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