Role of BK human polyomavirus in cancer

Jorge Levican,Aldo Gaggero,Mónica Acevedo,Francisco Aguayo,Oscar León

doi:10.1186/s13027-018-0182-9

Abstract

Human polyomaviruses (HPyV), which are small DNA viruses classified into the polyomaviridae family, are widely distributed in human populations. Thirteen distinct HPyVs have been described to date. Some of these viruses have been found in human tumors, suggesting an etiological relationship with cancer. In particular, convincing evidence of an oncogenic role has emerged for a specific HPyV, the Merkel cell polyomavirus (MCPyV). This HPyV has been linked to rare skin cancer, Merkel cell carcinoma (MCC). This finding may be just the tip of the iceberg, as HPyV infections are ubiquitous in humans. Many authors have conjectured that additional associations between HPyV infections and neoplastic diseases will likely be discovered. In 2012, the International Agency for Research on Cancer (IARC) evaluated the carcinogenicity of the BK virus (BKPyV), reporting that BKPyV is “possibly carcinogenic to humans.” This review explores the BKPyV infection from a historical point of view, including biological aspects related to viral entry, tropism, epidemiology and mechanisms potentially involved in BKPyV-mediated human carcinogenesis. In order to clarify the role of this virus in human cancer, more epidemiological and basic research is strongly warranted.

Highlights

Human polyomaviruses (HPyVs) are small, nonenveloped, double-stranded DNA viruses with approximately 5000-bp genome and icosahedral symmetry
The HPyV capsid harbors 72 pentamers of VP1, which interacts with the VP2/VP3 molecules associated with each pentamer [2]
This review evaluates the molecular mechanisms of BK polyomavirus (BKPyV) infection and its potential association with cancer

Summary

Introduction

Human polyomaviruses (HPyVs) are small, nonenveloped, double-stranded DNA viruses with approximately 5000-bp genome and icosahedral symmetry. Upon BKPyV infection in a permissive host cell, early gene expression leads to DNA replication, followed by late gene expression, production of progeny viral particles and cell death. Transfection of embryonic fibroblasts or cells cultured from kidney or brain tissues of diverse mammalian origin with complete or sub-genomic fragments of BKPyV DNA, containing the early coding region, lead to cell transformation [23].

Results

Conclusion