Download or read book Investigation of the Roles of Vaccinia Virus Protein F13 and Its Molluscum Contagiosum Virus Homolog MC021 at Steps Post Envelopment written by Peter J. Bryk and published by . This book was released on 2018 with total page 126 pages. Available in PDF, EPUB and Kindle. Book excerpt: The family Poxviridae encompasses a vast number of complex large, double-stranded DNA viruses. Among these are vaccinia virus (VACV), the virus used as the vaccine for smallpox, and molluscum contagiosum virus (MOCV), the only extant poxvirus that is human-specific and currently clinically relevant. VACV is the prototypic poxvirus and the protein F13 is conserved across the subfamily Chordopoxvirinae. It has been shown to be required to produce the wrapped forms of virus that are required for cell-to-cell spread. F13 is included on wrapped forms of virus, however what role it may play after virion envelopment remains unknown. During our investigations, two F13 temperature-sensitive VACV mutants were found to produce similar levels of extracellular virions (EV) compared to a virus with normal F13, yet displayed a small plaque phenotype similar to a F13L deletion mutant. Analysis of virions produced at the non-permissive temperature showed F13 was not incorporated, and that EV displayed delayed entry kinetics compared to virions containing F13. Furthermore, these virions were resistant to acid-induced dissolution of the EV envelope, suggesting F13 is involved in the modification or dissolution of this membrane. Little is known about MOCV virion morphogenesis, or if virion envelopment even occurs. Despite not having been shown to produce EV, MOCV encodes putative homologs of wrapped virion-specific proteins in VACV, of which the homolog of F13, MC021, shares the greatest amino acid sequence identity. A recombinant virus that expresses MC021 in place of F13 was capable of partially complementing EV production compared to an F13L deletion mutant, yet displayed markedly different localization from F13. We have identified interactions between MC021 and VACV proteins, including F13 and B5. Moreover, MC021 is incorporated into the EV envelope, and these EV enter cells at a rate similar to the parental strain, suggesting MC021 functionally replaces F13 on the EV membrane. Despite this, the virus has a plaque phenotype considerably smaller than that of the parental strain. Taken together, these results demonstrate a role for MC021 in the production of EV during infection, and suggest MOCV may produce wrapped forms of virus during its lifecycle.