Evasion of CD8+ T Cells Is Critical for Superinfection by Cytomegalovirus

Scott G. Hansen, Colin J. Powers, Rebecca Richards, Abigail B. Ventura, Julia C. Ford, Don Siess, Michael K. Axthelm, Jay A. Nelson, Michael A. Jarvis, Louis J. Picker, Klaus Früh

Research output: Contribution to journalArticle

178 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)102-106
Number of pages5
JournalScience
Volume328
Issue number5974
DOIs
StatePublished - Apr 2 2010

ASJC Scopus subject areas

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