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Journal of Virology, April 2005, p. 4908-4917, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4908-4917.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Human Immunodeficiency Virus (HIV)-Specific Gamma Interferon Secretion Directed against All Expressed HIV Genes: Relationship to Rate of CD4 Decline

Yoav Peretz,1 Galit Alter,2 Marie-Pierre Boisvert,1 George Hatzakis,1 Christos M. Tsoukas,1 and Nicole F. Bernard1*

McGill University Health Center, Montreal, Quebec, Canada,1 Massachusetts General Hospital, Boston, Massachusetts2

Received 31 August 2004/ Accepted 1 December 2004

Immune responses to human immunodeficiency virus (HIV) are detected at all stages of infection and are believed to be responsible for controlling viremia. This study seeks to determine whether gamma interferon (IFN-{gamma})-secreting HIV-specific T-cell responses influence disease progression as defined by the rate of CD4 decline. The study population consisted of 31 subjects naïve to antiretroviral therapy. All were monitored clinically for a median of 24 months after the time they were tested for HIV-specific responses. The rate of CD4+-T-cell loss was calculated for all participants from monthly CD4 counts. Within this population, 17 subjects were classified as typical progressors, 6 subjects were classified as fast progressors, and 8 subjects were classified as slow progressors. Peripheral blood mononuclear cells were screened for HIV-specific IFN-{gamma} responses to all expressed HIV genes. Among the detected immune responses, 48% of the recognized peptides were encoded by Gag and 19% were encoded by Nef gene products. Neither the breadth nor the magnitude of HIV-specific responses correlated with the viral load or rate of CD4 decline. The breadth and magnitude of HIV-specific responses did not differ significantly among typical, fast, and slow progressors. These results support the conclusion that although diverse HIV-specific IFN-{gamma}-secreting responses are mounted during the asymptomatic phase, these responses do not seem to modulate disease progression rates.

* Corresponding author. Mailing address: Research Institute of the McGill University Health Center, Montreal General Hospital, 1650 Cedar Ave., Rm. C10-160, Montreal, Quebec H3G 1A4, Canada. Phone: (514) 934-1934, ext. 44584. Fax: (514) 937-1424. E-mail: nicole.bernard{at}mcgill.ca.

Journal of Virology, April 2005, p. 4908-4917, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4908-4917.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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