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Longitudinal changes in HIV-1-specific T-cell quality associated with viral load dynamic.
J. Clin. Virol. 55, 114-120 (2012)
Background: Several correlates of HIV control have been described; however their predictive values remain unclear, since most studies have been performed in cross-sectional settings. Objectives: We evaluated the cause and consequence relationship between quality of HIV-specific T-cell response and viral load dynamic in a temporal perspective. Study design: HIV-1-specific T-cell responses were monitored over 7 years in a patient that following treatment interruption maintained a stable/low viral set point for 3.1 years before control of viral replication was lost and antiretroviral therapy restarted. Results: We observed that high frequencies of HIV-1-specific CD4 and CD8 T cells were unable to prevent loss of viral control. Gradual loss of functionality was observed in these responses, characterized by early loss of IL-2, viral load-dependent decrease of IFN-gamma and CD154 expression as well as increase of MIP-1 beta production. Terminally differentiated HIV-1-specific CD8 T cells expressing CD45RA were lost independently of viral load and preceded the loss-of-control phase of HIV infection. Conclusion: By describing qualitative changes in HIV-1-specific T-cell responses that coincide with loss of viral control, we identified specific correlates of disease progression and putative markers of viral control. Our findings suggest including the markers IL-2, IFN-gamma, MIP-1 beta, CD154 and CD45RA into monitoring of HIV-specific T-cell-responses to prospectively determine correlates of protection from disease-progression.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Hiv ; T-cell Response ; Correlates Of Protection ; Longitudinal Study; HIV; Responses; Infection; Type-1; Memory; Nonprogressors; Proliferation; Phenotype; Disease; Design
ISSN (print) / ISBN
1386-6532
e-ISSN
1386-6532
Journal
Journal of Clinical Virology
Quellenangaben
Volume: 55,
Issue: 2,
Pages: 114-120
Publisher
Elsevier
Non-patent literature
Publications
Reviewing status
Peer reviewed