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J Virol, June 1998, p. 5231-5238, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Similar Levels of Human Immunodeficiency Virus Type 1 Replication in Human TH1 and TH2 Clones

Judy A. Mikovits,1 Dennis D. Taub,2 Susan M. Turcovski-Corrales,2 and Francis W. Ruscetti3,*

Intramural Research Support Program, SAIC-Frederick,1 and the Laboratory of Leukocyte Biology,3 National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland, and Immunology Program, National Institute of Aging, Baltimore, Maryland2

Studies on the development and function of CD4+ TH1 and TH2 cells during the progression to AIDS may increase the understanding of AIDS pathogenesis. The preferential replication of human immunodeficiency virus (HIV) in either TH1 or TH2 cells could alter the delicate balance of the immune response. TH1 (gamma interferon [IFN-gamma ] positive, interleukin-4 [IL-4] and IL-5 negative) and TH2 (IFN-gamma negative, IL-4 and IL-5 positive) clones, developed from several healthy donors, pedigreed by reverse transcriptase PCR (RT-PCR) and enzyme linked immunosorbent assay have similar levels of cell surface expression of CD4 and several chemokine receptor cofactors necessary for viral entry. After activation by specific antigens and infection with T-cell-tropic strains of HIV type 1 (HIV-1), TH1 and TH2 clones showed similar levels of viral entry and reverse transcription. At days 3 through 14 postinfection, HIV replicated to similar levels in several TH1 and TH2 clones as measured by release of HIV p24 and total number of copies of gag RNA/total cell RNA as measured by RT-PCR. When values were normalized for viable cell number in three clones of each type, there was up to twofold more HIV RNA in TH1 than TH2 cells. In addition, several primary monocytotropic HIV-1 strains were able to replicate to similar levels in TH1 and TH2 cells. These studies suggest that the importance of TH1 and TH2 subsets in AIDS pathogenesis transcends clonal differences in their ability to support HIV replication.

* Corresponding author. Mailing address: Laboratory of Leukocyte Biology, NCI-Frederick Cancer Research and Development Center, Bldg. 567, Rm. 254, Frederick, MD 21702-1201. Phone: (301) 846-1504. Fax: (301) 846-7034. E-mail: RuscettF{at}ncifcrf.gov.

J Virol, June 1998, p. 5231-5238, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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