Transfusion associated HIV infection in patients with haematologic disorders in southern India.

Seventy patients with congenital coagulation disorders (group A) and 202 other patients (group B) attending the Haematology clinic at the Christian Medical College and Hospital, Vellore (India) were screened for HIV infection between March 1989 and April 1991. Fifty five patients in group A and 131 patients in group B had received blood or blood products in the past. Nineteen transfused patients (9 in group A and 10 in group B) had received blood or blood products exclusively from the hospital blood bank and none of them was HIV infected. Among the remaining 167 transfused patients, 14 (30.4%) of the 46 patients in group A and 6 (4.9%) of the 121 patients in group B were found to be positive for HIV. In group A, 13 of the 14 infected patients had received commercially available cryoprecipitate which was thus found to be the most frequent source of infection. In group B the source of infection was most probably unscreened HIV infected blood which was transfused.

High prevalence of HTLV antibodies in wild-caught bonnet monkeys in southern India.

The prevalence of human T-lymphotropic virus (HTLV) type-1 antibodies was determined in the bonnet monkeys, living naturally, within about 30 km radius of Vellore (south India). Sera from 157 animals, collected between January 1982 and May 1993 were screened for the presence of HTLV-I infection by a particle agglutination test (PAT). When sera repeatedly reactive in PAT were subjected to indirect immunofluorescence and western blot tests, 63 (40%) were confirmed to be positive for HTLV-1 antibody. These findings are significant in the light of recent reports that HTLV infection is endemic to southern India.

The detection of HIV-2 infection in southern India.

To determine the prevalence of HIV-2 infection in southern India, we tested two sets of sera, selected from among the samples which had been collected between January 1988 and October 1990 from high risk subjects and tested for HIV-1 antibody. They were screened for HIV-2 antibody by ELISA and repeatedly reactive sera confirmed by HIV-2 Western blot and line immunoassay. In the first set of 604 sera, only one (0.16%) was positive for HIV-2. In the second set of 24 sera, selected on the basis of having indeterminate HIV-1 Western blot profiles, again one (4%) was positive for HIV-2. The two HIV-2 infected subjects were residents of Madras or Visakhapatnam. Residents of Vellore region constituted 88 and 75 per cent of the two sets of subjects; none was positive for HIV-2. Our results show the prevalence of HIV-2 in the port-cities of southern India. Since it will spread to other regions continuous monitoring for this infection is essential in order to determine when to establish HIV-2 screening in addition to the existing HIV-1 screening of donor blood for transfusion.

Reduction of the cost of testing for antibody to human immunodeficiency virus, without losing sensitivity, by pooling sera.

The sensitivity of testing pooled sera instead of individual sera for antibody against human immunodeficiency virus (HIV) was evaluated using a non-competitive enzyme-linked immunosorbent assay (ELISA). For this purpose, 42 HIV antibody positive sera were titrated and introduced into 42 sets of pools of 2, 4, 8, 16, 32 or 64 sera in such a manner that each pool had one positive sample and the rest, HIV antibody negative sera. When the pools were tested in ELISA, all pools with high titred antibody positive sera were reactive irrespective of pool size, while some of the pools containing medium or low titred sera were non-reactive when pool size exceeded 16. Subsequently the pool size was limited to 16. When 208 previously unscreened samples were tested in 52 pools of 4, 26 pools of 8 or 13 pools of 16 sera, or individually, 6 antibody positive sera were correctly identified. Thus, it was found that the pooling method did not reduce the sensitivity of ELISA test, whereas the cost was reduced to less than half of that of individual testing.

T-lymphocyte mediated injury of beta cells in dual-aetiology diabetes mellitus in Swiss albino mouse.

Earlier we had described a dual aetiology diabetes mellitus (DADM) in mice injected with a sub-diabetogenic dose of streptozotocin (SD-SZN) and afterwards infected with coxsackie B3 virus (CBV). Further experiments were conducted to understand the mechanism of diabetogenesis. In in vitro stimulation and proliferation tests, the splenic lymphocytes (SLC) of mice given either SD-SZN or CBV infection showed lower responses to two T cell mitogens than those of control mice, indicating an immunosuppressive effect. Unexpectedly, SLC of mice given both SD-SZN and CBV showed enhanced response, indicating immunoactivation; they were not stimulated to proliferation in response to CBV antigen, indicating that the immunoactivation was not directed against CBV, but against streptozotocin or cellular elements. When mice were depleted of T cells by injecting with anti-thymocyte serum, the diabetogenic effect of SD-SZN and CBV infection was abrogated, without diminishing the replication of virus in the pancreas. Thus beta cell injury in DADM appears to be T cell-mediated.