Journal of acquired immune deficiency syndromes最新文献

This article extends existing methods for estimating reporting delays to allow nonparametric estimation of how delays are changing over time. Also implemented are refinements to estimate calendar month effects and to improve the accuracy of trend estimates by focusing on delays of > 6 months. Applying the method to 1987-definition adult and adolescent AIDS cases reported by June 1992 shows strong evidence for a nonlinear trend toward longer delays among cases diagnosed more recently and for slower reporting of cases diagnosed in January and June of each year. Combining estimated reporting delay corrections with the possibility of increasing underreporting produces a 14-16% higher estimated incidence by December 1991 and a 19-24% higher projected incidence by December 1993 than using the delay corrections provided with the public information AIDS data and assuming constant underreporting rates.

To quantify the number of human immunodeficiency virus type 1 (HIV-1) proviral copies per 1,000 CD4+ cells in cerebrospinal fluid (CSF) and blood in relationship to stage of infection and HIV-1 neurologic disease (HND), 87 HIV-1 seropositive men without CNS opportunistic infections, tumors, or neurosyphilis, 9 high-risk, and 14 not-at-risk seronegative controls underwent a structured interview, and physical and neurologic examination followed by blood and CSF collection. A custom-designed, fully automated polymerase chain reaction (PCR) system performed amplification with use of two HIV-1 gag primer pairs, Southern blotting, and hybridization with product-specific probes. Image analysis was used to quantify band intensities relative to a dilution series. Eighty-one of 87 (93%) seropositive patients, 1 of 9 high-risk patients, (11%) and none of 14 seronegative controls had PCR-detectable HIV-1 in their blood. Fifty-seven of 63 (90%) seropositive patients, 2 of 5 (40%) high-risk seronegative patients, and none of 14 controls had HIV-1 in their CSF. The proviral load in seropositive patients, all stages, was significantly greater in CSF than blood [median 25 vs. 0.6 copies/1,000 CD4+ cells (p = 0.0001)]. The median proviral load in blood was 0.09 copies/1,000 CD4+ cells in seropositive, asymptomatic subjects, 10.7 in patients with AIDS, and 1.4 in patients with AIDS-related complex (p = 0.0281). CSF proviral load was greater in seropositive patients with HND than those without HND, median 43.5 vs. 17.6 copies/1,000 CD4+ cells (p = 0.0614). Proviral load was greater in the blood and CSF of subjects with more advanced systemic disease and HND. There was a substantial penetration of HIV-1 into the CNS/CSF in both systemically and neurologically asymptomatic HIV-1 disease.

Human immunodeficiency virus (HIV)-infected gay and bisexual men (n = 609) randomly selected from two HIV outpatient clinics in Los Angeles completed confidential, self-administered questionnaires at the clinics, reporting sexual activities and disclosure during the previous 2 months. Approximately 9% had engaged in unprotected insertive anal intercourse with one or more partners. This activity was 3.27 times more likely to have occurred with seropositive partners than with partners who were seronegative or whose serostatus was unknown. Fourteen men (2.3% of total sample) had engaged in unprotected insertive anal sex with 25 seronegative or unknown serostatus partners who were not informed of their risk of infection. Thirty-three men (5.4% of total sample) had engaged in this activity with 37 seropositive partners who were informed. Clinicians and other health professionals can play an important role in helping to control the HIV epidemic by discussing with seropositive patients the importance of using safer sex and informing sexual partners. Such discussion should include information about the potentially negative health effects of unprotected sex between seropositive persons.

It has been reported that HIV-1 p24 antigen (p24 Ag) detection is improved after dissociation of immune complexes using acid treatment (ICD assay). In order to evaluate the clinical significance of p24 Ag detected by the standard assay and by the ICD assay in pediatric patients, we related these measurements to clinical status, level of p24 antibody, and percentage of CD4+ lymphocytes. Fifty-nine plasma specimens from 20 symptomatic HIV-1-infected children, collected prospectively over a 1-year period, were tested for these markers. Plasma was collected at the beginning of zidovudine therapy and approximately 7 and 12 months thereafter. Compared with the standard assay, the ICD assay showed a higher number of samples positive for p24 Ag (78% versus 34%) and an increase in the levels of p24 Ag (median value of 129 versus 24 pg/ml). The anti-p24 antibody level was inversely correlated with the p24 Ag level measured by either assay. Four children negative for p24 Ag by both assays had a stable clinical course. In contrast, 50% of the children negative by the standard assay but positive for ICD p24 Ag and 75% of the children positive by both assays had progression of disease. No patients were positive by the standard assay but negative by the ICD assay. Children whose plasma tested positive by both assays had lower percentages of lymphocytes that were CD4+ by comparison with children who were negative by both assays; children whose plasma tested positive only by the ICD assay formed an intermediate group.(ABSTRACT TRUNCATED AT 250 WORDS)

In response to recent laws regulating human immunodeficiency virus (HIV) antibody testing practices in all federal hospitals, our university-affiliated Veterans Affairs Hospital instituted several interventions designed to increase appropriate testing. Specific hospital policy requiring restriction of testing to high-risk individuals, provision of pre- and posttest counseling, and documentation of written consent was instituted. In addition, an education campaign to inform physicians of hospital policy and training of counselors as physician extenders was undertaken. To determine the efficacy of these interventions, we reviewed all HIV antibody tests performed during a subsequent six-month period (n = 221). Only 14% of tests met all hospital policy requirements. The decision to test was prompted by identification of a risk factor or other acceptable reason for testing for only 31% of patients. Risk reduction counseling was provided for only 28% of patients. Written consent was documented for 62% of patients. Health care providers on surgical services were less likely than others to comply with hospital policy (p < 0.0001). We conclude that an interventional program including specific hospital policy mandates, physician education, and provision of trained counselors was not adequate to ensure optimal HIV antibody testing practices. If this gap between policy and practice is to be closed, additional interventions, or alternatively modification of policy guidelines, will be needed.

Concerns are sometimes expressed at the extent to which HIV-1 is prioritized within international and national health budgets and as a research issue, on the grounds that much larger numbers of people in developing countries currently die from other diseases, such as malaria and tuberculosis. We use a previously described mathematical model to explore how the HIV-1 epidemic could develop within a sub-Saharan African context and investigate the trends and patterns of adult mortality which could follow. Two contrasting scenarios are studied, one which turns population growth rates negative and another which does not. In both cases, HIV-1-related disease accounts for over 75% of annual deaths among men and women aged 15-60 years by year 25 of the epidemic. Relatively little change in mortality is seen in the early years of the simulated epidemics. However, by year 15, expectation of life at age 15 has fallen from 50 to below 30 years. The fragmentary evidence now available from empirical studies supports the impression that HIV-1 is rapidly emerging as a leading cause of adult deaths in areas of sub-Saharan Africa. Observed patterns of age-dependent mortality reflect those projected in the model simulations.