Abstract
CD4+ T cells play a central role in the immunopathogenesis of HIV/AIDS, and their depletion during chronic HIV infection is a hallmark of disease progression. However, the relative contribution of CD4+ T cells as mediators of antiviral immune responses and targets for virus replication is still unclear. Here, we have generated data in SIV-infected rhesus macaques (RMs) that suggest that CD4+ T cells are essential in establishing control of virus replication during acute infection. To directly assess the role of CD4+ T cells during primary SIV infection, we in vivo depleted these cells from RMs prior to infecting the primates with a pathogenic strain of SIV. Compared with undepleted animals, CD4+ lymphocyte-depleted RMs showed a similar peak of viremia, but did not manifest any post-peak decline of virus replication despite CD8+ T cell- and B cell-mediated SIV-specific immune responses comparable to those observed in control animals. Interestingly, depleted animals displayed rapid disease progression, which was associated with increased virus replication in non-T cells as well as the emergence of CD4-independent SIV-envelopes. Our results suggest that the antiviral CD4+ T cell response may play an important role in limiting SIV replication, which has implications for the design of HIV vaccines.
Original language | English (US) |
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Pages (from-to) | 4433-45 |
Number of pages | 13 |
Journal | The Journal of clinical investigation |
Volume | 121 |
Issue number | 11 |
DOIs | |
State | Published - Nov 2011 |
Keywords
- Animals
- Antilymphocyte Serum/administration & dosage
- Base Sequence
- CD4 Antigens/immunology
- CD4-Positive T-Lymphocytes/immunology
- DNA Primers/genetics
- Lymphocyte Depletion
- Macaca mulatta
- RNA, Viral/genetics
- Simian Acquired Immunodeficiency Syndrome/immunology
- Simian Immunodeficiency Virus/genetics
- Viral Load/immunology
- Viremia/immunology
- Virus Replication/immunology
PubMed: MeSH publication types
- Journal Article
- Research Support, N.I.H., Extramural
- Research Support, U.S. Gov't, Non-P.H.S.