Plasma Stromal Cell–Derived Factor (SDF)‐1 Levels, SDF1‐3′A Genotype, and Expression of CXCR4 on T Lymphocytes: Their Impact on Resistance to Human Immunodeficiency Virus Type 1 Infection and Its Progression
Author(s) -
Álex Soriano,
Catalina Martínez,
Felipe García,
Montserrat Plana,
Eduard Palou,
Marylène Lejeune,
Juan I. Aróstegui,
Elisa de Lazzari,
Carmen Rodríguez,
Alicia Barrasa,
José Ignacio Lorenzo,
José Alcamı́,
Jorge del Romero,
José M. Miró,
José M. Gatell,
Teresa Gallart
Publication year - 2002
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 - 10.1086/343741
Subject(s) - biology , immunology , stromal cell derived factor 1 , cxcr4 , virus , lentivirus , virology , viral load , stromal cell , genotype , viral disease , immune system , chemokine , cancer research , genetics , gene
Plasma stromal cell-derived factor (SDF)-1 levels, SDF1-3'A polymorphism, and CXCR4(+) T lymphocytes in relation to resistance to human immunodeficiency virus (HIV)-1 infection and its progression were investigated in a study of HIV-positive patients, exposed but uninfected (EU) subjects, and healthy control subjects, all lacking CCR5 Delta 32 homozygosity. SDF1-3'A homozygosity was associated with low plasma SDF-1 levels in uninfected persons and was not related to long-term nonprogression. HIV-1 infection involved increased plasma SDF-1 levels, which were not attributable to any kind of chronic viral infection, because all EU hemophiliacs were hepatitis C virus-positive but had normal SDF-1 levels. High plasma SDF-1 levels and low CXCR4 expression on T lymphocytes was associated with long-term nonprogression, whereas in advancing disease expression of CXCR4 increased, accompanied by a decrease in plasma SDF-1 during the more advanced stages of HIV-1 infection. EU subjects with sexual exposure to HIV-1, but not EU hemophiliacs, showed an underpresentation of SDF1-3'A allele frequency, which was coupled with high plasma SDF-1 levels and low CXCR4 expression.
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