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- W2943634992 endingPage "e1007711" @default.
- W2943634992 startingPage "e1007711" @default.
- W2943634992 abstract "The human specific poxvirus molluscum contagiosum virus (MCV) produces skin lesions that can persist with minimal inflammation, suggesting that the virus has developed robust immune evasion strategies. However, investigations into the underlying mechanisms of MCV pathogenesis have been hindered by the lack of a model system to propagate the virus. Herein we demonstrate that MCV-encoded MC80 can disrupt MHC-I antigen presentation in human and mouse cells. MC80 shares moderate sequence-similarity with MHC-I and we find that it associates with components of the peptide-loading complex. Expression of MC80 results in ER-retention of host MHC-I and thereby reduced cell surface presentation. MC80 accomplishes this by engaging tapasin via its luminal domain, targeting it for ubiquitination and ER-associated degradation in a process dependent on the MC80 transmembrane region and cytoplasmic tail. Tapasin degradation is accompanied by a loss of TAP, which limits MHC-I access to cytosolic peptides. Our findings reveal a unique mechanism by which MCV undermines adaptive immune surveillance." @default.
- W2943634992 created "2019-05-09" @default.
- W2943634992 creator A5035615103 @default.
- W2943634992 creator A5061136971 @default.
- W2943634992 creator A5087099599 @default.
- W2943634992 date "2019-04-29" @default.
- W2943634992 modified "2023-10-14" @default.
- W2943634992 title "Molluscum contagiosum virus MC80 sabotages MHC-I antigen presentation by targeting tapasin for ER-associated degradation" @default.
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- W2943634992 doi "https://doi.org/10.1371/journal.ppat.1007711" @default.
- W2943634992 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6508746" @default.
- W2943634992 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31034515" @default.
- W2943634992 hasPublicationYear "2019" @default.
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