2005
DOI: 10.1128/jvi.79.14.9228-9235.2005
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CD8+T-Lymphocyte Response to Major Immunodominant Epitopes after Vaginal Exposure to Simian Immunodeficiency Virus: Too Late and Too Little

Abstract: In the acute stage of infection following sexual transmission of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV), virus-specific CD8؉ T-lymphocyte responses partially control but do not eradicate infection from the lymphatic tissues (LTs) or prevent the particularly massive depletion of CD4 ؉ T lymphocytes in gut-associated lymphatic tissue (GALT). We explored hypothetical explanations for this failure to clear infection and prevent CD4 ؉ T-lymphocyte loss in the SIV/rhesus macaque m… Show more

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Cited by 152 publications
(163 citation statements)
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“…During the initial expansion phase, the effector/target ratio at the local site of infection is apparently too low to control the pathogen. For SIV-vaccinated animals, this probably means that the CD8 ϩ effector cells appear too late in the mucosal tissues to control the initial virus growth (22,81,93). Whenever the CD8 ϩ T-cell immune response arrives late at the local scene of infection, virus-infected target cells outnumber the initial immune response, and the initial effector/target ratio will be too low for immediate immune control (see Appendix).…”
Section: Resultsmentioning
confidence: 99%
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“…During the initial expansion phase, the effector/target ratio at the local site of infection is apparently too low to control the pathogen. For SIV-vaccinated animals, this probably means that the CD8 ϩ effector cells appear too late in the mucosal tissues to control the initial virus growth (22,81,93). Whenever the CD8 ϩ T-cell immune response arrives late at the local scene of infection, virus-infected target cells outnumber the initial immune response, and the initial effector/target ratio will be too low for immediate immune control (see Appendix).…”
Section: Resultsmentioning
confidence: 99%
“…Monkeys vaccinated with SIV antigens carry expanded antigen-specific CD8 ϩ T cells and nevertheless fail to control initial viral replication when challenged with SIV (12,19,21,22,44,54,61,63,81,86). Because high effector/target ratios are required to control SIV infection, we have explained these observations with the time it takes these memory cells to be reactivated and recruited to the primary site of infection and/or to be expanded into a sufficiently large clone of effector cells.…”
Section: Discussionmentioning
confidence: 99%
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“…Remarkably, both MHC-identical animals exhibited mutations in these regions, though the affected amino acids were distinct in each animal. With the exception of the Tat [26][27][28][29][30][31][32][33][34][35][36] region, strong CTL responses were detected at 3 weeks postinfection in at least one of the two animals (data not shown), strongly suggesting that the shared variability results from immune escape.…”
Section: High Frequency Of Mhc Class I-and Mhc Class Ii-identical MCMmentioning
confidence: 91%
“…For the first time, it may be possible to study the in vivo correlates of protective cellular immunity by transferring SIV-specific lymphocytes from a donor animal into naive recipients immediately prior to SIV challenge. These studies could directly test the hypothesis that the failure of cellular immunity to control SIV infection results from an inability of CTL to mobilize to sites of viral replication early during infection (33). Additionally, in vitro data suggest that certain CTL specificities suppress SIV and HIV replication far more effectively than others (24,43).…”
Section: Vol 81 2007mentioning
confidence: 98%