Abstract
Viruses are intracellular parasites that require a permissive host cell to express the viral genome and to produce new progeny virus particles. However, not all viral infections are productive and some viruses can induce carcinogenesis. Irrespective of the type of infection (productive or neoplastic), viruses hijack the host cell machinery to permit optimal viral replication or to transform the infected cell into a tumor cell. One mechanism viruses employ to reprogram the host cell is through interference with signaling pathways. Polyomaviruses are naked, double-stranded DNA viruses whose genome encodes the regulatory proteins large T-antigen and small t-antigen, and structural proteins that form the capsid. The large T-antigens and small t-antigens can interfere with several host signaling pathways. In this case, we review the interplay between the large T-antigens and small t-antigens with host signaling pathways and the biological consequences of these interactions.
Highlights
The Polyomaviridae family consists of naked viruses with an icosahedral capsid structure
These results indicate that Merkel cell polyomavirus (MCPyV) does not interfere with the PI3K/AKT/mTOR pathway
ST associated with a PP4 regulatory subunit 1 (PP4R1)-PP4C complex, which mediated binding to NFκB essential modulator (NEMO) [46]. These results suggest that small t-antigen (sT) stimulates the interaction between NEMO and the protein phosphatase PP4C-PP4R1 complex
Summary
The Polyomaviridae family consists of naked viruses with an icosahedral capsid structure. 12 novel HPyV have been described: KIPyV [5], WUPyV [6], Merkel cell polyomavirus (MCPyV; [7]), HPyV6 [8], HPyV7 [8], Trichodysplasia spinulosa-associated polyomavirus (TSPyV; [9]), HPyV9 [10], MWPyV [11,12], STLPyV [13], HPyV12 [14], NJPyV [15], and LIPyV [16] They all encode at least two early proteins: large T-antigen (LT) and small t-antigen (sT), but other early proteins have been detected or may be encoded by the viral genome (Figure 1). We review the different pathways that are affected by HPyV and discuss the biological relevance of these interactions
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