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Human Immunodeficiency Virus (HIV) Type 1 Antibodies in Perinatal HIV‐1 Infection: Association with Human HIV‐1 Transmission, Infection, and Disease Progression
Author(s) -
Jane Pitt,
Denis Henrard,
Gordon FitzGerald,
Lynne Mofenson,
Judy Lew,
George V. Hillyer,
Hermann Mendez,
Ellen Cooper,
Celine Hanson,
Kenneth Rich
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 - 10.1086/315809
Subject(s) - antibody , immunology , medicine , transmission (telecommunications) , peripheral blood mononuclear cell , immune system , disease , virology , virus , viral disease , biology , biochemistry , electrical engineering , engineering , in vitro
Anti -human immunodeficiency virus (HIV) type 1 antibodies in 242 pregnant women and 238 infants were measured at birth and at 1, 2, 4, and 6 months after birth, to estimate their association with perinatal transmission and infant disease progression. Maternal anti-p24 (P=.01) and anti-gp120 (P=.04) antibodies were inversely associated with vertical transmission rates, independent of maternal percentage of CD4 cells, hard drug use, duration of ruptured membranes, serum albumin levels, serum vitamin A levels, and quantitative HIV-1 peripheral mononuclear blood cell culture, but not with maternal plasma immune complex dissociated p24 or HIV-1 RNA copy number, both of which were highly correlated with antibodies. From ages 1-2 months, anti-gp120, -gp41, -p31, and -p66 decayed to a greater extent in infected than in uninfected infants. Infected infants produced anti-p24 antibody by age 2 months, anti-p17 by 4 months, and anti-p41 and anti-gp120 by 6 months. As early as birth, infants with rapid disease progression had lower levels of anti-p24 than did infants whose disease did not rapidly progress, but not independently of HIV-1 RNA levels.

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