Polyomaviridae

Polyomaviridae include only the genus Polyomavirus. The family Polyomaviridae and the close family Papillomaviridae were created by splitting the former family Papovaviridae. They were elevated to the rank of class by the International Committee on Taxonomy of Viruses (ICTV) in March 2020 as Papovaviricetes to combine the two families of papovaviruses.

The former genus Polyomavirus was split into 4 genera (alpha-delta)

Genus Alphapolyomavirus (animal pathogenic

genera Orthopolyomavirus and Wukipolyomavirus separated)

• Species Human polyomavirus 1
• (Polyomavirus hominis 1, BK virus, en. BK polyomavirus, officially human polyomavirus 1, HPyV-1, BKPyV or BKV).
• Species Human polyomavirus 2
• (Polyomavirus hominis 2, JC virus, en. JC polyomavirus, officially Human polyomavirus 2, HPyV-2, JCPyV or JCV)
• Species Human polyomavirus 3
• (Polyomavirus hominis 3, AI virus, en. KI polyomavirus, officially Human polyomavirus 3, HPyV-3, KIPyV or KIV)
• Species Human polyomavirus 4 (polyomavirus hominis 4, WU virus, en. WU polyomavirus, officially human polyomavirus 4, HPyV-4, WUPyV or WUV)
• Species Human polyomavirus 5 (Merkel cell polyomavirus, MCPyV)

Genus Gammapolyomavirus (obsolete Avipolyomavirus) only animal pathogenic

Genus Deltapolyomavirus

• Species Human polyomavirus 6 (HPyV-6)
• Species Human polyomavirus 7 (HPyV-7)
• Species Human polyomavirus 10 (HPyV-10)
• Species Human polyomavirus 11 (HPyV-11)

Approximately 40-45 nm large, non-enveloped viruses with a double-stranded, circularly convalently closed DNA genome (DNA viruses) of approximately 5000 base pairs. The nucleocapsid, which is composed of 72 capsomeres, is formed by the three structural proteins VP1,-2 and-3, with VP1 being the main capsid. The nucleocapsid encloses the covalently closed DNA ring of the viral genome, which together with cellular histones forms a nucleoprotein complex. Of the five known histones, histones H2a, H2b, H3 and H4 are found.

To adsorb to the target cell, polyomamaviruses use receptors modified with sialic acid. Accordingly, infection can be blocked by treating the target cells with neuraminidase. The viruses are taken up by endocytosis. They are transported to the nucleus by the microtubular apparatus. The polyomaviruses themselves do not possess a DNA polymerase to amplify their viral DNA. During infection, two early regulatory proteins are expressed: the large tumor antigen (LTAg) and the small tumor antigen (STAg). The so-called late structural proteins (VP1, VP2, VP3) are synthesized after the onset of viral DNA replication.

In the nucleus, newly synthesized viral genomes that have formed a mini-chromosome with cellular histones are assembled with the imported structural proteins to form new viral particles.

In the normal population, antibodies against BK virus can be detected to 100% and against JC virus to about 80%. Infection occurs in early childhood and is usually asymptomatic. Under conditions of immunosuppression (see below organ transplants, skin changes), polyomaviruses persisting in the organism can be reactivated (reactivation with virus multiplication in the blood).

The disease that then breaks out typically becomes symptomatic in two forms, especially for transplanted patients, as:

• BK virus nephropathy (polyoma virus associated kidney disease) and as
• hemorrhagic cystitis.

JC virus (JCV) causes progressive multifocal leukoencephalopathy (PML) in cellular immunocompromised individuals (e.g., HIV-infected individuals, e.g., psoriatic patients treated long-term with efalizumab). PML is almost always fatal.

1. Imperiale MJ et al (2016) Polyomavirus Persistence. Annu Rev Virol 3:517-532.
2. Moens U et al (2008) Human polyomaviruses and cancer: further evidence. JDDG 6: 704-708