Journal
SCIENCE
Volume 328, Issue 5974, Pages 102-106Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1185350
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Funding
- Centocor, Inc [AI040101, RR016001]
- National Institutes of Health [RO1 AI059457, RO1 AI060392]
- International AIDS Vaccine Initiative
- National Center for Research Resources [RR016025, RR18107, RR00163]
- Ruth L. Kirschstein National Research Service [T32 AI007472, T32 HL007781]
- OHSU Tartar Trust fellowship
- Achievement Reward for College Scientists
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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.
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