Antigen‐Specific Production of RANTES, Macrophage Inflammatory Protein (MIP)–1α, and MIP‐1β In Vitro Is a Correlate of Reduced Human Immunodeficiency Virus Burden In Vivo
Author(s) -
John Ferbas,
Janis V. Giorgi,
Shamim Amini,
Kathie GrovitFerbas,
Dorothy J. Wiley,
Roger Detels,
Susan Plaeger
Publication year - 2000
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/315849
Subject(s) - macrophage inflammatory protein , in vivo , chemokine , immunology , in vitro , macrophage , biology , virus , virology , inflammation , biochemistry , microbiology and biotechnology
RANTES (regulated on activation, normal T expressed and secreted), macrophage inflammatory protein (MIP)-1alpha, and MIP-1beta are human immunodeficiency virus (HIV) suppressor factors by virtue of their ability to compete with HIV for access to cell surface R5. Their ability to block HIV infection in vitro is unequivocal; however, their role as HIV suppressor factors in vivo is not firmly established. We therefore conducted a study to test the hypothesis that production of these factors in vitro was a correlate of decreased virus burden in vivo. Moreover, we asked whether higher beta chemokine production could be demonstrated with cells from people who are R5D32 heterozygotes, compared with people who are R5 wild-type homozygotes. Our data support the thesis that RANTES, MIP-1alpha, and MIP-1beta production is associated with decreased in vivo virus load. Moreover, enhanced production of these factors may be explained in part by the genetic background of the host.
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