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HIV‐Specific Cellular Immune Response Is Inversely Correlated with Disease Progression as Defined by Decline of CD4+T Cells in Relation to HIV RNA Load
Author(s) -
Annette Oxenius,
David A. Price,
Martin Hersberger,
Erika Schlaepfer,
Rainer Weber,
Markus Weber,
Thomas M. Kündig,
Jürg Böni,
Helen Joller,
Rodney E. Phillips,
Markus Flepp,
Milos Opravil,
Roberto F. Speck
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/382028
Subject(s) - biology , immunology , human leukocyte antigen , immune system , coinfection , cd8 , virology , chemokine , virus , genotype , t cell , immunopathology , chemokine receptor , antigen , gene , genetics
The average time between infection with human immunodeficiency virus (HIV) and development of acquired immune deficiency syndrome is approximately 8 years. However, progression rates vary widely, depending on several determinants, including HIV-specific immunity, host genetic factors, and virulence of the infecting strain. In untreated HIV-infected patients with different progression rates, we examined HIV-specific T cell responses in combination with host genetic markers, such as chemokine/chemokine-receptor (CCR) polymorphisms and human leukocyte antigen (HLA) genotypes. HIV-specific CD4(+) T cell responses and, to a lesser extent, HIV-specific CD8(+) T cell responses were inversely correlated with progression rate. Slower progression was not related to polymorphisms in CCR genes, HLA genotype, or GB virus C coinfection. These data suggest that HIV-specific T cell responses are involved in protecting the host from disease progression.

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