During the past 6 years, focused virus hunting has led to the discovery of nine new human polyomaviruses, including Merkel cell polyomavirus, which has been linked to Merkel cell carcinoma, a lethal skin cell cancer. The discovery of so many new and highly divergent human polyomaviruses raises key questions regarding their evolution, tropism, latency, reactivation, immune evasion and contribution to disease. This Review describes the similarities and differences among the new human polyomaviruses and discusses how these viruses might interact with their human host.
"This virus family includes the human BK PyV that causes Pyassociated nephropathy and hemorrhagic cystitis (Bennett et al., 2012) and JC PyV responsible for progressive multifocal leukoencephalopathy (Maginnis et al., 2014). Strikingly within the past nine years, ten new human Pys have been discovered (DeCaprio & Garcea, 2013; White et al., 2013). Of these, the Merkel cell PyV has already been implicated as the causative agent of an aggressive skin cancer called Merkel cell carcinoma (Feng et al., 2008). "
[Show abstract][Hide abstract] ABSTRACT: A dedicated network of cellular factors ensures that proteins translocated into the endoplasmic reticulum (ER) are folded correctly before they exit this compartment en route to other cellular destinations or for secretion. When proteins misfold, selective ER-resident enzymes and chaperones are recruited to rectify the protein-misfolding problem in order to maintain cellular proteostasis. However, when a protein becomes terminally misfolded, it is ejected into the cytosol and degraded by the proteasome via a pathway called ER-associated degradation (ERAD). Strikingly, toxins and viruses can hijack elements of the ERAD pathway to access the host cytosol and cause infection. This review focuses on emerging data illuminating the molecular mechanisms by which these toxic agents co-opt the ER-to-cytosol translocation process to cause disease.
Critical Reviews in Biochemistry and Molecular Biology 09/2015; DOI:10.3109/10409238.2015.1085826 · 7.71 Impact Factor
"Polyomavirus and the DNA damage response VIROLOGICA SINICA 124 APRIL 2015 VOLUME 30 ISSUE 2 et al., 2014). The best characterized human polyomaviruses include BK polyomavirus (BKPyV), JC polyomavirus (JCPyV), and Merkel Cell polyomavirus (MCPyV) (DeCaprio and Garcea, 2013; Pinto and Dobson, 2014). BKPyV and JCPyV are found in the majority of the adult population as latent infections acquired in childhood and reside in the genitourinary tract (BKPyV and JCPyV) and bone marrow and brain (JCPyV) (Pinto and Dobson, 2014). "
[Show abstract][Hide abstract] ABSTRACT: Viruses are obligate intracellular parasites that subvert cellular metabolism and pathways to mediate their own replication-normally at the expense of the host cell. Polyomaviruses are a group of small DNA viruses, which have long been studied as a model for eukaryotic DNA replication. Polyomaviruses manipulate host replication proteins, as well as proteins involved in DNA maintenance and repair, to serve as essential cofactors for productive infection. Moreover, evidence suggests that polyomavirus infection poses a unique genotoxic threat to the host cell. In response to any source of DNA damage, cells must initiate an effective DNA damage response (DDR) to maintain genomic integrity, wherein two protein kinases, ataxia telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR), are major regulators of DNA damage recognition and repair. Recent investigation suggests that these essential DDR proteins are required for productive polyomavirus infection. This review will focus on polyomaviruses and their interaction with ATMand ATR-mediated DNA damage responses and the effect of this interaction on host genomic stability.
"To date, complete genome reference sequences for 46 polyomaviruses have been deposited at Genbank. Of those, 12 are human polyomaviruses
[10-13]. Several polyomaviruses have been associated to specific diseases, such as Progressive Multifocal Leukoencephalopathy (PML) for JCPyV, polyomavirus-associated nephropathy (PVAN) for BKPyV, Merkel cell carcinoma (MCC) for Merkel Cell Virus (MCPyV) and trichodysplasia spinulosa for Trichodysplasia spinulosa-associated Polyomavirus (TSPyV)
[Show abstract][Hide abstract] ABSTRACT: Polyomaviruses are a family of non-enveloped DNA viruses infecting several species, including humans, primates, birds, rodents, bats, horse, cattle, raccoon and sea lion. They typically cause asymptomatic infection and establish latency but can be reactivated under certain conditions causing severe diseases. MicroRNAs (miRNAs) are small non-coding RNAs that play important roles in several cellular processes by binding to and inhibiting the translation of specific mRNA transcripts. In this review, we summarize the current knowledge of microRNAs involved in polyomavirus infection. We review in detail the different viral miRNAs that have been discovered and the role they play in controlling both host and viral protein expression. We also give an overview of the current understanding on how host miRNAs may function in controlling polyomavirus replication, immune evasion and pathogenesis.
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