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KI polyomavirus (also known as KI virus, KIPyV, or Human polyomavirus 3) is a virus of the family Polyomaviridae. It was discovered in 2007 in stored samples of human respiratory secretions collected by the Karolinska Institute, after which the virus is named.[1]
| Human polyomavirus 3 | |
|---|---|
Virus classification  | |
| (unranked): | Virus |
| Realm: | Monodnaviria |
| Kingdom: | Shotokuvirae |
| Phylum: | Cossaviricota |
| Class: | Papovaviricetes |
| Order: | Sepolyvirales |
| Family: | Polyomaviridae |
| Genus: | Betapolyomavirus |
| Species: | Human polyomavirus 3 |
KI virus was discovered in 2007 in samples of human respiratory secretions being systematically searched as part of a program for identifying novel human viruses. It was identified by sequence homology to known human polyomaviruses BK virus and JC virus, and simian polyomavirus SV40.[1] KI virus was the third human polyomavirus described and the first to be discovered since BK and JC in 1971.[2] A very similar respiratory virus, WU virus, was also reported later in 2007.[3]
The complete genome of the KI virus has been sequenced and found to be a circular double-stranded DNA genome of 5040 base pairs containing genetic material characteristic of polyomaviruses, encoding five viral proteins: three capsid components, major capsid protein VP1, VP2, and VP3; and two additional proteins involved in replication, the large tumor antigen and small tumor antigen.[1]
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The prevalence of KI virus as detected by the presence of its DNA in human samples is generally estimated in the 1-5% range in various locations and populations, with some indication of age-dependence.[4] The virus has been detected in the respiratory secretions of children with respiratory infections in multiple locations.[5][6] By contrast, one 2009 study placed seroprevalence - that is, prevalence of antibodies against the virus (in this case the VP1 coat protein) - as high as 55% among a population of American adults and 56% among a population of American children.[7] Another 2009 study found around 70% seroprevalence for adults, with age patterns indicating that infants may inherit maternal antibodies against both WU and KI.[8] A 2016 study of polyomavirus seroprevalence found WU virus in 91.3% of samples from another American population.[9] Primary infection is generally believed to occur in childhood.[9]
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KI virus, like its close relative WU virus, is not known to be associated with any clinical disease despite its presence in respiratory secretions.[10] The rate of co-infection with other respiratory viruses is high, so it is difficult to assign causality to KI virus even where clinical symptoms are present.[4] Some polyomaviruses are well known as carcinogenic, including the human polyomavirus Merkel cell polyomavirus, but KI virus has also not been associated with cancer.[11] While no clear association with clinical symptoms has been identified, there is weak indication that WU and KI viruses may have pathogenic potential in immunocompromised patients.[12]
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KI virus got its name from the Karolinska Institute, the institutional affiliation of the researchers who discovered and reported the virus.[1]
Among the human polyomaviruses, KI is most similar to WU virus. A 2010 proposed classification recommended the division of the polyomaviruses into three genera, containing one genus of avian viruses and two of mammalian viruses; one of the latter was designated Wukipolyomavirus to indicate its two founding members.[13] In an updated classification system for the polyomavirus family proposed in 2016, WU virus is classified as a member of the genus Betapolyomavirus along with BK, JC, and KI.[2]
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