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Title: Partial protection of SIV-infected rhesus monkeys against superinfection with a heterologous SIV isolate

Abstract

Although there is increasing evidence that individuals already infected with human immunodeficiency virus type 1 (HIV-1) can be infected with a heterologous strain of the virus, the extent of protection against superinfection conferred by the first infection and the biologic consequences of superinfection are not well understood. We explored these questions in the simian immunodeficiency virus (SIV)/rhesus monkey model of HIV-1/AIDS. We infected cohorts of rhesus monkeys with either SIVmac251 or SIVsmE660 and then exposed animals to the reciprocal virus through intrarectal inoculations. Employing a quantitative real-time PCR assay, we determined the replication kinetics of the two strains of virus for 20 weeks. We found that primary infection with a replication-competent virus did not protect against acquisition of infection by a heterologous virus but did confer relative control of the superinfecting virus. In animals that became superinfected, there was a reduction in peak replication and rapid control of the second virus. The relative susceptibility to superinfection was not correlated with CD4(+) T-cell count, CD4(+) memory T-cell subsets, cytokine production by virus-specific CD8(+) or CD4(+) cells, or neutralizing antibodies at the time of exposure to the second virus. Although there were transient increases in viral loads of the primary virus andmore » a modest decline in CD4(+) T-cell counts after superinfection, there was no evidence of disease acceleration. These findings indicate that an immunodeficiency virus infection confers partial protection against a second immunodeficiency virus infection, but this protection may be mediated by mechanisms other than classical adaptive immune responses.« less

Authors:
 [1]
  1. Los Alamos National Laboratory
Publication Date:
Research Org.:
Los Alamos National Lab. (LANL), Los Alamos, NM (United States)
Sponsoring Org.:
USDOE
OSTI Identifier:
956516
Report Number(s):
LA-UR-09-00267; LA-UR-09-267
Journal ID: ISSN 0022-538X; JOVIAM; TRN: US201014%%1885
DOE Contract Number:  
AC52-06NA25396
Resource Type:
Journal Article
Journal Name:
Journal of Virology
Additional Journal Information:
Journal Name: Journal of Virology; Journal ID: ISSN 0022-538X
Country of Publication:
United States
Language:
English
Subject:
59; AIDS VIRUS; ANIMALS; ANTIBODIES; CONTROL; DISEASES; HUMAN POPULATIONS; KINETICS; LYMPHOKINES; MACACUS; MONKEYS; PATHOGENESIS; POLYMERASE CHAIN REACTION; REDUCTION; SIMIAN VIRUS

Citation Formats

Korber, Bette. Partial protection of SIV-infected rhesus monkeys against superinfection with a heterologous SIV isolate. United States: N. p., 2009. Web. doi:10.1128/JVI.00114-09.
Korber, Bette. Partial protection of SIV-infected rhesus monkeys against superinfection with a heterologous SIV isolate. United States. doi:10.1128/JVI.00114-09.
Korber, Bette. Thu . "Partial protection of SIV-infected rhesus monkeys against superinfection with a heterologous SIV isolate". United States. doi:10.1128/JVI.00114-09. https://www.osti.gov/servlets/purl/956516.
@article{osti_956516,
title = {Partial protection of SIV-infected rhesus monkeys against superinfection with a heterologous SIV isolate},
author = {Korber, Bette},
abstractNote = {Although there is increasing evidence that individuals already infected with human immunodeficiency virus type 1 (HIV-1) can be infected with a heterologous strain of the virus, the extent of protection against superinfection conferred by the first infection and the biologic consequences of superinfection are not well understood. We explored these questions in the simian immunodeficiency virus (SIV)/rhesus monkey model of HIV-1/AIDS. We infected cohorts of rhesus monkeys with either SIVmac251 or SIVsmE660 and then exposed animals to the reciprocal virus through intrarectal inoculations. Employing a quantitative real-time PCR assay, we determined the replication kinetics of the two strains of virus for 20 weeks. We found that primary infection with a replication-competent virus did not protect against acquisition of infection by a heterologous virus but did confer relative control of the superinfecting virus. In animals that became superinfected, there was a reduction in peak replication and rapid control of the second virus. The relative susceptibility to superinfection was not correlated with CD4(+) T-cell count, CD4(+) memory T-cell subsets, cytokine production by virus-specific CD8(+) or CD4(+) cells, or neutralizing antibodies at the time of exposure to the second virus. Although there were transient increases in viral loads of the primary virus and a modest decline in CD4(+) T-cell counts after superinfection, there was no evidence of disease acceleration. These findings indicate that an immunodeficiency virus infection confers partial protection against a second immunodeficiency virus infection, but this protection may be mediated by mechanisms other than classical adaptive immune responses.},
doi = {10.1128/JVI.00114-09},
journal = {Journal of Virology},
issn = {0022-538X},
number = ,
volume = ,
place = {United States},
year = {2009},
month = {1}
}