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Science 24 May 1996: Vol. 272. no. 5265, pp. 1167 - 1170 DOI: 10.1126/science.272.5265.1167
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Reports
Prognosis in HIV-1 Infection Predicted by the Quantity of Virus
in Plasma
John W. Mellors,
*
Charles R. Rinaldo Jr.,
Phalguni Gupta,
Roseanne M. White,
John A. Todd,
Lawrence A. Kingsley
The relation between viremia and clinical outcome in individuals
infected with human immunodeficiency virus-type 1 (HIV-1) has
important implications for therapeutic research and clinical care.
HIV-1 RNA in plasma was quantified with a branched-DNA signal
amplification assay as a measure of viral load in a cohort of 180 seropositive men studied for more than 10 years. The risk of acquired
immunodeficiency syndrome (AIDS) and death in study subjects, including
those with normal numbers of CD4+ T cells, was directly
related to plasma viral load at study entry. Plasma viral load was a
better predictor of progression to AIDS and death than was the number
of CD4+ T cells.
J. W. Mellors, Department of Medicine, School of Medicine,
University of Pittsburgh, Pittsburgh, PA 15213, USA; Department of
Infectious Diseases and Microbiology, Graduate School of Public Health,
University of Pittsburgh, Pittsburgh, PA 15261, USA; and Veterans
Affairs Medical Center, Pittsburgh, PA 15240, USA.
C. R. Rinaldo Jr., Department of Pathology, School of Medicine, and
Department of Infectious Diseases and Microbiology, Graduate School of
Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA.
P. Gupta, Department of Infectious Diseases and Microbiology, Graduate
School of Public Health, University of Pittsburgh, Pittsburgh, PA
15261, USA.
R. M. White and J. A. Todd, Chiron Corporation, Emeryville, CA 94608, USA.
L. A. Kingsley, Department of Infectious Diseases and Microbiology and
Department of Epidemiology, Graduate School of Public Health,
University of Pittsburgh, Pittsburgh, PA 15261, USA.
*
To whom correspondence should be addressed at University of
Pittsburgh Graduate School of Public Health, 403 Parran Hall,
Pittsburgh, PA 15261, USA.
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PNAS
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N. Engl. J. Med.
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- Evaluation of Two Commercially Available, Inexpensive Alternative Assays Used for Assessing Viral Load in a Cohort of Human Immunodeficiency Virus Type 1 Subtype C-Infected Patients from South Africa.
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- Direct Inoculation of Simian Immunodeficiency Virus from Sooty Mangabeys in Black Mangabeys (Lophocebus aterrimus): First Evidence of AIDS in a Heterologous African Species and Different Pathologic Outcomes of Experimental Infection.
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- Attenuated Central Nervous System Infection in Advanced HIV/AIDS With Combination Antiretroviral Therapy.
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Arch Neurol
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- Primary HIV-1 Infection Is Associated with Preferential Depletion of CD4+ T Lymphocytes from Effector Sites in the Gastrointestinal Tract.
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PNAS
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- A Human Immunodeficiency Virus Type 1-Infected Individual with Low Viral Load Harbors a Virus Variant That Exhibits an In Vitro RNA Dimerization Defect.
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- Immune Selection for Altered Antigen Processing Leads to Cytotoxic T Lymphocyte Escape in Chronic HIV-1 Infection.
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- Correlation between env V1/V2 Region Diversification and Neutralizing Antibodies during Primary Infection by Simian Immunodeficiency Virus sm in Rhesus Macaques.
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- Frequent Simian Foamy Virus Infection in Persons Occupationally Exposed to Nonhuman Primates.
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- Leishmania infantum Promotes Replication of HIV Type 1 in Human Lymphoid Tissue Cultured Ex Vivo by Inducing Secretion of the Proinflammatory Cytokines TNF-{alpha} and IL-1{alpha}.
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- Mycobacterium tuberculosis Recall Antigens Suppress HIV-1 Replication in Anergic Donor Cells via CD8+ T Cell Expansion and Increased IL-10 Levels.
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- Persistent Recognition of Autologous Virus by High-Avidity CD8 T Cells in Chronic, Progressive Human Immunodeficiency Virus Type 1 Infection.
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- Immune Failure in the Absence of Profound CD4+ T-Lymphocyte Depletion in Simian Immunodeficiency Virus-Infected Rapid Progressor Macaques.
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- Human Immunodeficiency Virus Type 1 Fitness Is a Determining Factor in Viral Rebound and Set Point in Chronic Infection.
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- Identification of Sequential Viral Escape Mutants Associated with Altered T-Cell Responses in a Human Immunodeficiency Virus Type 1-Infected Individual.
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