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Volume 336:1337-1342 May 8, 1997 Number 19 Next

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ABSTRACT

Background There are only limited data on human immunodeficiency virus type 1 (HIV-1) RNA in perinatally infected infants. Understanding the dynamics of HIV-1 infection and its relation to disease progression may help identify opportunities for effective antiviral treatment in infected infants.

Methods We obtained plasma samples from 106 HIV-infected infants at birth; at 1, 2, 4, 6, 9, 12, 15, and 18 months of age; and subsequently every 6 months. HIV-1 RNA was assayed by means of a reverse-transcription polymerase chain reaction. The infants were born between 1990 and 1993, and only 21 percent of the infants' mothers received any treatment with zidovudine during pregnancy.

Results Plasma HIV-1 RNA levels increased rapidly after birth, peaked at 1 to 2 months of age (median values at 1 and 2 months, 318,000 and 256,000 copies per milliliter, respectively), and then slowly declined to a median of 34,000 copies per milliliter at 24 months. Newborns with a first positive HIV-1 culture within 48 hours after birth had significantly higher HIV-1 RNA levels, although only during the first two months of life, than those with a first positive culture seven or more days after birth. Infants with a rapid progression of disease had higher peak HIV-1 RNA levels in the first two months of life than those without rapid progression (median value, 724,000 vs. 219,000 copies per milliliter; P = 0.006), as well as a higher geometric mean value during the first year of life (median value, 330,000 vs. 158,000 copies per milliliter; P = 0.001).

Conclusions In perinatally infected infants, HIV-1 RNA levels are high and decline only slowly during the first two years of life. Infants with very high viral loads in the first months of life are at increased risk for a rapid progression of disease, which suggests that early treatment with antiretroviral agents may be indicated for these infants.

Source Information

From the Department of Pediatrics, Section of Allergy and Immunology, Baylor College of Medicine, Houston (W.T.S.); Johns Hopkins University, Baltimore (T.C.Q.); the National Institute of Allergy and Infectious Diseases, Bethesda, Md. (T.C.Q., J.F.L.); the Virology Department, Columbia–Presbyterian Hospital, New York (P.L.); the National Institute of Child Health and Human Development, Bethesda, Md. (L.M.); the New England Research Institutes, Watertown, Mass. (S.A., L.A.K.); the University of Illinois at Chicago, Chicago (K.R.); the State University of New York Health Science Center at Brooklyn, Brooklyn (E.H.); the University of Puerto Rico, San Juan (C.D.); the Department of Biostatistics, Harvard School of Public Health, Boston (M.P.); and the National Institute on Drug Abuse, Rockville, Md. (V.S.).

Address reprint requests to Dr. Shearer at Texas Children's Hospital, 6621 Fannin St., MC 1-3291, Houston, TX 77030.

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