OBJECTIVES:This study assessed recent trends in HIV seroprevalence among injecting drug users in New York City.METHODS:We analyzed temporal trends in HIV seroprevalence from 1991 through 1996 in 5 studies of injecting drug users recruited from a detoxification program, a methadone maintenance program, research storefronts in the Lower East Side and Harlem areas, and a citywide network of sexually transmitted disease clinics. A total of 11,334 serum samples were tested.RESULTS:From 1991 through 1996, HIV seroprevalence declined substantially among subjects in all 5 studies: from 53% to 36% in the detoxification program, from 45% to 29% in the methadone program, from 44% to 22% at the Lower East Side storefront, from 48% to 21% at the Harlem storefront, and from 30% to 21% in the sexually transmitted disease clinics (all P < .002 by chi 2 tests for trend).CONCLUSIONS:The reductions in HIV seroprevalence seen among injecting drug users in New York City from 1991 through 1996 indicate a new phase in this large HIV epidemic. Potential explanatory factors include the loss of HIV-seropositive individuals through disability and death and lower rates of risk behavior leading to low HIV incidence.

Among a cohort of 152 infants perinatally infected with human immunodeficiency virus type 1, and their mothers, we correlated infant outcome with material CD4+ lymphocyte count and the presence of maternal acquired immunodeficiency syndrome near delivery. In a subset of 50 mother-infant pairs, we also correlated infant outcome with maternal quantitative viral burden as measured by the nucleic acid sequence based amplification system. We found that low maternal CD4+ cell count and high viral burden were associated with decreased time to category C disease or death in infants infected with human immunodeficiency virus type 1. In a multivariate analysis, high maternal viral load and maternal acquired immunodeficiency syndrome were independently associated with shorter time to category C disease or death in infants with human immunodeficiency virus type 1 infection. High viral load in pregnant women, independent of the presence of advanced maternal disease, appears to increase the risk of rapidly progressive disease in their infected offspring.

Objective: To investigate the hypothesis that labour and delivery events, perinatal characteristics, and maternal factors are only associated with intrapartum HIV transmission, and not with intrauterine HIV transmission.Methods: In the New York City Perinatal HIV Transmission Collaborative Study 276 infants of HIV-infected women were followed prospectively and had results of early polymerase chain reaction (PCR) tests available. Among infected children, intrauterine infection was presumed if HIV DNA was detected by PCR in samples collected from children aged less than or equal to 3 days, and intrapartum infection was presumed if HIV DNA was not detected in these early samples. The proportion of infants with presumed intrauterine and intrapartum infections were compared by selected intrapartum, perinatal and maternal characteristics.Results: Presumed intrapartum infection was found in 7% of infants delivered by Cesarean section and, among infants delivered vaginally, those with longer duration of membrane rupture (> 4 h) were significantly more likely to have presumed intrapartum HIV infection (22%) than those with shorter duration (9%; P = 0.02). There were no differences in presumed intrauterine HIV infection by mode of delivery or longer duration of membrane rupture. infants born preterm and small for gestational age had significantly higher risks of presumed intrapartum infection, but only those who were small for gestational age had higher risks of intrauterine infection.Conclusion: Our results support the notion that selected intrapartum conditions, long duration of membrane rupture prior to delivery in particular, are independent risk factors for maternal-infant transmission, and suggest that preterm infants may be especially vulnerable to intrapartum HIV exposure.

OBJECTIVE:To determine the effectiveness of primary prophylaxis in preventing Pneumocystis carinii pneumonia (PCP) in children with perinatally acquired human immunodeficiency virus 1 (HIV-1) infection.METHODS:We conducted a retrospective analysis of a cohort of infants followed from birth at six metropolitan hospitals and one outpatient clinic for pregnant, drug-using women in New York City. Outcomes measured were histologically confirmed PCP and/or death. The potential confounding effect of the infant's stage of illness, as determined by CD4 count, was controlled by including all CD4 determinations as time-dependant covariates in a Cox proportional hazards analysis. Cases were censored at PCP onset, death, loss to follow-up, and 18 months of age.RESULTS:One hundred twelve HIV-infected children were enrolled at birth between 1986 and 1993. Sixty of these were tracked beyond 18 months of age; of the others, 21 died before this age, 4 were considered lost to follow-up, and 27 had not reached 18 months of age at the last visit. Only 3 cases (4%) of confirmed PCP occurred among the 70 children who received primary PCP prophylaxis before 18 months of age, compared with 12 cases (28%) among 42 children not receiving PCP prophylaxis at any point before 18 months of age. The Kaplan-Meier estimated incidence of PCP in the first year among children not receiving prophylaxis was 25% (95% confidence interval [CI], 12 to 39). Using Cox methods, the unadjusted risk of PCP among infants not receiving prophylaxis, relative to those receiving it, was 4.1 (95% CI, 1.1 to 15); the relative risk was 4.4 (95% CI, 1.2 to 17) adjusting for the percentage of CD4-positive lymphocytes and 5.1 (95% CI, 1.3 to 20) adjusting for the absolute number of CD4-positive cells. Eight of 26 deaths were caused by PCP, and the likelihood of early death was significantly diminished if PCP prophylaxis was given (relative risk controlling for absolute CD4 cells, 2.57; 95% CI, 1.1 to 6.1).CONCLUSIONS:We report evidence that primary antimicrobial PCP prophylaxis is highly effective in decreasing the frequency of PCP and early death in infants with perinatal HIV infection. These findings support the revised National Pediatric HIV Resource Center and Centers for Disease Control and Prevention guidelines for PCP prophylaxis in children.

BACKGROUND AND METHODS:Differences in newborn outcome measures for human immunodeficiency virus (HIV)-1-infected and HIV-1-exposed but uninfected infants have been found in several studies, but not in others. Eighty-four infected and 248 uninfected children born to HIV-1-seropositive mothers followed prospectively in a multicenter, perinatal HIV-1 transmission cohort study were compared for differences in maternal demographics, health status, and newborn outcome measures, including delivery complications, physical examination findings, neonatal complications, and laboratory results.RESULTS:Mothers of HIV-1-infected infants were more likely than those of uninfected infants to have acquired immunodeficiency syndrome (AIDS) diagnosed through 2 weeks postpartum (21% vs 11%, P = .04); the transmission rate for the 38 women with AIDs was 37% compared with 22% for the 245 women without AIDS. Two of 27 (7%) women receiving zidovudine during pregnancy had infected infants compared with 73 (27%) of 275 women who did not receive zidovudine (P = .033). Mean gestational age was significantly lower among HIV-1-infected (37 weeks) than among uninfected infants (38 weeks; P < .001). Infected infants had significantly higher rates of prematurity (gestational age less than 37 weeks) (33% vs 19%, P = .01) and extreme prematurity (gestational age less than 34 weeks) (18% vs 6%, P = .001) than uninfected infants. Infection was associated with lower birth weight (2533 g vs 2862 g, P < .001) and smaller head circumference (32.0 cm vs 33.1 cm, P = .001). HIV-1-infected infants were significantly more likely to be small for gestational age (26% vs 16%, P = .04) and low birth weight (less than 2500 g) (45% vs 29%, P = .006) than infants who were uninfected. Twenty-two (26%) HIV-1-infected children died during a median follow-up of 27.6 months (range 1.9 to 98.3 months). Prematurity was predictive of survival: by Kaplan-Meier, an estimated 55% (95% confidence interval, 31% to 72%) of preterm infected children survived to 24 months compared with 84% (95% confidence interval, 70% to 92%) of full-term infected children (P = .005).CONCLUSION:Infants born to women with AIDS are at higher risk for HIV-1 infection than are infants born to HIV-1-infected women with AIDS not yet diagnosed. Women receiving zidovudine appear less likely to transmit HIV-1 to their infants. Significantly higher rates of prematurity and intrauterine growth retardation were found among HIV-1-infected infants than among those in the uninfected, HIV-1-exposed control group. Prematurity was associated with shortened survival in HIV-1-infected infants. Measures of intrauterine growth and gestation appear to be important predictors of HIV-1 infection status for seropositive infants and of prognosis for the infected infant.

Four methods of estimating mother-to-child transmission rates of human immunodeficiency virus type 1 (HIV-1), based on the 1992 Ghent workshop, were compared in a multicenter New York City prospective cohort study in 1986-1992. Of 833 infants born to women at risk of HIV-1 infection, 388 were born HIV-1 seropositive and 445 were HIV-1 seronegative. The four methods, the Antibody Only, Indirect, Direct, and Virologic Methods, yielded transmission rate estimates of 19-25%, classifying 59-89% of the cohort. Estimation based on persistence of HIV-1 antibody and clinical assessment yielded transmission rates similar to those methods that incorporated virologic testing.

This analysis sought to identify characteristics of pregnant human immunodeficiency virus type 1 (HIV-l)-infected women that predict mother-to-child HIV-1 transmission. Pregnant and immediately postpartum women at risk for HIV were enrolled at obstetric and pediatric care settings in New York City from 1986 to 1992. Demographic and behavioral characteristics, clinical illness, T lymphocyte subsets, immunoglobulin concentration and syphilis serology were collected on the women. Infants were followed to determine HIV infection classification according to Centers for Disease Control and Prevention criteria for HIV-1 in children. Transmission rates were calculated for women who gave birth more than 15 months before the analysis. Of 172 HIV-l-infected women with known outcome 49 (28%) had infected infants. The transmission rate (TR) was significantly higher among women with <280 CD4+ cells/mu l (lowest CD4+ quartile) than with CD4+ counts >280 (48% vs. 22%; P = 0.004; odds ratio, 3.4; 95% confidence interval (1.5, 7.8)); a similar trend was seen by CD4+% quartile. No difference in TR was seen comparing women by CD8+ count quartile but marginally higher TR was seen among women with CD8+% greater than or equal to 51% than with CD8+% <51% (TR = 41% us. 24%; P = 0.076; odds ratio, 2.2; confidence interval (1.0, 5.1)). The highest TR, 62%, was seen in women with both CD8+ count above the median and CD4+ count in the lowest quartile. No significant difference in TR was seen between women with and without HIV-related illness, although the TR was 53% among women hospitalized in the previous year for pneumonia compared with 25% in others (P = 0.03). TR was somewhat lower in women who delivered by cesarean section than vaginally (entire cohort: 18% vs. 32%, P = 0.11; prenatal enrollees only, 17% vs. 38%, P = 0.045). No factor or combination of factors was both highly sensitive and specific for predicting mother-to-child HIV transmission. A possible relationship between transmission and mode of delivery deserves further investigation.

We have used a human immunodeficiency virus type 1 (HIV-1)-specific IgG-Fc capture enzyme immunoassay (IgG-CEIA) to elucidate the dynamics of HIV-1 maternal antibody decay and de novo synthesis of HIV-1 antibodies in infants. Two hundred and thirty-nine serum specimens from 77 infants were analyzed by the IgG-CEIA and by two different conventional EIAs. With the IgG-CEIA, IgG was captured by an anti-human IgG monoclonal antibody (3C8) that reacts with all subclasses and was detected by recombinant HIV-1 envelope protein (CBre3)-peroxidase conjugate. Unlike the conventional EIAs, the IgG-CEIA showed a rapid decay of HIV-1-specific antibody in uninfected infants, with decline to background levels by 6 months (T1/2 [half-life] = 28-30 days). All 69 specimens collected from 39 uninfected infants between 6 and 15 months of age were negative by IgG-CEIA. However, HIV-1 antibodies remained high in infected infants; 20/22 infants (90.9%) with specimens between the ages of 6 to 23 months were positive by IgG-CEIA. Subtracting mean IgG-CEIA optical density values of seroreverting infants from those of HIV-1-infected infants in corresponding age groups provided a model for seroconversion in infected infants, with detectable IgG antibody synthesis starting about 3 months after birth. The IgG-CEIA may be a simple and important tool for early diagnosis of HIV-1 infection in infants at 6 months of age.