The Cell Tropism of Human Immunodeficiency Virus Type 1 Determines the Kinetics of Plasma Viremia in SCID Mice Reconstituted with Human Peripheral Blood Leukocytes
Autor: | Donald E. Mosier, Gaston Picchio, Kathy Wehrly, Bruce Chesebro, Richard J. Gulizia |
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Jazyk: | angličtina |
Rok vydání: | 1998 |
Předmět: |
CD4-Positive T-Lymphocytes
Author's Correction Chemokine viruses Kinetics Immunology Viral Pathogenesis and Immunity Viremia HIV Infections Mice SCID Biology Virus Replication Microbiology Mice Viral entry Virology medicine Animals Humans Tropism Transmission (medicine) Macrophages RNA virus diseases biochemical phenomena metabolism and nutrition medicine.disease Disease Models Animal Viral replication Insect Science biology.protein HIV-1 Leukocytes Mononuclear RNA Viral |
Popis: | Most individuals infected with human immunodeficiency virus type 1 (HIV-1) initially harbor macrophage-tropic, non-syncytium-inducing (M-tropic, NSI) viruses that may evolve into T-cell-tropic, syncytium-inducing viruses (T-tropic, SI) after several years. The reasons for the more efficient transmission of M-tropic, NSI viruses and the slow evolution of T-tropic, SI viruses remain unclear, although they may be linked to expression of appropriate chemokine coreceptors for virus entry. We have examined plasma viral RNA levels and the extent of CD4 + T-cell depletion in SCID mice reconstituted with human peripheral blood leukocytes following infection with M-tropic, dual-tropic, or T-tropic HIV-1 isolates. The cell tropism was found to determine the course of viremia, with M-tropic viruses producing sustained high viral RNA levels and sparing some CD4 + T cells, dual-tropic viruses producing a transient and lower viral RNA spike and extremely rapid depletion of CD4 + T cells, and T-tropic viruses causing similarly lower viral RNA levels and rapid-intermediate rates of CD4 + T-cell depletion. A single amino acid change in the V3 region of gp120 was sufficient to cause one isolate to switch from M-tropic to dual-tropic and acquire the ability to rapidly deplete all CD4 + T cells. |
Databáze: | OpenAIRE |
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