High HIV prevalence and risk behaviors in men who have sex with men in Chennai, India

OBJECTIVE: To estimate HIV and sexually transmitted disease (STD) prevalence and behavioral risk characteristics of men who have sex with men (MSM) in Chennai, India. METHODS: A cross-sectional population-based random sample survey was conducted in 2001. Randomly selected residents of 30 slums in Chennai were interviewed for behavioral risk factors through face-to-face interviews. Sera and urine were examined for syphilis, HIV-1, gonorrhea, and chlamydia. Logistic regression analyses were used to assess associations between MSM status and HIV infection and to identify risk characteristics of MSM. RESULTS: Of 774 men, 46 reported (5.9%) sex with other men. MSM were more likely to be seropositive for HIV (odds ratio [OR] = 8.57; 95% confidence interval [CI]: 1.83, 40.23) and were more likely to have a history of STD (OR = 2.66; 95% CI: 1.18, 6.02) than non-MSM. Men who used illicit drugs in past 3 months (adjusted odds ratio [AOR] = 4.01; 95% CI: 1.92, 8.41), ever exchanged money for sex (AOR = 3.93; 95% CI: 1.97, 7.84), or were ever tested for HIV (AOR = 3.72; 95% CI: 1.34, 10.34) were significantly more likely to report sex with men. CONCLUSIONS: MSM in Chennai slums are at high risk for HIV. HIV prevention strategies aimed at changing unsafe drug and sexual practices should target the general population of men, with specific attention to areas with high rates of MSM.     

Antigen-receptor degeneracy and immunological paradigms

This paper discusses some consequences of the discovery that antigen receptors are degenerate: Immune specificity, in contrast to the tenets of the clonal selection paradigm, must be generated by the immune response down-stream of initial antigen recognition; and specificity is a property of a collective of cells and not of single clones.     

The use of laboratory intervention to stem the flow of fresh-frozen plasma

Four methods of laboratory intervention were tested by the hospital blood bank in an effort to modify the use of fresh-frozen plasma (FFP). Over a one-year period, a utilization audit was serially initiated with feedback to physicians, a recurrent educational program was introduced for housestaff delineating guidelines for FFP use, a form was introduced requiring justification for FFP orders, and a policy was established requiring pathologist approval of FFP in patients with normal or no coagulation studies. Overall, in comparing the period following all forms of intervention (February 1986-October 1986) to the baseline period prior to any form of intervention (July 1984-March 1985), FFP use dropped 52% in the face of a 17% increase in red blood cell use. It was concluded that blood bankers can dramatically alter the use of this product using established methods for modifying physician ordering behavior.     

Confirmation that the Type I collagen gene on chromosome 17 is COL1A1 (α1(I)), using a human genomic probe

A cloned 15 kb genomic fragment from the human α1 (I) collagen gene (COL1A1) has been used as a probe on restriction digests of DNA from human-mouse somatic cell hybrids. Positive results on hybrids containing chromosome 17 as their only karyotypically visible human material confirm the assignment of this gene to chromosome 17. Hybrids which contain fragments of chromosome 17 are used to confirm the localization to 17q21-qter.     

The lipid raft microdomain-associated protein reggie-1/flotillin-2 is expressed in human B cells and localized at the plasma membrane and centrosome in PBMCs

Reggie-1/flotillin-2 is a plasma membrane-associated cytoplasmic protein, which defines non-caveolar raft microdomains. Reggie-1/flotillin-2 is enriched in detergent insoluble (TX100) membrane fractions (DIG), co-localizes with activated GPI-linked proteins and the fyn-kinase in neurons and T cells, and thus apparently participates in the assembly of protein complexes essential for signal transduction. In T cells activated by crosslinking the GPI-linked protein Thy-1 or by crosslinking the ganglioside GM1, reggie-1/flotillin-2 co-localizes with the T cell receptor. To determine whether reggie-1/flotillin-2 is also expressed in B cells, primary B cells from human blood and cell lines representing the developmental stages of pro, pre, mature and plasma B cells were analyzed by Western blotting, RT-PCR and immunofluorescence. Here, we show that reggie-1/flotillin-2 is expressed throughout B cell development, as well as in primary B cells, purified by cell sorting. On non-activated mature B cell Raji cell line we found reggie-1/flotillin-2 are exclusively in the detergent (TX100) insoluble membrane fractions that are staining positive for the raft marker GM1. Immunofluorescence microscopy showed that reggie-1/flotillin-2 is localized at the plasma membrane and marks intracellular spots in PBMCs. Confocal co-localization studies showed that reggie-1/flotillin-2 is associated with the plasma membrane, and the centrosomes (microtubule organizing centers) in these PBMCs. Comparison of reggie-1/flotillin-2 cDNA sequences with the genomic sequence database allowed us to determine the exon/intron structures in mouse and human. The gene organizations are highly conserved suggesting an important function of reggie-1/flotillin-2. Since reggie/flotillin proteins co-cluster with the T cell receptor and fyn kinases upon T cell stimulation, our findings of reggie-1/flotillin-2 in B cells suggest a similar role in B cell function.     

Plasmids of Ewingella americana: supplementary epidemiologic markers in an outbreak of pseudobacteremia.

During an outbreak of pseudobacteremia in a children's hospital, Ewingella americana was found in blood cultures from 20 patients. E. americana was inoculated into blood culture bottles at the time of specimen collection due to cross contamination from nonsterile, citrated blood collection tubes used for coagulation studies. Antimicrobial susceptibility testing and plasmid profiling were used to assess the association between patient isolates and isolates from unused blood collection tubes. All E. americana isolates had similar antibiograms (i.e., resistance only to cephalothin) when tested at 37 degrees C. However, when the same isolates were tested for antimicrobial susceptibility at 25 degrees C, a different antibiogram (i.e., resistance to chloramphenicol, ampicillin, and cephalothin) was found. The majority of these isolates also demonstrated a unique four-plasmid profile (130, 56, 4.6, and 3.1 megadaltons), and two of these plasmids (130 and 56 megadaltons) were characterized as temperature-sensitive plasmids. An epidemiologic link between outbreak-associated isolates obtained from different time periods in the outbreak was supported by evidence of a significant trend in the ability of the outbreak-associated isolates to reduce nitrate, together with the presence of the resistance antibiogram at 25 degrees C and the demonstration of the unique four-plasmid profile.     

Pathogenic anti-DNA antibodies in SLE: idiotypic families and genetic origins

We have adopted an idiotypic approach to study the double stranded DNA (dsDNA) binding antibodies of systemic lupus erythematosus (SLE). Three anti-idiotypic reagents, 8.12, 3I, and F4, identify cross reactive idiotypes that are each expressed on anti-dsDNA antibodies in the sera of many patients with SLE. These idiotypic antibodies are implicated in the pathogenesis of SLE as they are present in immune complex deposits in the kidneys of patients with SLE glomerulonephritis. The autoantibody associated idiotypes are also expressed on antibodies that do not bind DNA. We are investigating the origin of the pathogenic anti-dsDNA antibodies of SLE by comparing the autoantibodies, the antibodies to foreign antigens, and the myeloma proteins that express each SLE associated idiotype. In conjunction with serological analysis of these idiotypic systems, molecular genetic studies indicate that both the 8.12 and the 3I autoantibody associated idiotypes may be germline encoded, while the F4 idiotype is generated by somatic mutation. The data further suggest that the antigenic specificity of the pathogenic anti-DNA antibodies of SLE is acquired through somatic mutation of germline immunoglobulin genes. By studying the regulation of genes capable of encoding pathogenic autoantibodies, in both SLE patients and non-autoimmune individuals, we may be able to elucidate the pathogenesis of autoimmune disease and begin to design more effective therapeutic interventions.     

Ewingella americana: recurrent pseudobacteremia from a persistent environmental reservoir.

From September 1981 through April 1984, 20 patients at one hospital were identified with Ewingella americana pseudobacteremia. Case-control studies demonstrated an association between having a positive blood culture for E. americana and having blood for culture obtained simultaneously with blood obtained for coagulation studies (15 of 19 case patients versus 4 of 38 controls; P = 4.5 X 10(-7)). Review of blood-drawing procedures showed that blood for coagulation studies and culture was drawn with the same syringe, and coagulation tubes were filled before blood culture tubes. Some phlebotomists were not using new sterile needles to inoculate blood culture bottles. Collection tubes for coagulation studies were prepared in the hospital, and E. americana was isolated from all 52 unused coagulation tubes tested. Solutions prepared in the hospital may constitute a persistent inanimate environmental reservoir for this uncommon microorganism. Pseudobacteremia can result in unnecessary antimicrobial therapy for some patients, incurring the risks of adverse drug reactions, selection of drug-resistant bacteria, and increased health care costs.