Entry, infection, replication, and egress of human polyomaviruses: an update

Abstract

Polyomaviruses (PyVs), belonging to the family Polyomaviridae, are a group of small, nonenveloped, double-stranded, circular DNA viruses widely distributed in the vertebrates. PyVs cause no apparent disease in adult laboratory mice but cause a wide variety of tumors when artificially inoculated into neonates or semipermissive animals. A few human PyVs, such as BK, JC, and Merkel cell PyVs, have been unequivocally linked to pathogenesis under conditions of immunosuppression. Infection is thought to occur early in life and persists for the lifespan of the host. Over evolutionary time scales, it appears that PyVs have slowly co-evolved with specific host animal lineages. Host cell surface glycoproteins and glycolipids seem to play a decisive role in the entry stage of viral infection and in channeling the virions to specific intracellular membrane-bound compartments and ultimately to the nucleus, where the genomes are replicated and packaged for release. Therefore the transport of the infecting virion or viral genome to this site of multiplication is an essential process in productive viral infection as well as in latent infection and transformation. This review summarizes the major findings related to the characterization of the nature of the interactions between PyV and host protein and their impact in host cell invasion.

Merkel cell polyomavirus detected in head and neck carcinomas from Chile

“…BKPyV and JCPyV were discovered in 1971. In the last 15 years, mainly due to the development of new high-throughput sequencing techniques, other twelve HPyVs have been discovered (MCPyV, KIPyV, WUPyV, TSPyV, HPyV6, HPyV7, HPyV9, HPyV10, HPyV12, STLPyV, NJPyV and LIPyV) [2,3]. HPyV infection usually occurs early in life through a fecal-oral transmission mechanism and persists for the lifetime of the infected subject.…”

“…HPyV infection usually occurs early in life through a fecal-oral transmission mechanism and persists for the lifetime of the infected subject. In natural hosts, these viruses establish a productive infection, although in heterologous non-permissive hosts, the virus establishes latency with potential integration into the host genome [2]. HPyVs are very ubiquitous in nature and their association with some pathologies, cancer in particular, is under intensive investigation [4].…”

Role of DCP1-DCP2 complex regulated by viral and host microRNAs in DNA virus infection

“…The life cycle of a virus begins with the entry of the host cell. Replication of viral genomes, synthesis of viral proteins, assembly of viral particles, and release of viruses from host cells depend largely on host mechanisms (1, 2). It is reported that the stability of viral mrna is regulated by the dcp1-dcp2 complex located in the P-body (the processing bodies) (3, 4).…”

Mechanisms of nuclear lamina disruption and regulation of nuclear budding of herpes simplex virus type-1

“…Polyomaviruses are double stranded DNA, nonenveloped viruses that undergo genome replication and viral assembly in the nucleus. Most polyomaviruses, excluding JC virus (JCPyV), enter the cell via receptor binding at caveolae (151). JCPyV enters cells via clathrin-mediated endocytosis (151).…”

“…Most polyomaviruses, excluding JC virus (JCPyV), enter the cell via receptor binding at caveolae (151). JCPyV enters cells via clathrin-mediated endocytosis (151). Resulting caveosomes are trafficked to the ER using the microtubule network, where the viral capsid becomes inserted into the ER lumen (151).…”