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Immunotoxin Complementation of HAART to Deplete Persisting HIV-Infected Cell Reservoirs

Authors
Journal
PLoS Pathogens
1553-7366
Publisher
Public Library of Science
Publication Date
Volume
6
Issue
6
Identifiers
DOI: 10.1371/journal.ppat.1000803
Keywords
  • Opinion
  • Infectious Diseases/Antimicrobials And Drug Resistance
  • Infectious Diseases/Hiv Infection And Aids
  • Infectious Diseases/Viral Infections
  • Virology/Antivirals
  • Including Modes Of Action And Resistance
  • Virology/Immunodeficiency Viruses
  • Virology/New Therapies
  • Including Antivirals And Immunotherapy
  • Virology/Persistence And Latency
Disciplines
  • Medicine

Abstract

ppat.1000803 1..6 Opinion Immunotoxin Complementation of HAART to Deplete Persisting HIV-Infected Cell Reservoirs Edward A. Berger1*, Ira Pastan2 1 Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America, 2 Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America Achievements and Limitations of Antiretroviral Therapy The development of combinations of drugs that potently suppress HIV replica- tion, collectively given the acronym HAART (highly active antiretroviral ther- apy), has transformed the lives of people with HIV infection, particularly in high- income countries [1]. Though modern HAART regimens can drive HIV plasma viral loads below the detection limits of standard clinical assays ($50 copies HIV RNA/ml), long-term treatment fails to eradicate infectious virus as revealed by the persistence of HIV proviral DNA and infectious HIV in peripheral blood and lymphoid tissue, as well as by low level viremia (1–50 RNA copies/ml) in the majority of treated people as detected by ultrasensitive single copy assays [2–4]. Moreover, reservoirs of latently infected resting memory CD4+ T lymphocytes are established early after infection and persist throughout treatment with exceedingly slow decay rates; these latent reservoirs are unlikely to be eliminated by HAART alone, and thus have the potential to re- ignite the infection if activated after therapy is halted. A further complication is the existence of multiple sanctuaries of infection in cell types from various lineages (monocyte-macrophages, dendritic cells, hemapoietic stem cells, etc.) detected in distinct anatomical compartments (blood, peripheral lymph nodes, gut mucosa, central nervous system, genital tract, etc.). These findings raise a number of critical inter-related questions: Doe

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