Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 128, Issue 4, Pages 1627-1640Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI95127
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Funding
- ANRS
- Fundacao para a Ciencia e a Tecnologia (FCT) [IF/00021/2014]
- CIHR [MOP-133476]
- FCT [SFRH/BD/64064/2009]
- Canada Research Chair program
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [U42OD011023, P51OD011132] Funding Source: NIH RePORTER
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Apoptosis has been proposed as a key mechanism responsible for CD4(+) T cell depletion and immune dysfunction during HIV infection. We demonstrated that Q-VD-OPH, a caspase inhibitor, inhibits spontaneous and activation-induced death of T cells from SIV-infected rhesus macaques (RMs). When administered during the acute phase of infection, Q-VD-OPH was associated with (a) reduced levels of T cell death, (b) preservation of CD4(+)/CD8(+) T cell ratio in lymphoid organs and in the gut, (c) maintenance of memory CD4(+) T cells, and (d) increased specific CD4(+) T cell response associated with the expression of cytotoxic molecules. Although therapy was limited to the acute phase of infection, Q-VD-OPH-treated RMs showed lower levels of both viral load and cell-associated SIV DNA as compared with control SIV-infected RMs throughout the chronic phase of infection, and prevented the development of AIDS. Overall, our data demonstrate that Q-VD-OPH injection in SIV-infected RMs may represent an adjunctive therapeutic agent to control HIV infection and delaying disease progression to AIDS.
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