scholarly journals Autoantibodies to the alpha/beta T-cell receptors in human immunodeficiency virus infection: dysregulation and mimicry.

1994 ◽  
Vol 91 (23) ◽  
pp. 10849-10853 ◽  
Author(s):  
D. F. Lake ◽  
S. F. Schluter ◽  
E. Wang ◽  
R. M. Bernstein ◽  
A. B. Edmundson ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Virus Infection ◽  
Human Immunodeficiency Virus Infection ◽  
T Cell Receptors ◽  
Cell Receptors ◽  
Immunodeficiency Virus ◽  
Alpha Beta

Longitudinal analysis of T-cell receptor gene use by CD8+ T cells in early human immunodeficiency virus infection in patients receiving highly active antiretroviral therapy

Blood ◽  
2001 ◽  
Vol 97 (1) ◽  
pp. 214-220 ◽  
Author(s):  
Anna M. Schito ◽  
Eric Vittinghoff ◽  
Frederick M. Hecht ◽  
Mary K. Elkins ◽  
James O. Kahn ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Antiretroviral Therapy ◽  
Virus Infection ◽  
Human Immunodeficiency Virus Infection ◽  
T Cell Receptor ◽  
Highly Active Antiretroviral Therapy ◽  
Cell Receptor ◽  
Highly Active ◽  
Immunodeficiency Virus

Abstract The effects of early antiretroviral therapy on the peripheral CD8+ T-cell population were assessed by sequentially determining the T-cell receptor (TCR) repertoire complexity in a cohort of 15 individuals recently diagnosed with human immunodeficiency virus infection. Analysis was based on quantitative TCR variable B gene (TCRBV) usage and complementary-determining region 3 length assessment. Repertories were assessed at baseline and at weeks 2, 4, 12, 24, and 72 after initiation of therapy. Early administration of highly active antiretroviral therapy has a positive effect on the preservation and homeostasis of the CD8+ cell repertoire. Nevertheless, differences from average baseline and control TCR profiles and initial development of repertoire perturbations were observed. The findings suggest that additional therapeutic protocols will be required during primary infection to significantly prevent long-term erosion of the T-cell–mediated immune response.

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