Abstract
Human polyomaviruses, BK virus (BKV) and JC virus (JCV), are world widely distributed in human population. After primary infection, BKV and JCV establish latency in kidneys and upper part of urinary tract. In seropositive healthy individuals asymptomatic reactivation of both viruses occurs in in 0.5-20%. On the other hand, reactivation of these viruses in imunosuppressed patients, primarily in patients with T cell immunodeficiency, can lead to development of polyomavirus-associated diseases. Some of these diseases such as progressive multifocal leukoencephalopathy (PML), polyomavirus-induced nephropathy (PVN), hemorrhagic cystitis (HC) are life-threatening diseases with high mortality and morbidity rate. However, they do not affect all immunosuppressed patients, suggesting that other factors, such as genetic variability of BKV and JCV, can contribute to their occurrence. Immunosuppression leads to increased levels of replication of both viruses. Increased levels of replication are associated with higher incidence of mutations in the VP1 gene. Mutations, especially those located in outer loops, may lead to changed tropism and generation of more aggressive variants of BKV and JCV. This review is focused on clinical significance of BK and JC virus infection in immunosuppressed patients, especially in HIV-infected, and sequence changes in the VP1 gene that can contribute to selection of more virulent variants of BKV and JCV via adaptive evolution.
Highlights
Seroepidemiological studies have shown that between 27% and 80% of the human population is infected with two human polyomaviruses: BK virus (BKV) and JC virus (JCV)
It comprises 72 capsomers, where each capsomer is composed of 5 molecules of viral capsid protein 1 (VP1) that is associated with single molecule of VP2 and VP3
The genomes of BKV and JCV are divided into three regions: the early coding region, late coding region and hypervariable non-coding regulatory region (NCRR)
Summary
Seroepidemiological studies have shown that between 27% and 80% of the human population is infected with two human polyomaviruses: BK virus (BKV) and JC virus (JCV). The primary infection, which occurs during early childhood, is usually asymptomatic or is manifested as mild respiratory disease [1]. Both viruses establish latency in cells of the kidneys and upper parts of the urinary tract. JCV establishs latency in B lymphocytes and in other cells of monocytic lineage. During life of seropositive immunocompetent individuals sporadic asymptomatic reactivation of both viruses occurs in 0.5-20% [2].
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