RESUMO

While the worldwide AIDS epidemic continues to expand, directly measured incidence data are difficult to obtain. Methods to reliably estimate human immunodeficiency virus type 1 (HIV-1) incidence from more easily available data are particularly relevant in those parts of the world where prevalence is rising in heterosexually exposed populations. The authors set out to estimate HIV-1 incidence in a population of heterosexual sexually transmitted disease clinic attendees in Trinidad who had a known high prevalence of HIV-1 subtype B. Over the period 1987-1995, HIV-1 incidence estimates from serial cross-sectional studies of HIV-1 prevalence, passive follow-up of clinic recidivists, modeling of early markers of HIV-1 infection (p24 antigen screening), and a cohort study of seronegative genital ulcer disease cases were compared. Measuring incidence density in the genital ulcer disease cases directly gave the highest estimate, 6.9% per annum. Screening for the detection of early HIV-1 markers yielded an incidence of 5.0% per annum, while estimating incidence from serial cross-sectional prevalence data and clinic recidivists gave estimates of 3.5% and 4.5% per annum, respectively. These results were found to be internally consistent. Indirect estimates of incidence based on prevalence data can give accurate surrogates of true incidence. Within limitations, even crude measures of incidence are robust enough for health planning and evaluation purposes. For planning vaccine efficacy trials, consistent conservative estimates may be used to evaluate populations before targeting them for cohort studies.

PIP: HIV incidence data, necessary for the planning and evaluation of national AIDS control programs, are difficult to obtain directly. In this study, HIV-1 incidence in Trinidad was estimated in a population known to be at high risk: heterosexuals attending a sexually transmitted disease clinic in Port of Spain in 1987-95. HIV incidence estimates were obtained from serial cross-sectional studies of HIV-1 prevalence (n = 3625), passive follow-up of clinic recidivists (n = 98), modeling of early markers of HIV-1 infection (p24 antigen screening) (n = 12,154), and a cohort study of seronegative genital ulcer disease cases (n = 196). Measuring incidence density in genital ulcer disease cases directly gave the highest estimate: 6.9% per year. Screening for the detection of early HIV-1 markers yielded an incidence of 5.0% per year, while estimating incidence from serial cross-sectional prevalence data and clinic recidivists provided estimates of 3.5% and 4.5%, respectively. Although these estimates come from groups within the clinic population with differential HIV-1 risk, they were internally consistent. These findings suggest that indirect estimates of incidence based on prevalence data can provide accurate surrogates of true HIV incidence and may be used to target suitable populations for cohort studies.

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RESUMO

While the worldwide AIDS epidemic continues to expand, directly measured incidence data are difficult to obtain. Methods to reliably estimate human immunodeficiency virus type 1 (HIV-1) incidence from more easily available data are particularly relevant in those parts of the world where prevalence is rising in heterosexually exposed populations. The authors set out to estimate HIV-1 incidence in a population of heterosexual sexually transmitted disease clinic attended in Trinidad who had a known high prevalence of HIV-1 subtype B. Over the period 1987-1995, HIV-1 incidence estimates from serial cross-sectional studies of HIV-1 prevalence, passive follow-up of clinic recidivists, modeling of early markers of HIV-1 infection (p24 antigen screening), and a cohort study of seronegative genital ulcer disease cases were compared. Measuring incidence density in the genital ulcer disease cases directly gave the highest estimate, 6.9 percent per annum. Screening for the detection of early HIV-1 markers yielded an incidence of 5.0 percent per annum, while estimating incidence from serial cross-sectional prevalence data and clinic recidivists gave estimates of 3.5 percent and 4.5 percent per annum, respectively. These results were found to be internally consistent. Indirect estimates of incidence based on prevalence data can give accurate surrogates of true incidence. Within limitations, even crude measures of incidence are robust enough for health planning and evaluation purposes. For planning vaccine efficacy trails, consistent conservative estimates may be used to evaluate population before targeting them to cohort studies(AU)

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OBJECTIVES: To study trends in prevalence and to ascertain risk factors for HIV-1 among sexually transmitted disease (STD) clinic attenders in Trinidad. DESIGN AND METHODS: Serial cross-sectional studies were conducted in 1987-1988 and 1990-1991 at a centralized STD clinic in Port of Spain. A case-control study was carried out to examine in greater detail the demographic and behavioral risk factors for HIV-1 among self-declared heterosexuals in this population. RESULTS: HIV-1 prevalence increased from 3.0% [95% confidence interval (CI), 2.3-3.9] in 1987-1988 to 13.6% (95% CI, 11.8-15.6) in 1990-1991. Age > or = 40 years [odds ratio (OR), 2.0; 95% CI, 1.4-2.8], urban residence (OR, 2.2; 95% CI, 1.6-3.0), and human T-lymphotropic virus-I seropositivity (OR, 3.1; 95% CI, 1.6-6.0) were significant risk factors for HIV-1 in 1990-1991. In the case-control analysis, significant independent risk factors for men included current genital ulcer disease (OR, 5.2; 95% CI, 2.2-12.5), current genital warts (OR, 3.9; 95% CI, 1.2-12.0), having ever had syphilis (OR, 3.2; 95% CI 1.6-6.1), and use of crack cocaine in the preceding 6 months (OR, 6.2; 95% CI, 2.7-14.2). Corresponding risk factors for women were commercial sex work (OR, 5.7; 95% CI, 1.3-25.7), initiation of sexual activity before age 14 years (OR, 4.8; 95% CI, 1.5-16.0), and past non-gonococcal cervicitis (OR, 4.1; 95% CI, 1.3-13.1). CONCLUSIONS: HIV-1 in this setting is primarily heterosexually transmitted in a milieu of unprotected sexual activity fuelled by a crack cocaine epidemic. Targeted interventions to prevent, detect and treat STD and crack cocaine addiction, as well as disrupt their adverse synergism, may substantially reduce HIV-1 transmission in this population.

PIP: During mid-1987 to mid-1988 and mid-1990 to mid-1991, researchers conducted cross sectional serological surveys at the STD clinic in Port of Spain in Trinidad to examine trends in HIV-1 prevalence among 2019 and 1606 STD patients, respectively. They also conducted a case control study of risk factors for HIV-1 infection among heterosexual STD patients (131 cases and 173 age- and sex-matched controls) in 1992-1993. Between 1987-1988 and 1990-1991, HIV-1 seroprevalence increased markedly (3% to 13.6%). It increased more in women than in men (9- vs. 4-fold). During 1987-1988, men were more likely to be infected with HIV-1 (odds ratio [OR] = 3.1), but by 1990-1991, gender was no longer a significant risk factor (OR = 1.3). In 1990-1991, significant risk factors for HIV-1 infection were urban residence (OR = 2.2), HTLV-1 infection (OR = 3.1), and being at least 40 years old (OR = 1.8). None of these risk factors were significant in 1987-1988. HIV-1/HTLV-1 coinfection increased between the two surveys (0.05% to 1.5%). Significant independent HIV-1 risk factors in men identified in the case control study were: used crack cocaine in the past 6 months (adjusted OR [AOR] = 6.2; p = 0.0001); ever had anal sex (AOR = 7.2; p = 0.003); ever had syphilis (AOR = 3.2; p = 0.02); current genital ulcer disease (AOR = 5.2; p = 0.0001); and current genital warts (AOR = 3.9; p = 0.02). Significant independent HIV-1 risk factors in women were: less than 14 years old at first sex (OR = 4.8; p = 0.01); ever been a commercial sex worker (AOR = 5.7; p = 0.02); and ever had nongonococcal cervicitis (AOR = 4.1; p = 0.005). These findings suggest that sexual exposure to HIV-1 through ulcers for men and inflammatory STD and/or prostitution for women, all fueled by the crack cocaine epidemic, account for much of HIV-1 exploding in Trinidad. Public health interventions to prevent, detect, and treat STDs and crack cocaine addition may greatly reduce HIV-1 transmission.

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To address the hypothesis that increased infectious morbidity is associated with iron supplementation, 783 randomly selected infants were provided with a powdered full fat cow's milk (non-fortified group) and 872 with a powdered acidified full fat cow's milk fortified with 15 mg of iron as ferrous sulfate (fortified group). All infants were followed from birth to 15 months of age with a monthly home visit by a nurse who recorded morbidity occurring during the previous 30 days. At 9 months of age, 15% of infants in each cohort were receiving breast milk only; data for these infants were segregated to make the third group. Episodes (mean +/- SD) of diarrhea/infant/year were 1.06 +/- 1.29, 1.14 +/- 1.37, and 0.82 +/- 1.04 for the fortified, non-fortified and breast-fed groups, respectively; the fortified and non-fortified bottle-fed groups had a very similar incidence of respiratory illness; 2.66 +/- 2.07 and 2.74 +/- 2.24 episodes/infant/year, respectively. The incidence of respiratory illness for both bottle-fed groups was significantly higher than that for the breast-fed group (2.22 +/- 1.84 respiratory episodes/infant/year). We conclude that for the infants the tested form of iron fortified milk, which is sufficient to lower iron deficiency anemia, does not result in an increased incidence of diarrhea or respiratory illness.

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