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PLoS One. 2013 Sep 2;8(9):e72295. doi: 10.1371/journal.pone.0072295. eCollection 2013.

Repressive effect of primary virus replication on superinfection correlated with gut-derived central memory CD4(+) T cells in SHIV-infected Chinese rhesus macaques.

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  • 1Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) and Comparative Medicine Center, Peking Union Medical College (PUMC), Key Laboratory of Human Disease Comparative Medicine, Beijing, China.

Abstract

A possible mechanism of susceptibility to superinfection with simian-human immunodeficiency virus (SHIV)-1157ipd3N4 was explored in twelve SHIVSF162P3-infected Chinese rhesus macaques. Based on the kinetics of viral replication for the second infecting virus following SHIV-1157ipd3N4 inoculation, the monkeys were divided into two groups: those relatively resistant to superinfection (SIR) and those relatively sensitive to superinfection (SIS). We found that superinfection-resistant macaques had high primary viremia, whereas superinfection-sensitive macaques had low primary viremia, suggesting that primary SHIVSF162P3 infection with a high viral-replication level would repress superinfection with a heterologous SHIV-1157ipd3N4. Although no correlation of protection against superinfection with virus-specific CD4(+) T cell or CD8(+) T cell immune responses from gut was observed prior to superinfection, superinfection susceptibility was strongly correlated with CD4(+) Tcm cells from gut both prior to the second infecting virus inoculation and on day 7 after superinfection, but not with CD4(+) Tem cells from gut or with CD4(+) Tcm cells from peripheral blood and lymph node. These results point to the important roles of gut-derived CD4(+) Tcm cells for the study of the mechanisms of protection against superinfection and the evaluation of the safety and efficacy of vaccines and therapies against acquired immune deficiency syndrome (AIDS).

PMID:
24023734
[PubMed - indexed for MEDLINE]
PMCID:
PMC3759369
Free PMC Article
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