TY - JOUR
T1 - A tumor necrosis factor-α-inducible promoter variant of interferon-γ accelerates CD4+ t cell depletion in human immunodeficiency virus-1-infected individuals
AU - An, Ping
AU - Vlahov, David
AU - Margolick, Joseph B.
AU - Phair, John
AU - O'Brien, Thomas R.
AU - Lautenberger, James
AU - O'Brien, Stephen J.
AU - Winkler, Cheryl A.
N1 - Funding Information:
Received 18 November 2002; accepted 18 February 2003; electronically published 9 July 2003. Presented in part: 52nd Annual Meeting of American Society of Human Genetics, Baltimore, Maryland, 15–19 October 2002 (abstract 1136). Financial support: National Cancer Institute; National Institutes of Health (contract NO1-CO-124000). The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does the mention of trade names, commercial products, or organizations imply endorsement by the U. S. Government. Reprints or correspondence: Dr. Cheryl Winkler, Bldg. 560, NCI-FCRDC, Frederick, MD 21702 (winkler@ncifcrf.gov).
PY - 2003/7/15
Y1 - 2003/7/15
N2 - A polymorphism, -179G/T, in the promoter of the interferon (IFN)-γ gene (IFNG) confers differential tumor necrosis factor-α (TNF-α) inducibility to the IFNG promoter. The rarer allele, -179T, but not -179G, is inducible by TNF-α. We investigated the effects of IFNG -179G/T on AIDS pathogenesis. In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. It is possible that increased IFN-γ production induced by TNF-α when -179T is present causes CD4 cell depletion by apoptosis.
AB - A polymorphism, -179G/T, in the promoter of the interferon (IFN)-γ gene (IFNG) confers differential tumor necrosis factor-α (TNF-α) inducibility to the IFNG promoter. The rarer allele, -179T, but not -179G, is inducible by TNF-α. We investigated the effects of IFNG -179G/T on AIDS pathogenesis. In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG -179G/T genotype was associated with accelerated progression to CD4 <200 and AIDS-1993, a finding suggesting that IFNG -179T is a risk factor for AIDS progression, as measured by CD4 cell count. It is possible that increased IFN-γ production induced by TNF-α when -179T is present causes CD4 cell depletion by apoptosis.
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U2 - 10.1086/376455
DO - 10.1086/376455
M3 - Article
C2 - 12854077
AN - SCOPUS:0041314090
SN - 0022-1899
VL - 188
SP - 228
EP - 231
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 2
ER -