Prolonged CD4+ Cell/Virus Load Discordance during Treatment with Protease Inhibitor–Based Highly Active Antiretroviral Therapy: Immune Response and Viral Control

Mechanisms that underly discordant CD4+ cell/virus load (VL) responses in patients who receive highly active antiretroviral therapy (HAART) were studied in 30 human immunodeficiency virus (HIV)–positive patients, in 3 groups. Discordant responders maintained CD4+ cell levels >200/mm3 with stable...

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Bibliographic Details
Published in:The Journal of infectious diseases 2003-04, Vol.187 (7), p.1027-1037
Main Authors: Sufka, Susan A, Ferrari, Guido, Gryszowka, Victoria E, Wrin, Terri, Fiscus, Susan A, Tomaras, Georgia D, Staats, Herman F, Patel, Dhavalkumar D, Sempowski, Gregory D, Hellmann, Nicholas S, Weinhold, Kent J, Hicks, Charles B
Format: Article
Language:English
Subjects:
Adult
AIDS
Antiretroviral Therapy, Highly Active
CD4 Lymphocyte Count
Cell lines
Female
Highly active antiretroviral therapy
HIV
HIV - drug effects
HIV 1
HIV Infections - drug therapy
HIV Infections - immunology
HIV Infections - virology
HIV Protease Inhibitors - pharmacology
HIV Protease Inhibitors - therapeutic use
HIV/AIDS
Humans
Kidney cells
Male
Medical treatment failures
Middle Aged
T lymphocytes
Time Factors
Treatment Failure
Viral Load
Virology
Virus Replication - drug effects
Viruses
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Summary:Mechanisms that underly discordant CD4+ cell/virus load (VL) responses in patients who receive highly active antiretroviral therapy (HAART) were studied in 30 human immunodeficiency virus (HIV)–positive patients, in 3 groups. Discordant responders maintained CD4+ cell levels >200/mm3 with stable or increasing trend, despite sustained VLs of 500–5000 copies/mL, for >2 years. Treatment-success patients had CD4+ cell counts >200/mm3 with stable or increasing trend and VLs 2 years. Treatment-failure patients initially responded to HAART, followed by decreasing CD4+ cell counts and increasing VLs. Interferon-γ production to gag and noncytolytic CD8+ cell suppressive activity were greater in discordant responders. Cellular activation was greatest in patients with treatment failure. All discordant responders had non–syncytium-inducing (CCR5-tropic) viruses. Viruses from discordant responders and from patients with treatment failure had extensive resistance mutations; discordant responders had significantly lower viral replication capacities. These findings suggest that discordant responses may be related to enhanced HIV-directed immune responses, diminished cellular activation, decreased viral replication capacity, and preservation of non–syncytium-inducing virus strains
ISSN:0022-1899
1537-6613
DOI:10.1086/368359