republic broke up in 1984 and the two moved on to other projects: Sheldon played in a band with drummer James Nunn while Adkins tried various other musical projects, including one with Nunn. Adkins joined guitarists Eric "Derek" Davis and Barry Burnham, bassist Paul "Fang" Denis, and drummer Tim Baulch in their band Critical Noise. Baulch suggested the name Guttermouth for the new lineup, and this early incarnation of the band played shows, parties and skateboard demo's during 1988 until Davis relocated to nearby Huntington Beach in 1989, effectively dissolving the group. About a year later Adkins and Nunn also moved there. Adkins approached Burnham and Baulch about starting the band back up but the two declined. Adkins and Davis recruited Sheldon to replace Burnham and Nunn to replace Baulch. They also recruited an early fan of the band, bassist Clint Weinrich to join them. This solidified the "original" lineup of the band with Mark Adkins on vocals, Scott Sheldon and Eric Davis on guitars, Clint Weinrich on bass and James Nunn on drums, a lineup which would remain consistent over the next six years and two albums.

First album
By the summer of 1989, Guttermouth began performing in Huntington Beach and Orange County, building a small but enthusiastic local following. Their music was heavily influenced by the Los Angeles and Orange County punk rock scenes of the 1980s which included bands like the Adolescents, The Vandals, Social Distortion, Fear, the Descendents, Angry Samoans, Bad Religion and Black Flag. From these influences Guttermouth developed their own style of fast punk tempos with humorously sarcastic and offensive lyrics coupled with equally outrageous and offensive behavior, developing a reputation for chaotic live shows. In 1991, they were approached by local record label Dr. Strange about putting out an album, and entered Westbeach Recorders to record and release their first 7-inch record, Puke. Later that year they released another 7-inch, Balls, and finally their first LP, aptly titled Full Length LP.

Full Length proved to be a success for the band, expanding their fan base and giving them opportunities to perform throughout southern California alongside other popular punk rock bands. The album was soon re-released in CD format by Dr. Strange and an animated music video was made for the song "1, 2, 3…Slam!" to be played on local punk rock and skateboarding video programs. The band continued to play locally, developing friendships with fellow Orange County punk bands such as The Offspring and the Vandals. They played a show opening for the Vandals at the Ice House in Fullerton which was filmed for the Vandals live album Sweatin’ to the Oldies. Guttermouth continued to promote Full Length over the next few years and also released 7-inch vinyl singles for the new songs "Veggicide" and "P.C." In 1993, they recorded the 7-inch EP 11oz. as the first release put out by newly formed label Hopeless Records.

Friendly People and tours
By 1994, Full Length had been available for almost four years and the members of Guttermouth were preparing to write a second album. They originally considered releasing the album themselves, but were soon approached with an offer from Offspring singer Dexter Holland, who in the wake of his own band's success was starting an independent record label and wanted to put out Guttermouth's next album as his first release. They agreed and recorded the album Friendly People as the first release on Holland's new label Nitro Records, and filmed an independent music video for the song "End on 9." Guttermouth would remain with Nitro over the next five years, releasing an album each year on the label.

1994 also found the band playing to a much larger audience. The success that year of The Offspring's album Smash and Green Day's Dookie had brought the southern California punk rock scene into the national spotlight. Thanks to their friendship with The Offspring and their new record deal with Nitro, Guttermouth found themselves embarking on their first national and world tours opening for larger punk bands. However, their typically outrageous behavior would often find them at odds with the other bands, audiences, and venues at which they played. After about six months of touring with this reputation the band found themselves banned from performing in numerous cities and clubs and blacklisted by many of the bands with whom they had hoped to tour. To the band, however, this behavior was typical and in keeping with the anarchic ideals that were at the core of the punk movement.

At one point, the band found themselves ejected from a tour while in South Carolina, where they booked themselves at a club and recorded a performance which would later be released as Live From the Pharmacy. Adkins was arrested and briefly jailed in 1995 on charges of inciting a riot during a Guttermouth show at the Glen Helen Blockbuster Pavilion in San Bernardino, but evidence was insufficient to file charges.

Lineup change
The following year found the band returning home to California and experiencing a lineup change. Clint Weinrich married in the spring of 1995, and to fill in for him on a European tour the band recruited Steve "Stever" Rapp, a college friend of Nunn's who was playing in a band called The Grabbers. Things worked out well with Rapp on this tour and he soon became the band's permanent bass player. The new lineup entered the studio and recorded their third album Teri Yakimoto. By all accounts the recording process was plagued with problems, and at one point most of the recordings were scrapped and re-recorded with a new producer. The result was an album that continued the fast and sarcastic Guttermouth tradition but was more melodic and pop-influenced than their previous albums. The band continued to tour and expand their fan base, and filmed a music video for the song "Whiskey." With their popularity growing Nitro Records re-released Full Length in CD format with bonus tracks under the title The Album Formerly Known as Full Length LP.

In 1997, the band recorded Musical Monkey, an album which captured their chaotic energy and sharp sense of humor. It is considered by many to be the best representation of their "classic" sound, and songs such as "Lucky the Donkey," "Do the Hustle," "Lipstick" and "Perfect World" became staples in their live set. The following year they released Live From the Pharmacy, a recording of a live show from 1994 that also included four new songs engineered by Vandals guitarist Warren Fitzgerald and liner notes written by Nunn recounting the band's history. In 1998 Guttermouth was banned from performing in Canada for one year on charges of public indecency after Adkins exposed himself onstage in Saskatoon. According to Adkins: "oh, I was guilty [...] What I would do is grab two young girls out of the audience and I would have them hold up this sheet in front of me, and Jamie, the drummer at the time, would say this magical incantation, if you will, and I would be standing there stark naked." Combined with a drunk driving charge from the United States, the incident led Adkins to be arrested on immigration charges, detained for five days, and then deported, though Guttermouth would return to Canada a few years later. After obtaining a full pardon from the Canadian judicial system, no record remains on file.

Rapp left the band in 1999, at which point Nunn moved from drums to bass and new drummer William "Ty" Smith was brought in. That year the band recorded and released Gorgeous, their most aggressive album to date and their final album for Nitro.

Move to Epitaph
In 2000, Guttermouth appeared performing in the Kung Fu Films movie That Darn Punk, an appearance which stemmed from their longtime friendship with the Vandals. That year the band also signed to Epitaph Records, the label operated by Bad Religion's Brett Gurewitz which had grown throughout the 1990s into one of the largest independent labels in the country. For their 2001 album Covered With Ants the band combined their punk rock sound with instruments they had not used on albums before, including organ, banjo and fiddle. A music video was filmed for the song "She's Got the Look" and the band continued to tour.

As the band prepared to work on their next album in 2002, founding member James Nunn left the group. While original bassist Clint Weinrich filled in on tours, guitarists Eric Davis and Scott Sheldon played bass for the album's recording along with studio bassist Hedge. The musical direction shifted to territory the band had not hitherto explored, and the resulting album Gusto was substantially different from their previous efforts, with a slower speed and more melody and pop influence. Though the band's irreverent sense of humor remained intact, the music was much less characteristically "punk" than anything the band had played before. Response to the album was mixed, and the band members would later look back on it as something of a failed experiment. In 2003 Weinrich again rejoined the band for a series of shows including a performance at the House of Blues in Anaheim which was filmed and released by Kung Fu Records as a live concert CD and DVD package. The show's closing performance of "Perfect World" was removed from the DVD release of the show because a minor could be seen drinking alcohol on stage with the band. However, on the packaging of the DVD itself it is said that it was edited due to a frenzied crowd that damaged equipment, although the audio portion was preserved on the CD.

The band's next album Eat Your Face, released jointly through Epitaph and Volcom Entertainment in 2004, was hailed as a return to form. Founding guitarist Eric Davis had left the band and been replaced by Donald "Don" Horne, while former Slick Shoes bassist Kevin Clark filled the vacant bass position. Musically the album returned to the fast, loud punk rock style the band was known for, with many of the songs recorded in just a few takes. Lyrically it retained the band's sense of biting sarcasm and expressed dissatisfaction with the U.S. electoral system and the current state of punk rock in the mainstream, amongst other topics.

Warped Tour controversy
In the summer of 2004, Guttermouth embarked on the Vans Warped Tour, playing on the Volcom side stage. In keeping with their reputation for outrageous and offensive behavior, Adkins would often openly insult other acts from onstage, declaring that bands such as Simple Plan and My Chemical Romance cared more about their fashionable clothing and popularity than about the quality of their music. The band members also mocked what they saw as an uninformed political display of many bands on the tour by selling T-shirts and displaying banners that jokingly proclaimed support for President George W. Bush (many of the bands and media booths supported an anti-Republican stance in the months leading up to the 2004 presidential election). After several weeks on the tour Guttermouth was "politely" asked to leave, fueling rumors that other performers had petitioned to have them ejected. Eventually, however, Adkins issued a statement apologizing to Warped Tour manager Kevin Lyman and admitting that the band had left the tour voluntarily, due in part to his distaste for the political atmosphere surrounding it.

Recent activity
In 2005, drummer Ty Smith left Guttermouth and was replaced by Ryan Farrell. Bass player Kevin Clark departed the following year and founding member Clint Weinrich returned to the group. This lineup recorded the band's tenth album Shave the Planet, released in 2006 by Volcom Entertainment. The album found the band once again using their brand of humorous punk rock to poke fun at a number of subjects. Although Weinrich remains a member of the band, Clark has since rejoined the group and handles most of the touring. In June 2008, Farrell announced that Sheldon had left the band to focus on his family, having recently had a fourth child. The band's official Myspace profile lists Sheldon's replacement as Dave Luckett, with Donald Horne being replaced by Hunter Munich. In December 2008, Adkins announced that the band had returned to Hopeless Records, one of their first record labels, in celebration of their 20th Anniversary, and that Guttermouth is working on a new album. A further line-up change occurred in 2009, when Munich was replaced by Brandon Zinkil.

After a hiatus and further controversy on a 2013 tour, singer Adkins moved to Mexico and reformed the band in 2015.

Guttermouth with Bird Attack Records and Rude Records released Got it Made, a six-song EP, on July 15, 2016. The band followed up with another studio EP titled New Car Smell in 2017, along with a live recording titled The Whole Enchilada. Those two releases were also under the Bird Attack Records and Rude Records labels.

Guttermouth completed a successful tours of Australia in 2023 and 2024, and returned to touring in Florida and both Northern and Southern California.

Band members
Current members
 * Mark Adkins – vocals and MC (1989–present)
 * Justin Van Westbroek – bass (2009–2015, 2017–2018), drums (2015–2017), guitar (2018–present)
 * Matt Wills – guitar (2010–present)
 * AJ Condosta – drums (2017–present)
 * Taylor Beckemeyer – bass (2017–present)

Past members
 * Eric "Derek" Davis – guitar (1989–2004)
 * Scott Sheldon – guitar, keyboards (1989–2008)
 * Clint "Cliff" Weinrich – bass (1989–1995, 2002–2004 )
 * James Nunn (aka Captain/Admiral James T. Nunn) – drums (1989–1999), bass (1999–2001)
 * Steve "Stever" Rapp – bass (1995–1999)
 * William Tyler "Ty" Smith (credited as T. Bradford on Gorgeous) – drums (1999–2005)
 * Donald "Don" Horne – guitar (2004–2008)
 * Ryan Farrell – drums (2005–2011)
 * Dave Luckett – guitar (2008–2013)
 * Kevin Clark – bass (2004–2009, 2015–2017)
 * Hunter Munich – guitar (2008–2009)
 * Brandon Zinkil – guitar (2009–2010)
 * Alex Flamsteed – drums (2011–2015)
 * Geoff Armstrong – guitar (2013–2018)
 * Donnie Barnes - guitar (2018)

Former touring musicians
 * Chad Billhook – bass (2013–2014)
 * Adam the Woo (Adam Williams) – bass (2014)

Discography

 * Studio albums
 * Full Length LP (1991)
 * Friendly People (1994)
 * Teri Yakimoto (1996)
 * Musical Monkey (1997)
 * Gorgeous (1999)
 * Covered with Ants (2001)
 * Gusto (2002)
 * Eat Your Face (2004)
 * Shave the Planet (2006)

title: Guttermouth


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Gusto (album)

Gusto is the seventh album by California pop punk band Guttermouth, released in 2002 by Epitaph Records. It found the band taking their style of fast, abrasive punk rock in new directions, experimenting with elements of pop and other styles. Their usual tongue-in-cheek humor and sarcastic lyrics remain intact, but the album's overall sound is quite different from any of their others. This was due partly to a lineup change: founding member and frequent songwriter James Nunn had left the group the previous year, leaving guitarists Scott Sheldon and Eric Davis to fill in on bass, along with studio bassist Hedge. The album received generally poor reviews from both critics and longtime fans, and would later be regarded by the band as somewhat of a failed experiment.

Track listing
All songs written by Guttermouth.
 * 1) "Camp Fire Girl #62" 2:55
 * 2) "Scholarship in Punk" 2:15
 * 3) "Gusto" 2:13
 * 4) "Vacation" 2:52
 * 5) "Contagious" 2:51
 * 6) "Pee in the Shower" 2:29
 * 7) "Walk of Shame" 2:34
 * 8) "My Town" 2:36
 * 9) "Contribution" 2:17
 * 10) "Foot-Long" 1:56
 * 11) "Looking Out for #1" 1:48
 * 12) "Twins" 2:09
 * 13) "My Girlfriend" 2:35
 * 14) "Lemon Water" 3:19

Performers

 * Mark Adkins – vocals
 * Scott Sheldon – guitar, bass, guiro, backing vocals
 * Eric "Derek" Davis – guitar, bass, keyboards, vocals
 * Hedge – bass (tracks 1, 2, 5, 6 & 11)
 * William Tyler "Ty" Smith – drums
 * Eric Mayron – vocals on "Lemon Water"
 * Emily "Agent M" Whitehurst (Tsunami Bomb) – backing vocals on "My Town" and "Twins"

Album information

 * Record label: Epitaph Records
 * Recorded at Paramount Studios and Can Am Studios
 * Mixed at Paramount Studios by Jim Goodwin
 * Mastered by Gene Grimaldi at Oasis Mastering
 * Produced by Scott Sheldon, Eric Davis, Jim Goodwin, and Mark Adkins
 * All songs by Guttermouth
 * Art by Mark Adkins
 * Layout by C. Martin

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Gusto (album)


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Dexter Holland

Bryan Keith "Dexter" Holland (born December 29, 1965) is an American musician, singer, songwriter, virologist, and businessman. He is best known as the co-founder, lead vocalist, rhythm guitarist, main songwriter and composer, and only constant member of the rock band the Offspring. He is also the co-founder and former owner of the record label Nitro Records, creator of the hot sauce Gringo Bandito, and holds a PhD in molecular biology.

Early life
Bryan Keith Holland was born in Garden Grove, California, on December 29, 1965. He attended Pacifica High School in Garden Grove, graduating as class valedictorian in 1984. He was the best student in his year at mathematics, which he found "just as exciting as punk rock". He acquired the nickname "Dexter" for his academic prowess, taken from the slang term "Poindexter".

Holland attended the University of Southern California, where he earned a BSc in biology and an MSc in molecular biology. He suspended his studies to focus on music when the Offspring found success in 1994, but later resumed and earned a PhD in molecular biology in May 2017. He defended his thesis, "Discovery of mature microRNA sequences within the protein-coding regions of global HIV-1 genomes: predictions of novel mechanisms for viral infection and pathogenicity", under doctoral advisors Suraiya Rasheed and Bob Baker.

Music
In 1984, Holland started a punk band named Manic Subsidal with his friend and cross-country teammate Greg K. Holland played the drums. The band was formed when they failed to get into a Social Distortion concert. After James Lilja was hired as their drummer, Holland switched to vocals and guitars. Noodles then joined on guitar, and Manic Subsidal changed their name to the Offspring in 1986. After recording a demo in 1988, the Offspring signed a deal with a small-time label, Nemesis Records, for whom they recorded their first full-length album, The Offspring, in March 1989. This album would eventually be re-issued in 1995, by Holland's own record label, Nitro Records.

In 1991, the Offspring signed with Epitaph Records (home of Bad Religion, L7, NOFX, Pennywise and other similar bands). Their first release on the label was Ignition, which was released in 1992. Their last album for that label was 1994's Smash, which still holds the world record for most sales of an album on an independent label. The band then signed with Columbia Records in 1996 (after Brett Gurewitz, owner of Epitaph and guitarist for Bad Religion, sold the contract to Columbia, Holland claims) for whom they released their next six albums, Ixnay on the Hombre (1997), Americana (1998), Conspiracy of One (2000), Splinter (2003), Rise and Fall, Rage and Grace (2008) and Days Go By (2012). The albums, Let The Bad Times Roll (2021) and Supercharged (2024) were released on Concord Records. Holland is one of the two members (along with Noodles) to appear on all of The Offspring's albums, and as of Greg K.'s split from the band in November 2018, he is the only remaining original member left.

Holland sometimes plays the piano during live shows. Occasionally the band plays "Gone Away", with only Holland playing the song on piano. Holland sings in the tenor range.

He is also one of the co-founders of the record label Nitro Records, which he operated from 1994 to 2013, along with former bandmate Greg K.

Science

In a 1995 interview, Holland said that he would rather be a professor at a university than play music by the time he turns 40.

Holland was a doctoral student at the Laboratory of Viral Oncology and Proteomics Research, Keck School of Medicine, where he was supervised by Professor Suraiya Rasheed. In March 2013, Holland and co-authors published a paper in PLoS One regarding microRNA in HIV genomes, titled "Identification of Human MicroRNA-Like Sequences Embedded within the Protein-Encoding Genes of the Human Immunodeficiency Virus". The original academic paper describes the use of computational molecular biological (in silico) approaches to identify microRNA-like sequences in HIV. These sequences are suggested to have evolved to self-regulate survival of the virus in the host by evading its immune responses and thus influence the persistence, replication, and pathogenicity of HIV. Holland was awarded his Ph.D. in molecular biology during the USC Commencement on May 12, 2017.

Business
In 2004, Holland launched his own brand of hot sauce called Gringo Bandito. The label depicts Holland with bandoliers, revolvers, a sombrero and shades, a design that OC Weekly magazine described as parodying the logo for Tapatío hot sauce or Pancho Villa. Holland, who grew up in Southern California where Mexican cuisine is considered a "part of the way of life", wondered "if [he] could do [a hot sauce] better".

On the conception of the hot sauce, Holland states that in the early 2000s, while eating Mexican food, he began to read the label of a bottle of Tapatío; "It just clicked that I had to make one. People who like hot sauce are a certain type of people. They're passionate. They'll have a bottle with them wherever they go. I'm one of those people. And when I'm into something, I really get into it. It's like my music—I liked records, so I learned how to play a guitar. After that? A band."

It has sold over a million bottles and is available in over 500 restaurants and 7,000 stores, including being a top-ranked hot sauce on Amazon.

The headquarters for Gringo Bandito are located in a Huntington Beach industrial park, next to the Offspring's recording studio.

Philanthropy
In 1997, Holland and former Dead Kennedys singer Jello Biafra teamed up to form the FSU Foundation, which raised funds through charity concerts. The foundation organized benefit shows to raise money for various charities including AIDS Project Los Angeles, Poor People's United Fund, Trees Foundation, and Amnesty International.

Holland participated in the Los Angeles Marathon in 2006 and 2008 with his charity of choice being the Innocence Project, a non-profit legal clinic that handles legal cases where post-conviction DNA testing can yield conclusive proof of innocence.

Artistry
Holland's early musical influences include Aerosmith, the Beatles, the Sex Pistols, the Ramones, KISS, Bob Marley, Queen, and the Rolling Stones.

All of Holland's Ibanez RG body guitars are made out of mahogany and fitted with DiMarzio Super Distortion bridge pickups. During their latest recordings, Holland used a vintage Gibson SG Junior. He plays through a Mesa Boogie Dual Rectifier.

Personal life
Holland met hair stylist Kristine Luna in 1992, and they were married in 1995. She co-wrote the Offspring song "Session" and appeared in the music video for "I Choose". They divorced in 2012. He married Amber Sasse in 2013. His daughter from a previous relationship, Alexa (born 1986), is also a musician and goes by the stage name Lex Land.

A licensed aircraft pilot, Holland completed a 10-day solo flight around the world in November 2004. He also enjoys surfing and collecting postage stamps from the Isle of Man.

The Offspring
''All Offspring albums. For a complete list, see the Offspring discography''.

 * The Offspring (1989)
 * Ignition (1992)
 * Smash (1994)
 * Ixnay of the Hombre (1997)
 * Americana (1998)
 * Conspiracy of One (2000)
 * Splinter (2003)
 * Rise and Fall, Rage and Grace (2008)
 * Days Go By (2012)
 * Let the Bad Times Roll (2021)
 * Supercharged (2024)

Guest appearances

 * The Vandals – Hitler Bad, Vandals Good (1998) (co-wrote "Too Much Drama")
 * AFI – Black Sails in the Sunset (1999) (Backing vocals on "Clove Smoke Catharsis", "The Prayer Position" and "God Called in Sick Today")
 * The Aquabats – The Aquabats vs. the Floating Eye of Death! (1999) (co-wrote "Amino Man!")
 * The Vandals – Look What I Almost Stepped In... (2000) (co-wrote "Jackass" and does backing vocals on that song)
 * Dwarves – The Dwarves Must Die (2004) (Backing vocals on "Salt Lake City" and "Massacre")
 * Puffy AmiYumi – Splurge (2006) (co-wrote "Tokyo I'm on My Way ")
 * Ron Emory – Walk That Walk (2010) (backing vocals on "I'm Not Alone")
 * Dwarves – The Dwarves Are Born Again (2011) (Backing vocals on "Looking Out for Number One" and "Happy Birthday Suicide")
 * Dwarves – The Dwarves Invented Rock & Roll (2014) (backing vocals)
 * Dwarves – Take Back the Night (2018) (sings on "Julio")

Holland has also made cameo appearances in:
 * Idle Hands (Movie, 1999) as Band lead singer (with The Offspring)
 * Pauly Shore Is Dead (Movie, 2003) as Gas Station Guy
 * Punk's Not Dead (Documentary, 2007) as himself
 * One Nine Nine Four (Documentary, 2009) as himself
 * The Damned: Don't You Wish That We Were Dead (Documentary, 2015) as himself
 * The Last Sharknado: It's About Time (Movie, 2018) as British Captain

title: Dexter Holland


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ECMAScript

ECMAScript (ES) is a standard for scripting languages, including JavaScript, JScript, and ActionScript. It is best known as a JavaScript standard intended to ensure the interoperability of web pages across different web browsers. It is standardized by Ecma International in the document ECMA-262.

ECMAScript is commonly used for client-side scripting on the World Wide Web, and it is increasingly being used for server-side applications and services using runtime environments - Node.js, deno and bun.

ECMAScript, ECMA-262, JavaScript
ECMA-262, or the ECMAScript Language Specification, defines the ECMAScript Language, or just ECMAScript. ECMA-262 specifies only language syntax and the semantics of the core application programming interface (API), such as Array, Function, and globalThis, while valid implementations of JavaScript add their own functionality such as input/output and file system handling.

History
The ECMAScript specification is a standardized specification of a scripting language developed by Brendan Eich of Netscape; initially named Mocha, then LiveScript, and finally JavaScript. In December 1995, Sun Microsystems and Netscape announced JavaScript in a press release. In November 1996, Netscape announced a meeting of the Ecma International standards organization to advance the standardization of JavaScript. The first edition of ECMA-262 was adopted by the Ecma General Assembly in June 1997. Several editions of the language standard have been published since then. The name "ECMAScript" was a compromise between the organizations involved in standardizing the language, especially Netscape and Microsoft, whose disputes dominated the early standards sessions. Eich commented that "ECMAScript was always an unwanted trade name that sounds like a skin disease." ECMAScript has been formalized through operational semantics by work at Stanford University and the Department of Computing, Imperial College London for security analysis and standardization. "ECMA" stood for "European Computer Manufacturers Association" until 1994.

Features
The ECMAScript language includes structured, dynamic, functional, and prototype-based features.

Imperative and structured
ECMAScript JavaScript supports C-style structured programming. Previously, JavaScript only supported function scoping using the keyword, but ECMAScript 2015 added the keywords   and  , allowing JavaScript to support both block scoping and function scoping. JavaScript supports automatic semicolon insertion, meaning that semicolons that normally terminate a statement in C may be omitted in JavaScript.

Like C-style languages, control flow is done with the, , / ,  / , and  statements. Functions are weakly typed and may accept and return any type. Arguments not provided default to.

Weakly typed
ECMAScript is weakly typed. This means that certain types are assigned implicitly based on the operation being performed. However, there are several quirks in JavaScript's implementation of the conversion of a variable from one type to another. These quirks have been the subject of a talk entitled Wat.

Dynamic
ECMAScript is dynamically typed. Thus, a type is associated with a value rather than an expression. ECMAScript supports various ways to test the type of objects, including duck typing.

Transpiling
Since ES 2015, transpiling JavaScript has become very common. Transpilation is a source-to-source compilation in which newer versions of JavaScript are used, and a transpiler rewrites the source code so that it is supported by older browsers. Usually, transpilers transpile down to ES3 to maintain compatibility with all versions of browsers. The settings to transpile to a specific version can be configured according to need. Transpiling adds an extra step to the build process and is sometimes done to avoid needing polyfills. Polyfills create new features for older environments that lack them. Polyfills do this at runtime in the interpreter, such as the user's browser or on the server. Instead, transpiling rewrites the ECMA code itself during the build phase of development before it reaches the interpreter.

Conformance
In 2010, Ecma International started developing a standards test for Ecma 262 ECMAScript. Test262 is an ECMAScript conformance test suite that can be used to check how closely a JavaScript implementation follows the ECMAScript Specification. The test suite contains thousands of individual tests, each of which tests some specific requirement(s) of the ECMAScript specification. The development of Test262 is a project of the Ecma Technical Committee 39 (TC39). The testing framework and the individual tests are contributed to Ecma by member organizations of TC39.

Important contributions were made by Google (Sputnik test suite) and Microsoft, who both contributed thousands of tests. The Test262 test suite consisted of $38,014$ tests. ECMAScript specifications through ES7 are well-supported in major web browsers. The table below shows the conformance rate for current versions of software with respect to the most recent editions of ECMAScript.

title: ECMAScript


text:
Talk:ECMAScript

Influenced by CoffeeScript
the infobox claims "Influenced by: CoffeeScript", which, given there's not a single mention of that anywhere on the page nor this discussion, sounds a bit weird, especially given CoffeeScript is both way younger than ECMAScript, and a language that's designed to extend/modify and compile to it?

46.92.182.139 (talk) 08:30, 12 September 2021 (UTC)

 * Well, I think it's because newer versions of ECMAScript have features (like optional chaining) that are inspired by CoffeeScript's syntax.  AltoStev  Talk 13:46, 15 September 2021 (UTC)

Missing history
The introduction in https://tc39.es/ecma262/ has some information not included in this article. It's a primary source but there should be others...

Some quotes:

"Focused development of the sixth edition started in 2009, as the fifth edition was being prepared for publication. However, this was preceded by significant experimentation and language enhancement design efforts dating to the publication of the third edition in 1999."

"ECMAScript 2016 was the first ECMAScript edition released under Ecma TC39's new yearly release cadence and open development process"  AltoStev  Talk 13:50, 15 September 2021 (UTC)

title: Talk:ECMAScript


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Micropsia

Micropsia is a condition affecting human visual perception in which objects are perceived to be smaller than they actually are. Micropsia can be caused by optical factors (such as wearing glasses), by distortion of images in the eye (such as optically, via swelling of the cornea or from changes in the shape of the retina such as from retinal edema, macular degeneration, or central serous retinopathy), by changes in the brain (such as from traumatic brain injury, epilepsy, migraines, prescription drugs, and illicit drugs), and from psychological factors. Dissociative phenomena are linked with micropsia, which may be the result of brain-lateralization disturbance.

Micropsia is also commonly reported when the eyes are fixating at (convergence), or focusing at (accommodation), a distance closer than that of the object in accord with Emmert's law. Specific types of micropsia include hemimicropsia, a form of micropsia that is localized to one half of the visual field and can be caused by brain lesions in one of the cerebral hemispheres.

Related visual distortion conditions include macropsia, a less common condition with the reverse effect, and Alice in Wonderland syndrome, a condition that has symptoms that can include both micropsia and macropsia.

Signs and symptoms
Micropsia causes affected individuals to perceive objects as being smaller or more distant than they actually are.

The majority of individuals with micropsia are aware that their perceptions do not mimic reality. Many can imagine the actual sizes of objects and distances between objects. It is common for patients with micropsia to be able to indicate true size and distance despite their inability to perceive objects as they actually are. One specific patient was able to indicate the dimensions of specific objects with her hands. She was also able to estimate the distances between two objects and between an object and herself. She succeeded in indicating horizontal, vertical, and 45 degree positions and did not find it difficult to search for an object in a cluttered drawer, indicating that her figure-ground discrimination was intact despite having micropsia.

Individuals experiencing hemimicropsia often complain that objects in their left or right visual field appear to be shrunken or compressed. They may also have difficulty appreciating the symmetry of pictures. When drawing, patients often have a tendency to compensate for their perceptual asymmetry by drawing the left or right half of objects slightly larger than the other. In a case of one person with hemimicropsia asked to draw six symmetrical objects, the size of the picture on the left half was on average 16% larger than the corresponding right half.

Diagnosis
EEG testing can diagnose patients with medial temporal lobe epilepsy. Epileptiform abnormalities including spikes and sharp waves in the medial temporal lobe of the brain can diagnose this condition, which can in turn be the cause of an epileptic patient's micropsia.

The Amsler grid test can be used to diagnose macular degeneration. For this test, patients are asked to look at a grid, and distortions or blank spots in the patient's central field of vision can be detected. A positive diagnosis of macular degeneration may account for a patient's micropsia.

A controlled size comparison task can be employed to evaluate objectively whether a person is experiencing hemimicropsia. For each trial, a pair of horizontally aligned circles is presented on a computer screen, and the person being tested is asked to decide which circle is larger. After a set of trials, the overall pattern of responses should display a normal distance effect where the more similar the two circles, the higher the number of errors. This test is able to effectively diagnose micropsia and confirm which hemisphere is being distorted.

Due to the large range of causes that lead to micropsia, diagnosis varies among cases. Computed tomography (CT) and magnetic resonance imaging (MRI) may find lesions and hypodense areas in the temporal and occipital lobes. MRI and CT techniques are able to rule out lesions as the cause for micropsia, but are not sufficient to diagnose the most common causes.

Definition
Micropsia is the most common visual distortion, or dysmetropsia. It is categorized as an illusion in the positive phenomena grouping of abnormal visual distortions.
 * Convergence-accommodative micropsia is a physiologic phenomenon in which an object appears smaller as it approaches the subject.
 * Psychogenic micropsia can present itself in individuals with certain psychiatric disorders.
 * Retinal micropsia is characterized by an increase in the distance between retinal photoreceptors and is associated with decreased visual acuity.
 * Cerebral micropsia is a rare form of micropsia that can arise in children with chronic migraines.
 * Hemimicropsia is a type of cerebral micropsia that occurs within one half of the visual field.

Differential diagnosis
Of all of the visual distortions, micropsia has the largest variety of causes.

Migraines
Micropsia can occur during the aura phase of a migraine attack, a phase that often precedes the onset of a headache and is commonly characterized by visual disturbances. Micropsia, along with hemianopsia, quadrantopsia, scotoma, phosphene, teicopsia, metamorphopsia, macropsia, teleopsia, diplopia, dischromatopsia, and hallucination disturbances, is a type of aura that occurs immediately before or during the onset of a migraine headache. The symptom usually occurs less than thirty minutes before the migraine headache begins and lasts for five to twenty minutes. Only 10-20% of children with migraine headaches experience auras. Visual auras such as micropsia are most common in children with migraines.

Seizures
The most frequent neurological origin of micropsia is a result of temporal lobe seizures. These seizures affect the entire visual field of the patient. More rarely, micropsia can be part of purely visual seizures. This in turn only affects one half of the visual field and is accompanied by other cerebral visual disturbances. The most common cause of seizures which produce perceptual disturbances such as micropsia and macropsia is medial temporal lobe epilepsy in which the seizures originate in the amygdala-hippocampus complex. Micropsia often occurs as an aura signalling a seizure in patients with medial temporal lobe epilepsy. Most auras last for a very short period, ranging from a few seconds to a few minutes.

Drug use
Micropsia can result from the action of mescaline and other hallucinogenic drugs. Although drug-induced changes in perception usually subside as the chemical leaves the body, long-term cocaine use can result in the chronic residual effect of micropsia. Micropsia can be a symptom of Hallucinogen Persisting Perception Disorder, or HPPD, in which a person can experience hallucinogenic flashbacks long after ingesting a hallucinogen. A majority of these flashbacks are visual distortions which include micropsia, and 15-80% of hallucinogen users may experience these flashbacks. Micropsia can also be a rare side effect of zolpidem, a prescription medication used to temporarily treat insomnia.

Psychological factors
Psychiatric patients may experience micropsia in an attempt to distance themselves from situations involving conflict. Micropsia may also be a symptom of psychological conditions in which patients visualize people as small objects as a way to control others in response to their insecurities and feelings of weakness. In some adults who experienced loneliness as children, micropsia may arise as a mirror of prior feelings of separation from people and objects.

Epstein-Barr virus infection
Micropsia can be caused by swelling of the cornea due to infection by the Epstein-Barr virus (EBV) and can therefore present as an initial symptom of EBV mononucleosis, a disease caused by Epstein-Barr virus infection.

Retinal edema
Micropsia can result from retinal edema causing a dislocation of the receptor cells. Photoreceptor misalignment seems to occur following the surgical re-attachment for macula-off rhegmatogenous retinal detachment. After surgery, patients may experience micropsia as a result of larger photoreceptor separation by edematous fluid.

Macular degeneration
Macular degeneration typically produces micropsia due to the swelling or bulging of the macula, an oval-shaped yellow spot near the center of the retina in the human eye. The main factors leading to this disease are age, smoking, heredity, and obesity. Some studies show that consuming spinach or collard greens five times a week cuts the risk of macular degeneration by 43%.

Central serous chorioretinopathy
CSCR is a disease in which a serous detachment of the neurosensory retina occurs over an area of leakage from the choriocapillaris through the retinal pigment epithelium (RPE). The most common symptoms that result from the disease are a deterioration of visual acuity and micropsia.

Brain lesions
Micropsia is sometimes seen in individuals with brain infarctions. The damaged side of the brain conveys size information that contradicts the size information conveyed by the other side of the brain. This causes a contradiction to arise between the true perception of an object's size and the smaller perception of the object, and micropsic bias ultimately causes the individual to experience micropsia. Lesions affecting other parts of the extracerebral visual pathways can also cause micropsia.

Treatment
Treatment varies for micropsia due to the large number of different causes for the condition.

Treatments involving the occlusion of one eye and the use of a prism fitted over an eyeglass lens have both been shown to provide relief from micropsia.

Micropsia that is induced by macular degeneration can be treated in several ways. A study called AREDS (age-related eye disease study) determined that taking dietary supplements containing high-dose antioxidants and zinc produced significant benefits with regard to disease progression. This study was the first ever to prove that dietary supplements can alter the natural progression and complications of a disease state. Laser treatments also look promising but are still in clinical stages.

Epidemiology
Episodes of micropsia or macropsia occur in 9% of adolescents.

10-35% of those with migraines experience auras, with 88% of these patients experiencing both visual auras (which include micropsia) and neurological auras.

Micropsia seems to be slightly more common in boys than in girls among children who experience migraines.

Approximately 80% of temporal lobe seizures produce auras that may lead to micropsia or macropsia. They are a common feature of simple partial seizures and usually precede complex partial seizures of temporal lobe origin.

Central Serous Chorioretinopathy (CSCR) which can produce micropsia predominantly affects persons between the ages of 20 and 50. Women appear to be affected more than men by a factor of almost 3 to 1.

Comparison with Alice's Adventures in Wonderland
Alice in Wonderland Syndrome, a neurological condition associated with both micropsia and macropsia, is named after Lewis Carroll's famous 19th century novel Alice's Adventures in Wonderland. In the story, the title character, Alice, experiences numerous situations similar to those of micropsia and macropsia. Speculation has arisen that Carroll may have written the story using his own direct experience with episodes of micropsia resulting from the numerous migraines he was known to have. It has also been suggested that Carroll may have had temporal lobe epilepsy.

Comparison with Gulliver's Travels
Micropsia has also been related to Jonathan Swift's novel Gulliver's Travels. It has been referred to as "Lilliput sight" and "Lilliputian hallucination," a term coined by British physician Raoul Leroy in 1909, based on the small people that inhabited the island of Lilliput in the novel.

Research
Current experimental evidence focuses on the involvement of the occipitotemporal pathway in both the perceptual equivalence of objects across translations of retinal position and also across size modifications. Recent evidence points to this pathway as a mediator for an individual's perception of size. Even further, numerous cases suggest that size perception may be dissociated from other aspects of visual perception such as color and movement. However, more research is called for to correctly relate the condition to defined physiological conditions.

Current research is being done on macular degeneration which could help prevent cases of micropsia. A variety of drugs that block vascular endothelial growth factors (VEGFs) are being evaluated as a treatment option. These treatments for the first time have produced actual improvements in vision, rather than simply delaying or arresting the continued loss of vision characteristic of macular degeneration. A number of surgical treatments are also being investigated for macular degeneration lesions that may not qualify for laser treatment, including macular translocation to a healthier area of the eye, displacement of submacular blood using gas, and removing membranes by surgery.

title: Micropsia


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Human papillomavirus infection

Human papillomavirus infection (HPV infection) is caused by a DNA virus from the Papillomaviridae family. Many HPV infections cause no symptoms and 90% resolve spontaneously within two years. In some cases, an HPV infection persists and results in either warts or precancerous lesions. These lesions, depending on the site affected, increase the risk of cancer of the cervix, vulva, vagina, penis, anus, mouth, tonsils, or throat. Nearly all cervical cancer is due to HPV, and two strains – HPV16 and HPV18 – account for 70% of all cases. HPV16 is responsible for almost 90% of HPV-positive oropharyngeal cancers. Between 60% and 90% of the other cancers listed above are also linked to HPV. HPV6 and HPV11 are common causes of genital warts and laryngeal papillomatosis.

An HPV infection is caused by the human papillomavirus, a DNA virus from the papillomavirus family. Over 200 types have been described. An individual can become infected with more than one type of HPV, and the disease is only known to affect humans. More than 40 types may be spread through sexual contact and infect the anus and genitals. Risk factors for persistent infection by sexually transmitted types include early age of first sexual intercourse, multiple sexual partners, smoking, and poor immune function. These types are typically spread by sustained direct skin-to-skin contact, with vaginal and anal sex being the most common methods. HPV infection can also spread from a mother to baby during pregnancy. There is no evidence that HPV can spread via common items like toilet seats, but the types that cause warts may spread via surfaces such as floors. HPV is not killed by common hand sanitizers and disinfectants, increasing the possibility of the virus being transferred via non-living infectious agents called fomites.

HPV vaccines can prevent the most common types of infection. To be most effective, inoculation should occur before the onset of sexual activity, and are therefore recommended between the ages of 9–13 years. Cervical cancer screening, such as the Papanicolaou test ("pap smear"), or examination of the cervix after applying acetic acid, can detect both early cancer and abnormal cells that may develop into cancer. Screening allows for early treatment which results in better outcomes. Screening has reduced both the number of cases and the number of deaths from cervical cancer. Genital warts can be removed by freezing.

Nearly every sexually active individual is infected by HPV at some point in their lives. HPV is the most common sexually transmitted infection (STI), globally. High-risk HPVs cause about 5% of all cancers worldwide and about 37,300 cases of cancer in the United States each year. Cervical cancer is among the most common cancers worldwide, causing an estimated 604,000 new cases and 342,000 deaths in 2020. About 90% of these new cases and deaths of cervical cancer occurred in low- and middle-income countries. Roughly 1% of sexually active adults have genital warts. Cases of skin warts have been described since the time of ancient Greece, but that they were caused by a virus was not determined until 1907.

HPV types
HPV is a group of more than 200 related viruses, which are designated by a number for each virus type. Some HPV types, such as HPV5, may establish infections that persist for the lifetime of the individual without ever manifesting any clinical symptoms. HPV types 1 and 2 can cause common warts in some infected individuals. HPV types 6 and 11 can cause genital warts and laryngeal papillomatosis.

Many HPV types are carcinogenic. About twelve HPV types (including types 16, 18, 31, and 45) are called "high-risk" types because persistent infection has been linked to cancer of the oropharynx, larynx, vulva, vagina, cervix, penis, and anus. These cancers all involve sexually transmitted infection of HPV to the stratified epithelial tissue. HPV type 16 is the strain most likely to cause cancer and is present in about 47% of all cervical cancers, and in many vaginal and vulvar cancers, penile cancers, anal cancers, and cancers of the head and neck.

The table below lists common symptoms of HPV infection and the associated types of HPV.

Available HPV vaccines protect against either two, four, or nine types of HPV. There are six prophylactic HPV vaccines licensed for use: the bivalent vaccines Cervarix, Cecolin, and Walrinvax; the quadrivalent vaccines Cervavax and Gardasil; and the nonavalent vaccine Gardasil 9. All HPV vaccines protect against at least HPV types 16 and 18, which cause the greatest risk of cervical cancer. The quadrivalent vaccines also protect against HPV types 6 and 11. The nonavalent vaccine Gardasil 9 provides protection against those four types (6, 11, 16, and 18), along with five other high-risk HPV types responsible for 20% of cervical cancers (types 31, 33, 45, 52, and 58).

Warts
Skin infection ("cutaneous" infection) with HPV is very widespread. Skin infections with HPV can cause noncancerous skin growths called warts (verrucae). Warts are caused by a rapid growth of cells on the outer layer of the skin. While cases of warts have been described since the time of ancient Greece, their viral cause was not known until 1907.

Skin warts are most common in childhood and typically appear and regress spontaneously over the course of weeks to months. Recurring skin warts are common. All HPVs are believed to be capable of establishing long-term "latent" infections in small numbers of stem cells present in the skin. Although these latent infections may never be fully eradicated, immunological control is thought to block the appearance of symptoms such as warts. Immunological control is HPV type-specific, meaning an individual may become resistant to one HPV type while remaining susceptible to other types.

Types of warts include: Common, flat, and plantar warts are much less likely to spread from person to person.
 * Common warts are usually found on the hands and feet, but can also occur in other areas, such as the elbows or knees. Common warts have a characteristic cauliflower-like surface and are typically slightly raised above the surrounding skin. Cutaneous HPV types can cause genital warts but are not associated with the development of cancer.
 * Plantar warts are found on the soles of the feet; they grow inward, generally causing pain when walking.
 * Subungual or periungual warts form under the fingernail (subungual), around the fingernail, or on the cuticle (periungual). They are more difficult to treat than warts in other locations.
 * Flat warts are most commonly found on the arms, face, or forehead. Like common warts, flat warts occur most frequently in children and teens. In people with normal immune function, flat warts are not associated with the development of cancer.

Genital warts
HPV infection of the skin in the genital area is the most common sexually transmitted infection worldwide. Such infections are associated with genital or anal warts (medically known as condylomata acuminata or venereal warts), and these warts are the most easily recognized sign of genital HPV infection.

The strains of HPV that can cause genital warts are usually different from those that cause warts on other parts of the body, such as the hands or feet, or even the inner thighs. A wide variety of HPV types can cause genital warts, but types 6 and 11 together account for about 90% of all cases. However, in total more than 40 types of HPV are transmitted through sexual contact and can infect the skin of the anus and genitals. Such infections may cause genital warts, although they may also remain asymptomatic.

The great majority of genital HPV infections never cause any overt symptoms and are cleared by the immune system in a matter of months. Moreover, people may transmit the virus to others even if they do not display overt symptoms of infection. Most people acquire genital HPV infections at some point in their lives, and about 10% of women are currently infected. A large increase in the incidence of genital HPV infection occurs at the age when individuals begin to engage in sexual activity. As with cutaneous HPVs, immunity to genital HPV is believed to be specific to a specific strain of HPV.

Laryngeal papillomatosis
In addition to genital warts, infection by HPV types 6 and 11 can cause a rare condition known as recurrent laryngeal papillomatosis, in which warts form on the larynx or other areas of the respiratory tract. These warts can recur frequently, may interfere with breathing, and in extremely rare cases can progress to cancer. For these reasons, repeated surgery to remove the warts may be advisable.

Case statistics
Cervical cancer is among the most common cancers worldwide, causing an estimated 604,000 new cases and 342,000 deaths in 2020. About 90% of these new cases and deaths of cervical cancer occurred in low- and middle-income countries, where screening tests and treatment of early cervical cell changes are not readily available.

In the United States, about 37,300 cases of cancer due to HPV occur each year.

Cancer development
In some infected individuals, their immune systems may fail to control HPV. Lingering infection with high-risk HPV types, such as types 16, 18, 31, and 45, can favor the development of cancer. Co-factors such as cigarette smoke can also enhance the risk of such HPV-related cancers.

HPV is believed to cause cancer by integrating its genome into nuclear DNA. Some of the early genes expressed by HPV, such as E6 and E7, act as oncogenes that promote tumor growth and malignant transformation. HPV genome integration can also cause carcinogenesis by promoting genomic instability associated with alterations in DNA copy number.

E6 produces a protein (also called E6) that simultaneously binds to two host cell proteins called p53 and E6-Associated Protein (E6-AP). E6AP is an E3 Ubiquitin ligase, an enzyme whose purpose is to tag proteins with a post-translational modification called Ubiquitin. By binding both proteins, E6 induces E6AP to attach a chain of ubiquitin molecules to p53, thereby flagging p53 for proteosomal degradation. Normally, p53 acts to prevent cell growth and promotes cell death in the presence of DNA damage. p53 also upregulates the p21 protein, which blocks the formation of the cyclin D/Cdk4 complex, thereby preventing the phosphorylation of retinoblastoma protein (RB), and in turn, halting cell cycle progression by preventing the activation of E2F. In short, p53 is a tumor-suppressor protein that arrests the cell cycle and prevents cell growth and survival when DNA damage occurs. Thus, the degradation of p53, induced by E6, promotes unregulated cell division, cell growth and cell survival, all characteristics of cancer.

It is important to note, that while the interaction between E6, E6AP and p53 was the first to be characterized, there are multiple other proteins in the host cell which interact with E6 and assist the induction of cancer.

Squamous cell carcinoma of the skin
Studies have also shown a link between a wide range of HPV types and squamous cell carcinoma of the skin. In such cases, in vitro studies suggest that the E6 protein of the HPV virus may inhibit apoptosis induced by ultraviolet light.

Cervical cancer
Nearly all cases of cervical cancer are associated with HPV infection, with two types, HPV16 and HPV18, present in 70% of cases. In 2012, twelve HPV types were considered carcinogenic for cervical cancer by the International Agency for Research on Cancer: 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, and 59. One study found that 74% of squamous cell carcinomas and 78% of adenocarcinomas tested positive for HPV types 16 or 18. Persistent HPV infection increases the risk for developing cervical carcinoma. Individuals who have an increased incidence of these types of infection are women with HIV/AIDS, who are at a 22-fold increased risk of cervical cancer.

The carcinogenic HPV types in cervical cancer belong to the alphapapillomavirus genus and can be grouped further into HPV clades. The two major carcinogenic HPV clades, alphapapillomavirus-9 (A9) and alphapapillomavirus-7 (A7), contain HPV16 and HPV18, respectively. These two HPV clades were shown to have different effects on tumour molecular characteristics and patient prognosis, with clade A7 being associated with more aggressive pathways and an inferior prognosis.

In 2020, about 604,000 new cases and 342,000 deaths from cervical cancer occurred worldwide. Around 90% of these occurred in the developing world.

Most HPV infections of the cervix are cleared rapidly by the immune system and do not progress to cervical cancer (see below the Clearance subsection in Virology). Because the process of transforming normal cervical cells into cancerous ones is slow, cancer occurs in people having been infected with HPV for a long time, usually over a decade or more (persistent infection). Furthermore, both the HPV infection and cervical cancer drive metabolic modifications that may be correlated with the aberrant regulation of enzymes related to metabolic pathways.

Non-European (NE) HPV16 variants are significantly more carcinogenic than European (E) HPV16 variants.

Anal cancer
The risk for anal cancer is 17 to 31 times higher among HIV-positive individuals who were coinfected with high-risk HPV, and 80 times higher for particularly HIV-positive men who have sex with men.

Anal Pap smear screening for anal cancer might benefit some subpopulations of men or women engaging in anal sex. No consensus exists, though, that such screening is beneficial, or who should get an anal Pap smear.

Penile cancer
HPV is associated with approximately 50% of penile cancers. In the United States, penile cancer accounts for about 0.5% of all cancer cases in men. HPV16 is the most commonly associated type detected. The risk of penile cancer increases 2- to 3-fold for individuals who are infected with HIV as well as HPV.

Head and neck cancers
Oral infection with high-risk carcinogenic HPV types (most commonly HPV 16) is associated with an increasing number of head and neck cancers. This association is independent of tobacco and alcohol use.

The local percentage varies widely, from 70% in the United States to 4% in Brazil. Engaging in anal or oral sex with an HPV-infected partner may increase the risk of developing these types of cancers.

In the United States, the number of newly diagnosed, HPV-associated head and neck cancers has surpassed that of cervical cancer cases. The rate of such cancers has increased from an estimated 0.8 cases per 100,000 people in 1988 to 4.5 per 100,000 in 2012, and, as of 2021, the rate has continued to increase. Researchers explain these recent data by an increase in oral sex. This type of cancer is more common in men than in women.

The mutational profile of HPV-positive and HPV-negative head and neck cancer has been reported, further demonstrating that they are fundamentally distinct diseases.

Lung cancer
Some evidence links HPV to benign and malignant tumors of the upper respiratory tract. The International Agency for Research on Cancer has found that people with lung cancer were significantly more likely to have several high-risk forms of HPV antibodies compared to those who did not have lung cancer. Researchers looking for HPV among 1,633 lung cancer patients and 2,729 people without the lung disease found that people with lung cancer had more types of HPV than noncancer patients did, and among lung cancer patients, the chances of having eight types of serious HPV were significantly increased. In addition, expression of HPV structural proteins by immunohistochemistry and in vitro studies suggest HPV presence in bronchial cancer and its precursor lesions. Another study detected HPV in the exhaled breath condensate (EBC), bronchial brushing and neoplastic lung tissue of cases, and found a presence of an HPV infection in 16.4% of the subjects affected by nonsmall cell lung cancer, but in none of the controls. The reported average frequencies of HPV in lung cancers were 17% and 15% in Europe and the Americas, respectively, and the mean number of HPV in Asian lung cancer samples was 35.7%, with a considerable heterogeneity between certain countries and regions.

Skin cancer
In very rare cases, HPV may cause epidermodysplasia verruciformis (EV) in individuals with a weakened immune system. The virus, unchecked by the immune system, causes the overproduction of keratin by skin cells, resulting in lesions resembling warts or cutaneous horns which can ultimately transform into skin cancer, but the development is not well understood. The specific types of HPV that are associated with EV are HPV5, HPV8, and HPV14.

Transmission
Sexually transmitted HPV is divided into two categories: low-risk and high-risk. Low-risk HPVs cause warts on or around the genitals. Type 6 and 11 cause 90% of all genital warts and recurrent respiratory papillomatosis that causes benign tumors in the air passages. High-risk HPVs cause cancer and consist of about twelve identified types. Types 16 and 18 are responsible for causing most of HPV-caused cancers. These high-risk HPVs cause 5% of the cancers in the world. In the United States, high-risk HPVs cause 3% of all cancer cases in women and 2% in men.

Risk factors for persistent genital HPV infections, which increases the risk for developing cancer, include early age of first sexual intercourse, multiple partners, smoking, and immunosuppression. Genital HPV is spread by sustained direct skin-to-skin contact, with vaginal, anal, and oral sex being the most common methods. Occasionally, it can spread from manual sex or from a mother to her baby during pregnancy. HPV is difficult to remove via standard hospital disinfection techniques, and may be transmitted in a healthcare setting on re-usable gynecological equipment, such as vaginal ultrasound transducers. The period of communicability is still unknown, but probably at least as long as visible HPV lesions persist. HPV may still be transmitted even after lesions are treated and no longer visible or present.

Perinatal
Although genital HPV types can be transmitted from mother to child during birth, the appearance of genital HPV-related diseases in newborns is rare. However, the lack of appearance does not rule out asymptomatic latent infection, as the virus has proven to be capable of hiding for decades. Perinatal transmission of HPV types 6 and 11 can result in the development of juvenile-onset recurrent respiratory papillomatosis (JORRP). JORRP is very rare, with rates of about 2 cases per 100,000 children in the United States. Although JORRP rates are substantially higher if a woman presents with genital warts at the time of giving birth, the risk of JORRP in such cases is still less than 1%.

Genital infections
Genital HPV infections are transmitted primarily by contact with the genitals, anus, or mouth of an infected sexual partner.

Of the 120 known human papilloma viruses, 51 species and three subtypes infect the genital mucosa. Fifteen are classified as high-risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82), three as probable high-risk (26, 53, and 66), and twelve as low-risk (6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81, and 89).

Condoms do not completely protect from the virus because the areas around the genitals including the inner thigh area are not covered, thus exposing these areas to the infected person's skin.

Hands
Studies have shown HPV transmission between hands and genitals of the same person and sexual partners. Hernandez tested the genitals and dominant hand of each person in 25 heterosexual couples every other month for an average of seven months. She found two couples where the man's genitals infected the woman's hand with high-risk HPV, two where her hand infected his genitals, one where her genitals infected his hand, two each where he infected his own hand, and she infected her own hand. Hands were not the main source of transmission in these 25 couples, but they were significant.

Partridge reports men's fingertips became positive for high risk HPV at more than half the rate (26% per two years) as their genitals (48%). Winer reports 14% of fingertip samples from sexually active women were positive.

Non-sexual hand contact seems to have little or no role in HPV transmission. Winer found all fourteen fingertip samples from virgin women negative at the start of her fingertip study. In a separate report on genital HPV infection, 1% of virgin women (1 of 76) with no sexual contact tested positive for HPV, while 10% of virgin women reporting non-penetrative sexual contact were positive (7 of 72).

Shared objects
Sharing of possibly contaminated objects, for example, razors, may transmit HPV. Although possible, transmission by routes other than sexual intercourse is less common for female genital HPV infection. Fingers-genital contact is a possible way of transmission but unlikely to be a significant source.

Blood
Though it has traditionally been assumed that HPV is not transmissible via blood – as it is thought to only infect cutaneous and mucosal tissues – recent studies have called this notion into question. Historically, HPV DNA has been detected in the blood of cervical cancer patients. In 2005, a group reported that, in frozen blood samples of 57 sexually naive pediatric patients who had vertical or transfusion-acquired HIV infection, 8 (14.0%) of these samples also tested positive for HPV-16. This seems to indicate that it may be possible for HPV to be transmitted via blood transfusion. However, as non-sexual transmission of HPV by other means is not uncommon, this could not be definitively proven. In 2009, a group tested Australian Red Cross blood samples from 180 healthy male donors for HPV, and subsequently found DNA of one or more strains of the virus in 15 (8.3%) of the samples. However, it is important to note that detecting the presence of HPV DNA in blood is not the same as detecting the virus itself in blood, and whether or not the virus itself can or does reside in blood in infected individuals is still unknown. As such, it remains to be determined whether HPV can or cannot be transmitted via blood. This is of concern, as blood donations are not currently screened for HPV, and at least some organizations such as the American Red Cross and other Red Cross societies do not presently appear to disallow HPV-positive individuals from donating blood.

Surgery
Hospital transmission of HPV, especially to surgical staff, has been documented. Surgeons, including urologists and/or anyone in the room, is subject to HPV infection by inhalation of noxious viral particles during electrocautery or laser ablation of a condyloma (wart). There has been a case report of a laser surgeon who developed extensive laryngeal papillomatosis after providing laser ablation to patients with anogenital condylomata.

Virology
HPV infection is limited to the basal cells of stratified epithelium, the only tissue in which they replicate. The virus cannot bind to live tissue; instead, it infects epithelial tissues through micro-abrasions or other epithelial trauma that exposes segments of the basement membrane. The infectious process is slow, taking 12–24 hours for initiation of transcription. It is believed that involved antibodies play a major neutralizing role while the virions still reside on the basement membrane and cell surfaces.

HPV lesions are thought to arise from the proliferation of infected basal keratinocytes. Infection typically occurs when basal cells in the host are exposed to the infectious virus through a disturbed epithelial barrier as would occur during sexual intercourse or after minor skin abrasions. HPV infections have not been shown to be cytolytic; rather, viral particles are released as a result of degeneration of desquamating cells. HPV can survive for many months and at low temperatures without a host; therefore, an individual with plantar warts can spread the virus by walking barefoot.

HPV is a small double-stranded circular DNA virus with a genome of approximately 8000 base pairs. The HPV life cycle strictly follows the differentiation program of the host keratinocyte. It is thought that the HPV virion infects epithelial tissues through micro-abrasions, whereby the virion associates with putative receptors such as alpha integrins, laminins, and annexin A2 leading to entry of the virions into basal epithelial cells through clathrin-mediated endocytosis and/or caveolin-mediated endocytosis depending on the type of HPV. At this point, the viral genome is transported to the nucleus by unknown mechanisms and establishes itself at a copy number of 10-200 viral genomes per cell. A sophisticated transcriptional cascade then occurs as the host keratinocyte begins to divide and become increasingly differentiated in the upper layers of the epithelium.

Evolution
The phylogeny of the various strains of HPV generally reflects the migration patterns of Homo sapiens and suggests that HPV may have diversified along with the human population. Studies suggest that HPV evolved along five major branches that reflect the ethnicity of human hosts, and diversified along with the human population.

Researchers initially identified two major variants of HPV16, European (HPV16-E), and Non-European (HPV16-NE). More recent analyses based on thousands of HPV16 genomes show that indeed two major clades exist, that are further subdivided into four lineages (designated A-D) and even further subdivided into 16 sublineages (A1–4, B1–4, C1–4 and D1–4). The A1-A3 sublineages constitute the European variant, A4 the Asian variant, B1-B4 the African type I variant, C1–C4 the African type II variant, D1 the North American variant, D2 the Asian American type I variant, D3 the Asian American type II variant. The various lineages and sublineages have different oncogenic capacity, where overall, the non-European lineages are considered to increase the risk for cancer. Although HPV16 is a DNA virus, there are signs of recombination among the different lineages. Based on an analysis of more than 3600 genomes, between 0.3 and 1.2% of them could be recombinant. Thus, ideally, genotyping (for cancer-risk assessment) of HPV16 should not be based only on certain genes, but on all genes from the entire genome.

A bioinformatics tool named HPV16-Genotyper performs i) HPV16 lineage genotyping, ii) it detects potential recombination events, iii) it identifies, within the submitted sequences, mutations/SNPs that have been reported (in literature) to increase the risk for cancer.

E6/E7 proteins
The two primary oncoproteins of high risk HPV types are E6 and E7. The "E" designation indicates that these two proteins are early proteins (expressed early in the HPV life cycle), while the "L" designation indicates that they are late proteins (late expression). The HPV genome is composed of six early (E1, E2, E4, E5, E6, and E7) open reading frames (ORF), two late (L1 and L2) ORFs, and a non-coding long control region (LCR). After the host cell is infected viral early promoter is activated and a polycistronic primary RNA containing all six early ORFs is transcribed. This polycistronic RNA then undergoes active RNA splicing to generate multiple isoforms of mRNAs. One of the spliced isoform RNAs, E6*I, serves as an E7 mRNA to translate E7 protein. However, viral early transcription subjects to viral E2 regulation and high E2 levels repress the transcription. HPV genomes integrate into host genome by disruption of E2 ORF, preventing E2 repression on E6 and E7. Thus, viral genome integration into host DNA genome increases E6 and E7 expression to promote cellular proliferation and the chance of malignancy. The degree to which E6 and E7 are expressed is correlated with the type of cervical lesion that can ultimately develop.

Sometimes papillomavirus genomes are found integrated into the host genome, and this is especially noticeable with oncogenic HPVs. The E6/E7 proteins inactivate two tumor suppressor proteins, p53 (inactivated by E6) and pRb (inactivated by E7). The viral oncogenes E6 and E7 are thought to modify the cell cycle so as to retain the differentiating host keratinocyte in a state that is favourable to the amplification of viral genome replication and consequent late gene expression. E6 in association with host E6-associated protein, which has ubiquitin ligase activity, acts to ubiquitinate p53, leading to its proteosomal degradation. E7 (in oncogenic HPVs) acts as the primary transforming protein. E7 competes for retinoblastoma protein (pRb) binding, freeing the transcription factor E2F to transactivate its targets, thus pushing the cell cycle forward. All HPV can induce transient proliferation, but only strains 16 and 18 can immortalize cell lines in vitro. It has also been shown that HPV 16 and 18 cannot immortalize primary rat cells alone; there needs to be activation of the ras oncogene. In the upper layers of the host epithelium, the late genes L1 and L2 are transcribed/translated and serve as structural proteins that encapsidate the amplified viral genomes. Once the genome is encapsidated, the capsid appears to undergo a redox-dependent assembly/maturation event, which is tied to a natural redox gradient that spans both suprabasal and cornified epithelial tissue layers. This assembly/maturation event stabilizes virions, and increases their specific infectivity. Virions can then be sloughed off in the dead squames of the host epithelium and the viral lifecycle continues. A 2010 study has found that E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.
 * Role in cancer

Latency period
Once an HPV virion invades a cell, an active infection occurs, and the virus can be transmitted. Several months to years may elapse before squamous intraepithelial lesions (SIL) develop and can be clinically detected. The time from active infection to clinically detectable disease may make it difficult for epidemiologists to establish which partner was the source of infection.

Clearance
Most HPV infections are cleared up by most people without medical action or consequences. The table provides data for high-risk types (i.e. the types found in cancers).

Clearing an infection does not always create immunity if there is a new or continuing source of infection. Hernandez' 2005-6 study of 25 couples reports "A number of instances indicated apparent reinfection [from partner] after viral clearance."

Diagnosis
Over 200 types of HPV have been identified, and they are designated by numbers. They may be divided into "low-risk" and "high-risk" types. Low-risk types cause warts and high-risk types can cause lesions or cancer.

Cervical testing
Guidelines from the American Cancer Society recommend different screening strategies for cervical cancer based on a woman's age, screening history, risk factors and choice of tests. Because of the link between HPV and cervical cancer, the ACS currently recommends early detection of cervical cancer in average-risk asymptomatic adults primarily with cervical cytology by Pap smear, regardless of HPV vaccination status. Women aged 30–65 should preferably be tested every 5 years with both the HPV test and the Pap test. In other age groups, a Pap test alone can suffice unless they have been diagnosed with atypical squamous cells of undetermined significance (ASC-US). Co-testing with a Pap test and HPV test is recommended because it decreases the rate of false-negatives. According to the National Cancer Institute, "The most common test detects DNA from several high-risk HPV types, but it cannot identify the types that are present. Another test is specific for DNA from HPV types 16 and 18, the two types that cause most HPV-associated cancers. A third test can detect DNA from several high-risk HPV types and can indicate whether HPV-16 or HPV-18 is present. A fourth test detects RNA from the most common high-risk HPV types. These tests can detect HPV infections before cell abnormalities are evident.

"Theoretically, the HPV DNA and RNA tests could be used to identify HPV infections in cells taken from any part of the body. However, the tests are approved by the FDA for only two indications: for follow-up testing of women who seem to have abnormal Pap test results and for cervical cancer screening in combination with a Pap test among women over age 30."

Mouth testing
Guidelines for oropharyngeal cancer screening by the Preventive Services Task Force and American Dental Association in the U.S. suggest conventional visual examination, but because some parts of the oropharynx are hard to see, this cancer is often only detected in later stages.

The diagnosis of oropharyngeal cancer occurs by biopsy of exfoliated cells or tissues. The National Comprehensive Cancer Network and College of American Pathologists recommend testing for HPV in oropharyngeal cancer. However, while testing is recommended, there is no specific type of test used to detect HPV from oral tumors that is currently recommended by the FDA in the United States. Because HPV type 16 is the most common type found in oropharyngeal cancer, p16 immunohistochemistry is one test option used to determine if HPV is present, which can help determine course of treatment since tumors that are negative for p16 have better outcomes. Another option that has emerged as a reliable option is HPV DNA in situ hybridization (ISH) which allows for visualization of the HPV.

Testing men
There is not a wide range of tests available even though HPV is common; most studies of HPV used tools and custom analysis not available to the general public. Clinicians often depend on the vaccine among young people and high clearance rates (see Clearance subsection in Virology) to create a low risk of disease and mortality, and treat the cancers when they appear. Others believe that reducing HPV infection in more men and women, even when it has no symptoms, is important (herd immunity) to prevent more cancers rather than just treating them. Where tests are used, negative test results show safety from transmission, and positive test results show where shielding (condoms, gloves) is needed to prevent transmission until the infection clears.

Studies have tested for and found HPV in men, including high-risk types (i.e. the types found in cancers), on fingers, mouth, saliva, anus, urethra, urine, semen, blood, scrotum and penis.

The aforementioned Qiagen/Digene kit was successfully used off-label to test the penis, scrotum and anus of men in long-term relationships with women who were positive for high-risk HPV. Of these men, 60% were found to carry the virus, primarily on the penis. Similar studies have been conducted on women using cytobrushes - an endocervical brush for sampling the cervix in females - and custom analysis.

In one study researchers sampled subjects' urethra, scrotum and penis. Samples taken from the urethra added less than 1% to the HPV rate. Studies like this led Giuliano to recommend sampling the glans, shaft and crease between them, along with the scrotum, since sampling the urethra or anus added very little to the diagnosis. Dunne recommends the glans, shaft, their crease, and the foreskin.

In one study the subjects were asked not to wash their genitals for 12 hours before sampling, including the urethra as well as the scrotum and the penis. Other studies are silent on washing – a particular gap in studies of the hands.

One small study used wet cytobrushes, rather than wet the skin. It found a higher proportion of men to be HPV-positive when the skin was rubbed with a 600 grit emery paper before being swabbed with the brush, rather than swabbed with no preparation. It's unclear whether the emery paper collected the virions or simply loosened them for the swab to collect.

Studies have found self-collection (with emery paper and Dacron swabs) as effective as collection done by a clinician, and sometimes more so, since patients were more willing than a clinician to scrape vigorously. Women had similar success in self-sampling using tampons, swabs, cytobrushes and lavage.

Several studies used cytobrushes to sample fingertips and under fingernails, without wetting the area or the brush.

Other studies analyzed urine, semen, and blood and found varying amounts of HPV, but there is not a publicly available test for those yet.

Other testing
Although it is possible to test for HPV DNA in other kinds of infections, there are no FDA-approved tests for general screening in the United States or tests approved by the Canadian government, since the testing is inconclusive and considered medically unnecessary.

Genital warts are the only visible sign of low-risk genital HPV and can be identified with a visual check. These visible growths, however, are the result of non-carcinogenic HPV types. Five percent acetic acid (vinegar) is used to identify both warts and squamous intraepithelial neoplasia (SIL) lesions with limited success by causing abnormal tissue to appear white, but most doctors have found this technique helpful only in moist areas, such as the female genital tract. At this time, HPV tests for males are used only in research.

Research into testing for HPV by antibody presence has been done. The approach is looking for an immune response in blood, which would contain antibodies for HPV if the patient is HPV positive. The reliability of such tests has not been proven, as there has not been a FDA approved product as of August 2018; testing by blood would be a less invasive test for screening purposes.

Prevention
The HPV vaccines can prevent the most common types of infection. To be effective they must be used before an infection occurs and are therefore recommended between the ages of nine and thirteen. Cervical cancer screening, such as with the Papanicolaou test (pap) or looking at the cervix after using acetic acid, can detect early cancer or abnormal cells that may develop into cancer. This allows for early treatment which results in better outcomes. Screening has reduced both the number and deaths from cervical cancer in the developed world. Warts can be removed by freezing.

Vaccines
Three vaccines are available to prevent infection by some HPV types: Gardasil, Gardasil 9 and Cervarix; all three protect against initial infection with HPV types 16 and 18, which cause most of the HPV-associated cancer cases. Gardasil also protects against HPV types 6 and 11, which cause 90% of genital warts. Gardasil is a recombinant quadrivalent vaccine, whereas Cervarix is bivalent, and is prepared from virus-like particles (VLP) of the L1 capsid protein. Gardasil 9 is nonavalent, having the potential to prevent about 90% of cervical, vulvar, vaginal, and anal cancers. It can protect for HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58; the latter five cause up to 20% of cervical cancers which were not previously covered.

The vaccines provide little benefit to women already infected with HPV types 16 and 18. For this reason, the vaccine is recommended primarily for those women not yet having been exposed to HPV during sex. The World Health Organization position paper on HPV vaccination clearly outlines appropriate, cost-effective strategies for using HPV vaccine in public sector programs.

There is high-certainty evidence that HPV vaccines protect against precancerous cervical lesions in young women, particularly those vaccinated aged 15 to 26. HPV vaccines do not increase the risk of serious adverse events. Longer follow-up is needed to monitor the impact of HPV vaccines on cervical cancer.

The CDC recommends the vaccines be delivered in two shots at an interval of least 6 months for those aged 11–12, and three doses for those 13 and older. In most countries, they are funded only for female use, but are approved for male use in many countries, and funded for teenage boys in Australia. The vaccine does not have any therapeutic effect on existing HPV infections or cervical lesions. In 2010, 49% of teenage girls in the US got the HPV vaccine.

Following studies suggesting that the vaccine is more effective in younger girls than in older teenagers, the United Kingdom, Switzerland, Mexico, the Netherlands and Quebec began offering the vaccine in a two-dose schedule for girls aged under 15 in 2014.

Cervical cancer screening recommendations have not changed for females who receive HPV vaccine. It remains a recommendation that women continue cervical screening, such as Pap smear testing, even after receiving the vaccine, since it does not prevent all types of cervical cancer.

Both men and women are carriers of HPV. The Gardasil vaccine also protects men against anal cancers and warts and genital warts.

Duration of both vaccines' efficacy has been observed since they were first developed, and is expected to be longlasting.

In December 2014, the FDA approved a nine-valent Gardasil-based vaccine, Gardasil 9, to protect against infection with the four strains of HPV covered by the first generation of Gardasil as well as five other strains responsible for 20% of cervical cancers (HPV-31, HPV-33, HPV-45, HPV-52, and HPV-58).

Condoms
The Centers for Disease Control and Prevention says that male "condom use may reduce the risk for genital human papillomavirus (HPV) infection" but provides a lesser degree of protection compared with other sexual transmitted infections "because HPV also may be transmitted by exposure to areas (e.g., infected skin or mucosal surfaces) that are not covered or protected by the condom."

Disinfection
The virus is unusually hardy, and is immune to most common disinfectants. It is the first virus ever shown to be resistant to inactivation by glutaraldehyde, which is among the most common strong disinfectants used in hospitals. Diluted sodium hypochlorite bleach is effective, but cannot be used on some types of re-usable equipment, such as ultrasound transducers. As a result of these difficulties, there is developing concern about the possibility of transmitting the virus on healthcare equipment, particularly reusable gynecological equipment that cannot be autoclaved. For such equipment, some health authorities encourage use of UV disinfection or a non-hypochlorite "oxidizing‐based high‐level disinfectant [bleach] with label claims for non‐enveloped viruses", such as a strong hydrogen peroxide solution or chlorine dioxide wipes. Such disinfection methods are expected to be relatively effective against HPV.

Management
There is currently no specific treatment for HPV infection. However, the viral infection is usually cleared to undetectable levels by the immune system. According to the Centers for Disease Control and Prevention, the body's immune system clears HPV naturally within two years for 90% of cases (see Clearance subsection in Virology for more detail). However, experts do not agree on whether the virus is eliminated or reduced to undetectable levels, and it is difficult to know when it is contagious.

Follow up care is usually recommended and practiced by many health clinics. Follow-up is sometimes not successful because a portion of those treated do not return to be evaluated. In addition to the normal methods of phone calls and mail, text messaging and email can improve the number of people who return for care. As of 2015 it is unclear the best method of follow up following treatment of cervical intraepithelial neoplasia.

Epidemiology
Globally, 12% of women are positive for HPV DNA, with rates varying by age and country. The highest rates of HPV are in younger women, with a rate of 24% in women under 25 years. Rates decline in older age groups in Europe and the Americas, but less so in Africa and Asia. The rates are highest in Sub-Saharan Africa (24%) and Eastern Europe (21%) and lowest in North America (5%) and Western Asia (2%).

The most common types of HPV worldwide are HPV16 (3.2%), HPV18 (1.4%), HPV52 (0.9%), HPV31 (0.8%), and HPV58 (0.7%). High-risk types of HPV are also distributed unevenly, with HPV16 having a rate around 13% in Africa and 30% in West and Central Asia.

Like many diseases, HPV disproportionately affects low-income and resource-poor countries. The higher rates of HPV in Sub-Saharan Africa, for example, may be related to high exposure to human immunodeficiency virus (HIV) in the region. Other factors that impact the global spread of disease are sexual behaviors including age of sexual debut, number of sexual partners, and ease of access to barrier contraception, all of which vary globally.

United States
HPV is estimated to be the most common sexually transmitted infection in the United States. Most sexually active men and women will probably acquire genital HPV infection at some point in their lives. The American Social Health Association estimates that about 75–80% of sexually active Americans will be infected with HPV at some point in their lifetime. By the age of 50 more than 80% of American women will have contracted at least one strain of genital HPV. It was estimated that, in the year 2000, there were approximately 6.2 million new HPV infections among Americans aged 15–44; of these, an estimated 74% occurred to people between ages of 15 and 24. Of the STIs studied, genital HPV was the most commonly acquired. In the United States, it is estimated that 10% of the population has an active HPV infection, 4% has an infection that has caused cytological abnormalities, and an additional 1% has an infection causing genital warts.

Estimates of HPV prevalence vary from 14% to more than 90%. One reason for the difference is that some studies report women who currently have a detectable infection, while other studies report women who have ever had a detectable infection. Another cause of discrepancy is the difference in strains that were tested for.

One study found that, during 2003–2004, at any given time, 26.8% of women aged 14 to 59 were infected with at least one type of HPV. This was higher than previous estimates; 15.2% were infected with one or more of the high-risk types that can cause cancer.

The prevalence for high-risk and low-risk types is roughly similar over time.

Human papillomavirus is not included among the diseases that are typically reportable to the CDC as of 2011.

Ireland
On average 538 cases of HPV-associated cancers were diagnosed per year in Ireland during the period 2010 to 2014. Cervical cancer was the most frequent HPV-associated cancer with on average 292 cases per year (74% of the female total, and 54% of the overall total of HPV-associated cancers). A study of 996 cervical cytology samples in an Irish urban female, opportunistically screened population, found an overall HPV prevalence of 19.8%, HPV 16 at 20% and HPV 18 at 12% were the commonest high-risk types detected. In Europe, types 16 and 18 are responsible for over 70% of cervical cancers. Overall rates of HPV-associated invasive cancers may be increasing. Between 1994 and 2014, there was a 2% increase in the rate of HPV-associated invasive cancers per year for both sexes in Ireland.

As HPV is known to be associated with ano-genital warts, these are notifiable to the Health Protection Surveillance Centre (HPSC). Genital warts are the second most common STI in Ireland. There were 1,281 cases of ano-genital warts notified in 2017, which was a decrease on the 2016 figure of 1,593. The highest age-specific rate for both male and female was in the 25–29 year old age range; 53% of cases were among males.

Sri Lanka
In Sri Lanka, the prevalence of HPV is 15.5% regardless of their cytological abnormalities.

Inner Mongolia
In the Autonomous Region of Inner Mongolia overall HPV prevalence is 14.5% but shows substantial ethnical disparity, the prevalence in Mongolian women (14.9%) being much higher than that of Han participants (4.3%). Urbanization, the number of sex partners, and PAP history appear as risk factors for HPV infection in Han, but not in Mongolian women. The region is thus an important example that epidemiology of HPV is more related to cultural and ethnical factors and not to geography per se.

History
In 1972, the association of the human papillomaviruses with skin cancer in epidermodysplasia verruciformis was proposed by Stefania Jabłońska in Poland. In 1976 Harald zur Hausen published the hypothesis that human papilloma virus plays an important role in the cause of cervical cancer. In 1978, Jabłońska and Gerard Orth at the Pasteur Institute discovered HPV-5 in skin cancer. In 1983 and 1984 zur Hausen and his collaborators identified HPV16 and HPV18 in cervical cancer.

The HeLa cell line contains extra DNA in its genome that originated from HPV type 18.

Research
The Ludwig-McGill HPV Cohort is one of the world's largest longitudinal studies of the natural history of human papillomavirus (HPV) infection and cervical cancer risk. It was established in 1993 by Ludwig Cancer Research and McGill University in Montreal, Canada.

title: Human papillomavirus infection