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The disruption of macaque CD4 + T‐cell repertoires during the early simian immunodeficiency virus infection
Author(s) -
Zhou Dejiang,
Kou ZhongChen,
Ibegbu Chris,
Shen Yun,
LeeParritz David,
Shen Ling,
Sehgal Prabhat K.,
McClure Harold M.,
Morrison Paul,
Bogle Christine,
Sehgal Neetu,
Nahmias Andre J.,
Chen Zheng W.
Publication year - 1999
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1111/j.1600-0684.1999.tb00267.x
Subject(s) - simian immunodeficiency virus , biology , rhesus macaque , macaque , virology , t cell receptor , virus , simian , t cell , immunology , dominance (genetics) , immunodeficiency , t lymphocyte , immune system , genetics , gene , paleontology
T‐cell receptor (TCR) complementarity determining region 3 (CDR3) spetratyping analysis was employed to assess the ability of an AIDS virus to disrupt CD4 + T‐cell repertoires during the primary infection. Rhesus and pig‐tailed macaques infected with simian immunodeficiency virus (SIV)mac 251 and SIVsmmFGb, respectively, were evaluated. Following SIV infection, the macaques exhibited an apparent decline of CD4 + peripheral blood lymphocyte (PBL) counts, which was associated with a change in CDR3 profiles from multiple‐length distribution to one‐ or two‐length dominance in the selected TCR Vβ‐expressing CD4 + PBL subpopulations. Molecular analysis of the perturbed cell subpopulations suggested that the CD4 + T cells bearing the dominant CDR3 length were clonally expanded. These results indicate that SIV infection can induce a disruption of macaque CD4 + T‐cell repertoires during the primary infection. The finding in this study, therefore, suggests that the virus‐induced clonal dominance can contribute to the disruption of CD4 + T‐cell repertoires.