Microsatellite instability in primary neoplasms from HIV + patients.

AIDS is associated with a high risk of certain malignancies, notably Kaposi's sarcoma (KS) and B-cell non-Hodgkin's lymphoma (NHL). The pathogenesis of these malignancies is not fully understood. One mechanism of malignant transformation recently described in colon tumorigenesis results from defects in DNA mismatch repair, manifest as widespread microsatellite instability. We demonstrate a high rate of microsatellite instability in KS and aggressive lymphomas obtained from HIV-infected patients, whereas there is no evidence of instability in similar lesions from HIV-negative patients. Further elucidation of the underlying mechanisms responsible for HIV-associated instability in primary tumours may provide insight into the pathogenesis of these AIDS-related neoplasms.

Tampons as a self-administered collection method for the detection and quantification of genital HIV-1.

OBJECTIVE: To assess the detection and quantitation of HIV-1 from tampon eluents in comparison with cervicovaginal lavage (CVL) and plasma specimens from the same women. METHODS: Ninety-seven tampon, 105 CVL, and 104 plasma specimens from 105 HIV-1 seropositive women were analyzed using Version 3 of the Chiron bDNA assay, with sensitivity of 50 HIV-1 RNA copies/ml. Data analyses used McNemar's test, Wilcoxon signed rank test, and Mantel--Haenszel chi-squared and odds ratios with 95% confidence intervals to assess differences in proportions. RESULTS: In women for whom both plasma and genital specimens were available, HIV-1 was detected less frequently in genital specimens: [tampons (33/97, 34%) and CVL (48/104, 46%)] than plasma specimens (86/104, 83%) (P < 0.001 for both plasma versus tampon and for plasma versus CVL). However, the proportion of genital specimens with detectable virus did not differ significantly by collection method (P = 0.14). Among women with detectable virus using both collection methods (n = 23), viral load was similar for tampon eluents (median, 355 copies/ml; range, 52--120,898) and CVL specimens (median, 265 copies/ml; range, 61--35,637;P = 0.88). CONCLUSION: Tampon eluent specimens are slightly less sensitive than CVL specimens in the detection of genital HIV-1, although quantification of viral load, when detectable by both methods, was similar.

Short tandem repeat methodology for genotypic identification of single-person versus multi-person use of syringes.

OBJECTIVE: To develop laboratory methods to differentiate between single- versus multi-person use of syringes by injection drug users. METHODS: Forensic short tandem repeat (STR) genetic analysis was undertaken to cross-validate a test panel of trace blood contents from syringes representing single- versus multi-person syringe use. Laboratory-simulated scenarios of needle sharing generated 34 syringe washes that were blinded for evaluation. Polymerase chain reaction was used to amplify the polymorphic STR locus D6S502 from blood trace contents in used syringes. Alleles were sized and quantified using a commercial gene sequencer. A statistical algorithm was developed to determine the number of alleles present in the amplified DNA fragments. Syringes with more than two expected alleles were considered to represent multi-person syringe use. Sensitivity, specificity and the kappa coefficient were calculated. RESULTS: Allelic matrix-based analysis of alleles from the single STR successfully characterized single-use (n = 12) and multiple-use (n = 22) syringes with 68% sensitivity and 100% specificity upon re-analysis. The extent of agreement over and above chance (kappa = 0.6; P < 0.0001) indicated good agreement for differentiating single- versus multi-person syringe use. CONCLUSIONS: These findings suggest that improved genotypic STR analysis of syringe material could be an adjunct to methods for validating self-reported needle sharing, conducting behavioral surveillance of needle-sharing behaviors, and evaluating interventions such as needle-exchange programs. Assays based on multiple STR loci will undoubtedly improve upon the promising results obtained from laboratory simulations of needle sharing.

Detection of HIV-1 proviral DNA in sperm from HIV-1-infected men.

OBJECTIVE: Sexual transmission is a major mode of the spread of HIV-1, although the cellular and molecular mechanisms are poorly defined. In this study, we sought to assess the cellular reservoirs of HIV-1 proviral DNA in the semen of HIV-1-infected men. DESIGN AND METHODS: An in situ polymerase chain reaction (IS-PCR), which amplifies specific genes within intact cells, was used to evaluate levels of HIV-1 provirus in seminal cells from HIV-1-infected men in various stages of clinical disease. RESULTS: Initial studies demonstrated HIV-1 provirus in relatively low numbers (1:100 to 1:6000) of both the seminal mononuclear cells and sperm from certain HIV-1-infected men. To extend these findings, 94 seminal samples from HIV-1-infected men were evaluated. HIV-1 proviral DNA was detected in seminal cells of a significant percentage of HIV-1-infected men (45%) at all stages of clinical immunodeficiency. Both seminal mononuclear cells and sperm (35 and 33% of samples studied, respectively) harbored HIV-1 proviral sequences. HIV-1-harboring sperm are shown to stain positively for HIV-1 in the mid-pieces of these cells, with rarer staining of the sperm heads. CONCLUSIONS: HIV-1 proviral DNA can be demonstrated by IS-PCR in seminal mononuclear cells and sperm from certain HIV-1-infected men. The role played by proviral DNA in these cells in the sexual transmission of this retroviral agent will require further study.

Racial differences in rate of CD4 decline in HIV-1-infected homosexual men.

OBJECTIVE: To determine whether racial differences exist in the rate of CD4 lymphocyte decline in HIV-1-infected homosexual men. DESIGN: Prospective cohort study. STUDY POPULATION: Non-Hispanic white (n = 321) and black (n = 102) HIV-1-seropositive homosexual and bisexual men were recruited from the Baltimore/Washington, DC metropolitan areas between 1984-1985 and 1987-1990, and evaluated semiannually. MAIN MEASUREMENTS: Changes in CD4 lymphocyte count and CD4 percentage over time were analysed using linear regression methods for the 271 white and 69 black participants who had at least four semiannual CD4 lymphocyte measurements. RESULTS: Rate of decline in CD4 lymphocyte count over 6 months was much slower among black than white seroprevalent men at all levels of baseline CD4 count (baseline 201-400 x 10(6)/l: + 0.24 versus -17.7 x 10(6)/l; 401-600 x 10(6)/l: -11.3 versus -23.9 x 10(6)/l; 601-800 x 10(6)/l: -15.1 versus -35.2 x 10(6)/l; > 800 x 10(6)/l: -4.3 versus -42.7 x 10(6)/l for black versus white, respectively), although this was only statistically significant for the lowest and highest strata of baseline CD4 count. These racial differences persisted after adjustment for recruitment period (1984-1985 or 1987-1990), follow-up duration, age and zidovudine therapy or Pneumocystis carinii pneumonia prophylaxis. Similar findings were observed among the 70 white and 11 black seroconverters. Black participants were also less likely than a subgroup of white participants matched on baseline CD4 lymphocyte count to be HIV-1 p24 antigen-positive. However, after acid dissociation of samples initially p24 antigen-negative, there were no significant differences in the prevalence of p24 antigenemia at enrollment or after 1 year of follow-up. CONCLUSIONS: This analysis suggests a more gradual decline in CD4 lymphocyte count among black than white Americans. The clinical significance of and reasons for this are unclear, but the lower prevalence of p24 antigenemia due to immune complexing among black Americans suggests that racial differences in the immune response to HIV may exist. Additional studies are needed to validate these findings in a larger cohort of non-whites, and to assess their relationship with other measures of cell-mediated immune function.

Racial heterogeneity of HIV antigenemia in people with HIV infection.

We compared the prevalence of HIV p24 antigenemia in black and white US patients with HIV infection. The prevalence of HIV antigenemia increased with severity of HIV disease (P less than 0.001). In all clinical categories, whites were more likely to be HIV-antigenemic than blacks (overall prevalence 38 versus 18%; P less than 0.01). Anti-p24 antibodies were detected in a higher proportion of blacks (84%) than whites (65%; P = 0.02). Blacks had significantly higher total serum immunoglobulin levels than whites (median 3.8 versus 3.2 mg/dl; P less than 0.00001). Racial differences in HIV antigen expression may result from differences in humoral response to HIV infection. These differences should be considered when HIV antigen is used as a surrogate marker in clinical trials.

Longitudinal study of homosexual couples discordant for HIV-1 antibodies in the Baltimore MACS Study.

Thirty-six sexually active couples serologically discordant for human immunodeficiency virus, type 1 (HIV-1), within the Baltimore Multicenter AIDS Cohort Study (MACS) were assessed to determine whether evidence of HIV-1 infection could be detected in the HIV-1-antibody-negative partners and whether factors associated with lack of transmission of HIV from the seropositive to the seronegative partner could be ascertained. Six HIV-1 seropositive couples and 18 seronegative couples were followed concurrently for comparison. None of the seropositive subjects had an AIDS-defining illness at entry into the study, and all subjects were followed for 1 year. A separate evaluation of unprotected anal receptive and insertive intercourse between discordant couples indicated high-risk activities for a median of 40 months, as reported by the HIV seropositive partner. Despite this finding, none of the HIV-1 seronegative men in discordant couples had evidence of HIV-1 infection by viral culture, p24 antigen testing, or polymerase chain reaction for HIV-1 DNA. Discordant seronegatives and seropositives did not differ from concordant seronegatives and seropositives in numbers of circulating CD4, CD8, and natural killer lymphocytes or in prevalence of antibodies to herpes simplex virus, type 1, Epstein-Barr virus, or cytomegalovirus, except that discordant seronegative men were less likely than their seropositive partners to have antibodies to herpes simplex virus, type 2. The reason for the apparent lack of HIV-1 infection in seronegative discordant individuals remains unexplained and did not appear to be associated with type of sexual activity, T-lymphocyte subsets or natural killer cells, or early stage of HIV-1 disease.

The effect of fresh lymphocytes on increased sensitivity of HIV-1 isolation: a multicenter study.

A multicenter study was undertaken to determine the sensitivity and reproducibility of markers for human immunodeficiency virus type 1 (HIV-1) viral growth and the effect of various preparations of lymphocytes on the sensitivity of standard and routinely used procedures for HIV-1 isolation. In phase 1, cocultivated culture supernatants obtained from 10 HIV-1 cultures were transported to three Multicenter AIDS Cohort Study (MACS) Virology Laboratories. Three commercial HIV-p24 antigen capture (AC) tests and two reverse transcriptase (RT) assays were used to ascertain the replication of HIV-1. The Du Pont and Abbott AC assays were found to be most sensitive (85-100%), and the RT assay with 24-h incubation period had comparable sensitivity (75-100%). In phase II, the sensitivity of standard cocultivation procedure for HIV-1 isolation was compared using freshly phytohemagglutinin-P (PHA-P)-stimulated, stimulated-frozen, and frozen-thawed and then stimulated normal human peripheral blood mononuclear cells (PBMCs) as cocultivating cells. Blood samples from 13 HIV-1 infected individuals with various CD4+ cell counts were cocultivated in each of the three MACS laboratories using one of the aforementioned normal PBMCs. The PHA-P-stimulated fresh normal PBMC showed a maximum isolation rate of 100% (13 of 13) with an average of 8 days to positivity. This rate of isolation was significantly greater than other rates using any one of the other PBMC preparations. These findings demonstrated that the use of freshly PHA-P stimulated PBMCs maximized HIV-1 isolation from blood when a sensitive HIV-1 p24 AC assay or RT assay with overnight incubation is employed for the detection of HIV in culture supernatant.

Diagnosis and differentiation of HTLV-I and HTLV-II infection by enzyme immunoassays using synthetic peptides.

Synthetic peptides from the major envelope protein of HTLV-I (ENV-I, amino acid 177-213) and HTLV-II (ENV-II, amino acid 173-209) and a conserved region of the transmembrane protein (TM, amino acid 378-402) were used as antigens in microtiter plate enzyme immunoassays (EIA) to detect and discriminate antibodies to HTLV-I and II. The ENV-I and ENV-II peptide EIAs were able to correctly discriminate HTLV-I and II infections in 17 of 18 subjects whose infections were determined by a gene amplification method. Sera from 100 of 107 subjects with serologically confirmed infection with HTLV-I/II and 0 of 218 seronegative controls reacted with one or more of the peptides (sensitivity, 93.5%; specificity, 100%). Ninety-six of the 100 peptide positive sera reacted exclusively with either the ENV-I or the ENV-II peptide, thereby differentiating the two viral infections. The pattern of reactivity to the ENV peptides was distinct in different populations. Patients attending an Emergency Department, who had a history of drug abuse, and male inmate entering a correctional facility only had antibody reactivity to the ENV-II peptide. Subjects from Haiti and patients with HTLV-associated neurological disease only had antibody reactivity to the ENV-I peptide. Peptide-based enzyme immunoassays that distinguish antibodies to HTLV-I and HTLV-II will facilitate studies of the epidemiology of HTLV.

Mutual confounding and interactive effects between hepatitis C and hepatitis B viral infections in hepatocellular carcinogenesis: a population-based case-control study in Taiwan.

A population-based case-control study was conducted in Taiwan to determine the hepatitis C virus (HCV)-associated risk of hepatocellular carcinoma (HCC) in a hyperendemic area for hepatitis B virus (HBV) infection. A total of 58 recently diagnosed HCC patients and 225 matched community controls, who participated in a community-based liver cancer screening program, were recruited between March 1991 and March 1994. Control subjects were matched to HCC patients by age (+/- 5 years), sex, residence, and date of serum sample collection (+/- 3 months). Serum samples from all study subjects were tested for hepatitis B surface antigen (HBsAg) and antibodies to HCV (anti-HCVs) by enzyme immunoassays, as well as HCV RNA by reverse transcription-PCR assays. Accordingly, patients with HCC were more likely than were controls to be positive for HBsAg (82.8% versus 12.9%, with an odds ratio (OR) of 22.9), anti-HCVs (13.8% versus 4.4%, with an OR of 3.9), and HCV RNA (13.8% versus 5.8%, with an OR of 2.7). After adjustment for anti-HCVs and HCV RNA positivities, the matched ORs associated with HBsAg increased to 27.6 and 28.1, respectively, whereas the corresponding adjusted ORs for anti-HCVs and HCV RNA after controlling for HBsAg status were increased to 8.8 and 6.2, respectively. In the meantime, interactive effects between HCV and HBV on risk were also observed. Compared with those who were negative for both anti-HCVs and HBsAg, the matched ORs associated with the sole positivity of anti-HCVs and HBsAg were 4.0 (95% confidence interval = 0.7-24.0) and 24.6 (95% confidence interval = 9.5-64.1), respectively, whereas 6 HCC cases but none of control subjects were positive for both anti-HCVs and HBsAg. These results indicate that there are mutual confounding and interactive effects between HCV and HBV with respect to their links to HCC in this endemic area of chronic HBV infections.

Steroid-responsive myeloneuropathy in a man dually infected with HIV-1 and HTLV-I.

Two human retroviruses, HIV-1 and HTLV-I, have been associated with myelopathies in addition to other neurologic disorders. We report an American dually infected with HIV-1 and HTLV-I who developed steroid-responsive myeloneuropathy. This 28-year-old bisexual man developed interstitial pneumonitis and a transient midthoracic sensory level followed by the evolution of a slowly progressive spastic paraparesis and sensorimotor neuropathy. Serologic studies demonstrated coinfection with both HIV-1 and HTLV-I. Peripheral blood absolute CD4 count was persistently within the normal range. Cranial MRI was normal and spinal MRI showed T3-T10 atrophy. Serial CSF analyses demonstrated marked intrathecal synthesis of anti-HTLV-I IgG, lymphocytic pleocytosis, elevated protein and immunoglobulin G, and oligoclonal bands. HIV-1 was isolated from CSF but not from peripheral nerve. Lymphoproliferative studies confirmed spontaneous proliferation in both blood and CSF. Soluble interleukin 2 receptor and soluble CD8 were greatly elevated in blood and CSF when compared with patients with HIV-related vacuolar myelopathy and seronegative patients with other causes of myelopathy. Nerve biopsy showed epi- and endoneurial CD8+ lymphocytic infiltration without vasculitis; muscle biopsy showed features of acute and chronic denervation. A 6-week course of prednisone produced sustained improvement in leg strength and walking times. We speculate that the myeloneuropathy was caused by HTLV-I in the setting of coinfection with HIV-1.

Intrathecal synthesis of anti-HIV IgG: correlation with increasing duration of HIV-1 infection.

We determined intrathecal synthesis (ITS) of anti-HIV-1 immunoglobulin in 62 CSF samples from 51 HIV-1 seropositive homosexual men using an ELISA technique with paired serum and CSF samples diluted to a concentration of IgG of 10 micrograms/ml. All subjects were neurologically normal and none was taking zidovudine. We estimated duration of HIV-1 infection from semiannual serologic testing during the 3-year period before CSF analysis and detected ITS of anti-HIV-1 immunoglobulin in 2 of 12 (17%) of those with less than 18 months of HIV-1 seropositivity, in 3 of 21 (14%) with 19 to 36 months, and in 13 of 29 (45%) with greater than 36 months of HIV-1 seropositivity (p = 0.037). There was a trend toward an inverse relationship between level of ITS and the peripheral blood T-helper lymphocyte count. This study demonstrates that increasing ITS of anti-HIV-1 IgG is related to duration of HIV-1 infection and suggests an inverse correlation with systemic immune status. The detection of ITS of anti-HIV-1 immunoglobulin is not necessarily a marker of clinically overt neurologic involvement.

The diagnostic utility of elevation in cerebrospinal fluid beta 2-microglobulin in HIV-1 dementia. Multicenter AIDS Cohort Study.

We measured serum and CSF beta 2-microglobulin (beta 2M) levels in HIV-1 seropositive individuals with and without dementia to determine the frequency and diagnostic utility of elevation of CSF beta 2M. We compared 34 samples from 27 patients with HIV-1 dementia with 110 samples from 54 HIV-1 seropositive participants in the Multicenter AIDS Cohort Study, none of whom had progressive dementia. Neurosyphilis and CNS opportunistic processes were excluded in all subjects. We stratified the nondemented subjects by duration of HIV seropositivity and peripheral blood CD4 count. Compared with the nondemented group, demented subjects had significantly higher CSF total protein, IgG%, and CSF albumin/serum albumin ratios. A highly significant association was found between elevated CSF beta 2M and reduced CD4 count (p less than 0.0001). No significant differences were noted between the demented and nondemented groups in CSF WBC count or in the frequency of CSF HIV-1 isolation. The mean CSF beta 2M was 1.9 mg/l in the nondemented subjects compared with 4.2 mg/l in those with dementia (p less than 0.0001). We derived a cutoff of 3.8 mg/l from the distribution of CSF beta 2M in the nondemented group. The determination of CSF beta 2M had a sensitivity of 44%, specificity of 90%, and a positive predictive value of 88% for diagnosis of HIV dementia when compared with nondemented subjects with CD4 counts less than 200. In those without dementia, there was a strong correlation between serum and CSF beta 2M (r = 0.50, p less than 0.0001), but in demented subjects CSF beta 2M was elevated independently of serum levels, suggesting that CSF beta 2M is produced within the brain in HIV dementia. In the absence of CNS opportunistic processes, elevated CSF beta 2M greater than 3.8 mg/l is a clinically useful marker for HIV dementia.

Flow cytometric quantitation of T cell phenotypes in cerebrospinal fluid and peripheral blood of homosexual men with and without antibodies to human immunodeficiency virus, type I.

Two-color flow cytometry was used to analyze T cell subsets (total (CD3), helper-inducer (CD4), and suppressor-cytotoxic (CD8] in paired specimens of cerebrospinal fluid (CSF) and peripheral blood of 66 homosexual men, including 62 with antibodies to human immunodeficiency virus, type 1 (HIV-1). With the exception of one traumatic specimen, all of the CSF specimens, 52 of which had less than or equal to 5 lymphocytes/mm3, were evaluated fully, with the number of lymphocytes counted for each antibody ranging from 200 to 2933 (mean = 1129). Proportions of CD3, CD4, and CD8 lymphocytes in CSF were very highly correlated with the proportions of these cells in the peripheral blood (r = 0.87, 0.96, and 0.94, respectively), as was the CD4/CD8 ratio (r = 0.98). These strong correlations were present in each of seven subgroups of study subjects defined on the basis of detailed neurologic examination, neuropsychological testing, and the presence or absence of antibodies to HIV-1. In the population studied, T cell phenotypes in CSF as analyzed by two-color flow cytometry were largely determined by the corresponding proportions in the peripheral blood.

Localization of human immunodeficiency virus core antigen in term human placentas.

Evidence of human immunodeficiency virus (HIV) replication was sought in human placentas obtained at term from pregnancies complicated by maternal HIV infection. Placentas were obtained from the pregnancies of 19 HIV-seropositive women, 4 women who were seronegative, and 4 untested women with no risk factors for HIV infection. These placentas were each examined by immunoperoxidase immunocytochemistry using monoclonal anti-p24/55 antibodies. In addition, minced placental tissue from 11 of the seropositive pregnancies and the 3 seronegative pregnancies were co-cultivated with stimulated human peripheral blood mononuclear cells. The clinical status of the infants born to the HIV-seropositive women was assessed when the infants were 8 to 28 months of age. P24/55 antigen was detected in 5 of the 19 placentas of the HIV-seropositive pregnancies and in none of the 8 placentas of seronegative or low-risk pregnancies. This HIV core viral antigen was located exclusively in the cytoplasm of villous cells with morphological characteristics of macrophages. The HIV antigen-containing cells were very sparsely distributed. Staining of the trophoblast was not observed in any placental specimen. Human immunodeficiency virus was isolated in culture from 3 of the 11 placentas from seropositive pregnancies. Clinical follow-up has not revealed a relationship between infection of the infant and either p24/55 antigen identification or isolation of virus from the placenta. Virological and histological evidence of HIV replication is found in approximately one fourth of placentas obtained at term from pregnancies complicated by maternal HIV infection. Replicating virus appears localized to sparse macrophages located within the chorionic villi, but specifically not within the trophoblastic layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-HIV type 1 memory cytotoxic T lymphocyte responses associated with changes in CD4+ T cell numbers in progression of HIV type 1 infection.

We investigated memory cytotoxic T lymphocyte (CTLm) responses to HIV-1 as a determinant of HIV-1 disease progression, in relation to plasma HIV-1 load and T lymphocyte numbers in a longitudinal study of 14 homosexual men with incident HIV-1 infection. Study participants were selected who exhibited failure of T cell homeostasis, i.e., a downward inflection in CD3+ T cells that occurs in >75% of persons 1.5 to 2.5 years before development of AIDS, and compared with participants who developed low CD4+ T cell counts associated with possible T cell homeostasis failure, a subject who progressed rapidly to AIDS without well-defined T cell inflection, and subjects who had long-term preservation of T cell homeostasis (nonprogressors). High CTLm responses against Gag, but not Pol or Env, soon after seroconversion were associated with a slower loss of CD4+ T cells 1-4 years after seroconversion. Anti-Env CTLm responses decreased in most subjects around the time that T cell homeostasis failed. Plasma HIV-1 RNA increased exponentially (1.59-fold per year) over the 5 years preceding failure of T cell homeostasis, and there was a shift from a non-syncytium-inducing/CCR5 coreceptor phenotype of HIV-1 to a syncytium-inducing/CXCR4 phenotype, regardless of high or increasing levels of anti-HIV-1 CTLm during this time. These observations suggest that decreases in CTLm and increasing virus load are independent factors contributing to HIV-1 disease progression.

Differences in neutralization of simian lentivirus (SIVMAC) in lymphocyte and macrophage cultures.

Comparison of neutralization of SIVmac251 in primary macrophage cultures with neutralization in lymphocytes (CEM174 cells) showed that neutralizing antibodies induced by SIV251 in infected rhesus macaques protected both macrophages and T lymphocytes against infection when the virus was preincubated with the antibodies. In macrophages, the neutralizing antibodies also protected against infection when added 1 hour after the virus. Addition of antisera to macrophages between 24 and 48 hours after virus inoculation resulted in infection with continuous release of small amounts of p24 into the supernatant fluids but these antibody-treated cultures failed to exhibit cytopathic virus replication. In contrast, the same neutralizing antisera did not protect lymphocytes against infection and subsequent cytopathic replication of the virus when added only 1 hour after virus inoculation. This distinction in the effect that neutralizing antibodies had on the development of cytopathic infection in lymphocytes and macrophages when added after virus inoculation, suggests that they could alter the dynamics of virus replication and therefore the pathogenesis of disease.

Occupational risk of human immunodeficiency virus, hepatitis B virus, and hepatitis C virus infections among funeral service practitioners in Maryland.

OBJECTIVE: To estimate the risk of exposure and infection with bloodborne pathogens, a seroepidemiologic survey was conducted among funeral service practitioners (FSPs) in Maryland. METHOD: Of 262 members of the Maryland State Funeral Directors Association, 130 (49%) volunteered to participate in the study. In addition to a brief questionnaire, designed to assess both occupational and non-occupational risk factors for bloodborne pathogen infection, participants were screened for markers of human immunodeficiency virus (HIV), hepatitis C virus (HCV), and past hepatitis B virus (HBV). Titers for antibodies to hepatitis B surface antigen (anti-HBs) also were examined and compared with history of hepatitis B vaccination. RESULTS: Seroprevalence for HIV, HBV, and HCV infection was 0.8%, 4.6%, and 0%, respectively. Nearly 19% of participants reported at least one bloodborne exposure in the past 6 months. The one HIV infection and all but two of the HBV infections were correlated with well-established non-occupational risk behaviors. Disposable gloves were worn by 96%, and eating, drinking, or smoking during embalming were infrequent. Sixty-one percent of FSPs reported having received one or more doses of hepatitis B vaccine at some time in the past. Of those who reported having received all three doses of vaccine, 67% had adequate titers to hepatitis B surface antibody, the marker of protection related to vaccination. CONCLUSION: Compared with prior studies of FSPs, this study found a low rate of occupational exposures and a high rate of hepatitis B vaccination, suggesting improved compliance with recommendations for preventing transmission of bloodborne pathogens in the workplace.

HIV-1 antibodies and serology.

This article reviews various laboratory assays for screening and detection of antibodies against HIV-1 and viral components. The prognostic role of these assays in the course of HIV-1 infection is described as well as functional aspects of anti-HIV antibodies.

Epidemiology of viral hepatitis among Iranian population--a viral marker study.

Our studies revealed that the incidence of viral hepatitis in Iran is more common than in the western countries. Although the incidence of hepatitis type A in the region is not thoroughly investigated, our first report on this disease in our region reveals an almost complete immunity among adults after 30 years of age. The incidence of HBsAg among our voluntary blood donors is 3.5%. If it is assumed that the incidence rate in the whole country is also 3.5%, then it is possible that there are one million HBsAg carriers among 35 million Iranians. These carriers constitute a major health problem in Iran. There is a good possibility that the HBsAg incidence rate in the other countries of the region is similarly high. Therefore it is highly recommended that control and preventive measures such as third generation HB teting of donated blood and blood products become mandatory. All HBsAg positive donors should be interviewed and informed that their blood contains an infectious agent and this must be carefully considered at the times of bleeding. Other high risk groups such as haemodialysis patients and staff and haemophiliacs also should be investigated as possible candidates for HB vaccination.