Abstract
Members of the Polyomaviridae family differ in their host range, pathogenesis, and disease severity. To date, some of the most studied polyomaviruses include human JC, BK, and Merkel cell polyomavirus and non-human subspecies murine and simian virus 40 (SV40) polyomavirus. Although dichotomies in host range and pathogenesis exist, overlapping features of the infectious cycle illuminate the similarities within this virus family. Of particular interest to human health, JC, BK, and Merkel cell polyomavirus have all been linked to critical, often fatal, illnesses, emphasizing the importance of understanding the underlying viral infections that result in the onset of these diseases. As there are significant overlaps in the capacity of polyomaviruses to cause disease in their respective hosts, recent advancements in characterizing the infectious life cycle of non-human murine and SV40 polyomaviruses are key to understanding diseases caused by their human counterparts. This review focuses on the molecular mechanisms by which different polyomaviruses hijack cellular processes to attach to host cells, internalize, traffic within the cytoplasm, and disassemble within the endoplasmic reticulum (ER), prior to delivery to the nucleus for viral replication. Unraveling the fundamental processes that facilitate polyomavirus infection provides deeper insight into the conserved mechanisms of the infectious process shared within this virus family, while also highlighting critical unique viral features.
Highlights
In order to infect a host, all viruses must transverse cellular barriers to access the interior of the cell where viruses replicate and propagate infection [1,2]
JCPyV internalization has been identified to occur through clathrin-mediated endocytosis [106,110,111]
One theme is apparent among polyomaviruses; while these viruses are attributed to using distinct cellular attachment and entry factors and enter cells by differing mechanisms, all polyomaviruses are targeted to the endoplasmic reticulum (ER) [15,16,17,18,19,20,21]
Summary
In order to infect a host, all viruses must transverse cellular barriers to access the interior of the cell where viruses replicate and propagate infection [1,2]. Nonproductive routes of infection may result in identification of the virus by the host immune system, resulting in targeting of the virus and clearance of the infection To avoid this fate, viruses have developed mechanisms to orchestrate attachment, entry, and trafficking to the appropriate compartment that supports either fusion or penetration for release of the viral genetic material. The capsids of these viruses are comprised primarily of viral protein 1 (VP1), and secondarily of VP2 and VP3 [4,7] Due to their importance in human health, infection strategies of polyomaviruses BK (BKPyV), JC (JCPyV), and Merkel cell (MCPyV) are of significant interest. This review details the mechanisms by which several human and non-human polyomaviruses attach and transverse biologically relevant membranes, traffic through the cytoplasm to the endoplasmic reticulum, and uncoat for delivery of the virion to the nucleus for viral replication. Understanding the mechanisms by which polyomaviruses arrive at the nucleus could identify targets for the prevention of infection and spread of disease
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