Endogenous Production of beta -Chemokines by CD4+, but Not CD8+, T-Cell Clones Correlates with the Clinical State of Human Immunodeficiency Virus Type 1 (HIV-1)-Infected Individuals and May Be Responsible for Blocking Infection with NonSyncytium-Inducing HIV-1 In Vitro

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J Virol, January 1998, p. 876-881, Vol. 72, No. 1
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Endogenous Production of $beta$ -Chemokines by CD4⁺, but Not CD8⁺, T-Cell Clones Correlates with the Clinical State of Human Immunodeficiency Virus Type 1 (HIV-1)-Infected Individuals and May Be Responsible for Blocking Infection with NonSyncytium-Inducing HIV-1 In Vitro

Kunal Saha,¹ Galina Bentsman,¹ Leonard Chess,² and David J. Volsky¹^,^*

Molecular Virology Laboratory, St. Luke's-Roosevelt Hospital Center, College of Physicians & Surgeons, Columbia University, New York, New York 10019,¹ and Division of Rheumatology, Department of Medicine, College of Physicians & Surgeons, Columbia University, New York, New York 10032²

Received 24 June 1997/Accepted 28 September 1997

Recent studies have demonstrated that the $beta$ -chemokines RANTES, MIP-1 $alpha$ , and MIP-1 $beta$ suppress human immunodeficiency virus type1 (HIV-1) replication in vitro and may play an important rolein protecting exposed but uninfected individuals from HIV-1 infection.However, levels of $beta$ -chemokines in AIDS patients are comparableto and can exceed levels in nonprogressing individuals, indicatingthat global $beta$ -chemokine production may have little effect on HIV-1disease progression. We sought to clarify the role of $beta$ -chemokinesin nonprogressors and AIDS patients by examination of $beta$ -chemokineproduction and HIV-1 infection in patient T-lymphocyte clonesestablished by herpesvirus saimiri immortalization. Both CD4⁺ and CD8⁺ clones were established, and they resembled primary T cells intheir phenotypes and expression of activated T-cell markers. CD4⁺ T-cell clones from all patients had normal levels of mRNA-encodingCCR5, a coreceptor for non-syncytium-inducing (NSI) HIV-1. CD4⁺ clones from nonprogressors and CD8⁺ clones from AIDS patients secreted high levels of RANTES, MIP1 $alpha$ ,and MIP-1 $beta$ . In contrast, CD4⁺ clones from AIDS patients produced no RANTES and little or noMIP-1 $alpha$ or MIP-1 $beta$ . The infection of CD4⁺ clones with the NSI HIV-1 strain ADA revealed an inverse correlationto $beta$ -chemokine production; clones from nonprogressors were poorlysusceptible to ADA replication, but clones from AIDS patientswere highly infectable. The resistance to ADA infection in CD4⁺ clones from nonprogressors could be partially reversed by treatmentwith anti- $beta$ -chemokine antibodies. These results indicate thatCD4⁺ cells can be protected against NSI-HIV-1 infection in culturethrough endogenously produced factors, including $beta$ -chemokines,and that $beta$ -chemokine production by CD4⁺, but not CD8⁺, T cells may constitute one mechanism of disease-free survivalfor HIV-1-infected individuals.

^* Corresponding author. Mailing address: Molecular Virology Laboratory, 432 W. 58th St., St. Luke's-Roosevelt Hospital Center,New York, NY 10019. Phone: (212) 582-4451. Fax: (212) 582-5027.E-mail: djv4{at}columbia.edu.

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Endogenous Production of -Chemokines by CD4+, but Not CD8+, T-Cell Clones Correlates with the Clinical State of Human Immunodeficiency Virus Type 1 (HIV-1)-Infected Individuals and May Be Responsible for Blocking Infection with NonSyncytium-Inducing HIV-1 In Vitro

Endogenous Production of $beta$ -Chemokines by CD4⁺, but Not CD8⁺, T-Cell Clones Correlates with the Clinical State of Human Immunodeficiency Virus Type 1 (HIV-1)-Infected Individuals and May Be Responsible for Blocking Infection with NonSyncytium-Inducing HIV-1 In Vitro