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The role of plasma RNA as a determinant of risk in maternal-fetal HIV transmission and early progression of disease in perinatally-infected infants.
Bryson YJ; UCLA School of Medicine, Department of Pediatrics.
November 30, 1996
3rd Conf Retro and Opportun Infect. 1996 Jan 28-Feb 1;:175. Unique

ZDV treatment during pregnancy, delivery and to the infant has been shown to significantly reduce perinatal transmission which could be related to reduction of maternal virus load and/or prophylaxis of the infant several studies have shown a significant increase in transmission risk associated with high maternal virus load at or near delivery. In a prospective cohort study of HIV infected pregnant mothers and their infants, we measured virus load over time by Roche RNA PCR, quantitative DNA PCR, co-culture, plasma viremia and ICD p24 AG and correlated resuls with infant outcome, timing of infection, and clinical disease progression in infants. We quantitated virus load at delivery in 97 mother infant pairs including 50 women followed over gestation (mean 13 weeks). Transmitters (n=20) had significantly higher median RNA copy numers (94,000 vs. 4,597), HIV copy/micrograms PBMC DNA (253 vs. 20) and lower CD4 counts (349/mm3 at delivery compared to nontransmitter whereas untreated nontransmitters had stable low HIV levels. The highest HIV levels were found in in utero transmitters whereas intrapartum transmitters had lower levels (n= 75)).In 2 nontransmitters treated with ZDV (mean 53 weeks) there was a median 5-fold drop in RNA copy number by delivery. Transmitters showed either a persistently elevated HIV RNA copy number or an increase in late gestation, HIV levels suggesting that other factors at delivery may also play a role. This study suggests that maternal virus load is a critical factor in the risk of transmission, that single determinations of virus load early in pregnancy do not necessarily predict outcome and delivery factors may account for transmission in some cases with low virus load. We also found that both the timing of infection and the pattern and magnitude of HIV replication soon after birth were important determinants of outcome in infants. In 32 infected infants followed from birth intrapartum infected infants (n=14) with negative virus at birth also had undetectable HIV RNA whereas all 18 infants with positive virus at birth were positive by HIV RNA. Infants with early rapid disease progression showed a rapid burst of HIV replication after birth (mean peak 3,753,300 RNA/copies/ml (890,000 - 7 million range) compared to infants with slow disease progression who had a lower virus load (mean peak 793,578 RNA copies /ml (190,000 - 1.5 million range, p=.0002). The presence of virus at birth and rapid high levels of HIV replication should target infants who are a thigh risk of rapid disease progression.

*Disease Transmission, Vertical Female HIV Core Protein p24/BLOOD HIV Infections/PHYSIOPATHOLOGY/*TRANSMISSION HIV-1/GENETICS/*ISOLATION & PURIF Human Infant Polymerase Chain Reaction Pregnancy Pregnancy Complications, Infectious RNA, Viral/*BLOOD Risk Factors ABSTRACT