Page 248 - AIDSBK23C

Page 248

PREGNANCY AND THE PLACENTA IN AIDS

HIV infected women should be monitored with viral loads every month until the virus is
undetectable and then every 2–3 months, along with CD4 counts each trimester. Resistance
testing can be done if they have recently seroconverted or if they have failed therapy. HIV
infected women in labor can be treated with either: 1) zidovudine in labor and 6 weeks to the
neonate, 2) nevirapine, a single dose to the mother in labor and a single dose to the neonate, 3)
zidovudine–lamivudine in labor and to the neonate for 1 week, or 4) both nevirapine as above
and the zidovudine regimen as above. Cesarean delivery should be recommended to all women
with an HIV-1 viral load greater than 1000 copies/mL. Discontinuation of antiretroviral therapy
in the postpartum period is appropriate in those circumstances in which it would not have been
used in the first instance if the woman had not been pregnant.[291] The use of nevirapine during
labor to prevent perinatal HIV transmission has been shown to increase the rate of virologic
resistance, but only when antiretroviral regimens including nevirapine were instituted within 6
months following delivery.[1001]
There is no solid evidence to suggest that pregnancy accelerates the progression of HIV
infection to AIDS in women, though pregnancy increases the infectivity of women to sexual
partners.[217,1002] Pregnancies in HIV-infected women are more likely to result in
prematurity, intrauterine growth retardation, spontaneous abortion, and perinatal death.[214]
The 50% rate of HIV infection in stillbirths from HIV-infected mothers is much greater than that
for liveborns, suggesting that fetal HIV infection increases fetal demise.[1003]
The placenta in mothers with HIV infection has been shown by immunocytochemistry
and in situ hybridization to contain HIV-1 antigen by 8 weeks gestational age. Placental tissue
also contains cells with CD4 receptors, and HIV infection can occur with transplacental spread
of HIV to the fetus. Vertical transmission may occur through either endothelial tissues or
Hofbauer cells that have CD4 receptors. Trophoblasts also have CD4 receptors, and placental
cytokines and chemokines influence HIV replication within trophoblasts. The CCR5 strain of
HIV-1 appears to be preferentially transmitted through the placenta.[1004]
The histology of the placenta does not appear to be altered by HIV infection. The most
common inflammatory lesion is chorioamnionitis, observed in a third of cases. The most
common non-inflammatory lesion is cytotrophoblastic hyperplasia, observed in about three-
fourths of cases. Antiretroviral therapy does not appear to diminish the incidence of these
lesions.[1005]
The risk for perinatal HIV infection is increased when chorioamnionitis, plasmacellular
deciduitis, and decidual cell necrosis is present.[179,1006] When placental infection with
malarial parasites is present, then the risk of mother-to-child transmission of HIV
increases.[1007] An immune restoration syndrome in pregnant women starting antiretroviral
therapy may lead to placental villitis and fetal loss.[1008]
Very rarely, opportunistic infections have occurred in placenta of mothers with AIDS.
Placental cryptococcosis may be manifested grossly as multiple white nodules and
microscopically by numerous encapsulated budding yeasts in the intervillous spaces and
chorionic villi.[1009]