Abstract
In this article, we show that passage in SCID mice rendered a human CD4(+) T-cell line (CEM cells) highly susceptible to infection by macrophage-tropic (M-tropic) strains and primary clinical isolates of human immunodeficiency virus type 1 (HIV-1). This in vivo-acquired permissiveness of CEM cells was associated with the induction of a CD45RO+ phenotype as well as of some beta-chemokine receptors. Regulated upon activation, normal T-cell expressed and secreted chemokine entirely inhibited the ability of M-tropic HIV-1 strains to infect these cells. These findings may lead to new approaches in investigating in vivo the capacity of different HIV strains to exploit chemokine receptors in relation to the dynamics of the activation and/or differentiation state of human CD4(+) T cells.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acquired Immunodeficiency Syndrome / etiology*
-
Acquired Immunodeficiency Syndrome / immunology
-
Acquired Immunodeficiency Syndrome / virology
-
Animals
-
Base Sequence
-
CD4-Positive T-Lymphocytes / immunology*
-
CD4-Positive T-Lymphocytes / pathology
-
CD4-Positive T-Lymphocytes / virology*
-
Cell Differentiation
-
Cell Line
-
DNA Primers / genetics
-
Female
-
HIV-1 / immunology*
-
HIV-1 / pathogenicity*
-
Humans
-
Leukocyte Common Antigens / physiology
-
Lymphocyte Activation
-
Macrophages / virology*
-
Mice
-
Mice, SCID
-
Phenotype
-
Protein Tyrosine Phosphatase, Non-Receptor Type 1
-
Receptors, CCR5 / genetics
-
Receptors, CCR5 / physiology*
-
Receptors, Chemokine / genetics
-
Receptors, Chemokine / physiology
-
Up-Regulation
-
Virus Cultivation
Substances
-
DNA Primers
-
Receptors, CCR5
-
Receptors, Chemokine
-
Leukocyte Common Antigens
-
Protein Tyrosine Phosphatase, Non-Receptor Type 1