Evasion of CD8+ T cells is critical for superinfection by cytomegalovirus.
Science, 2010/4/02;328(5974):102-6.
Hansen SG[1], Powers CJ, Richards R, Ventura AB, Ford JC, Siess D, Axthelm MK, Nelson JA, Jarvis MA, Picker LJ, Früh K
Affiliations
PMID: 20360110DOI: 10.1126/science.1185350
Impact factor: 63.714
Abstract
Cytomegalovirus (CMV) can superinfect persistently infected hosts despite CMV-specific humoral and cellular immunity; however, how it does so remains undefined. We have demonstrated that superinfection of rhesus CMV-infected rhesus macaques (RM) requires evasion of CD8+ T cell immunity by virally encoded inhibitors of major histocompatibility complex class I (MHC-I) antigen presentation, particularly the homologs of human CMV US2, 3, 6, and 11. In contrast, MHC-I interference was dispensable for primary infection of RM, or for the establishment of a persistent secondary infection in CMV-infected RM transiently depleted of CD8+ lymphocytes. These findings demonstrate that US2-11 glycoproteins promote evasion of CD8+ T cells in vivo, thus supporting viral replication and dissemination during superinfection, a process that complicates the development of preventive CMV vaccines but that can be exploited for CMV-based vector development.
MeSH terms
Animals; Antigen Presentation; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cytomegalovirus; Cytomegalovirus Infections; Cytomegalovirus Vaccines; Disease Models, Animal; Gene Products, gag; Genes, Viral; Histocompatibility Antigens Class I; Immune Evasion; Immunologic Factors; Macaca mulatta; Male; Simian Immunodeficiency Virus; Superinfection; Viral Proteins; Virus Replication; Virus Shedding
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