False-positive self-reports of HIV-1 infection.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S S Gould.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Six of 11 human immunodeficiency virus (HIV)-infected patients with chronic diarrhea, shedding only Candida spp. in their stools, elicited a Candida-specific secretory immunoglobulin A response. Similar responses were identified in only 1 of 10 HIV-positive patients with chronic diarrhea but without Candida spp. and in none of 10 HIV-negative subjects without diarrhea. Candida spp. may play a role in the etiology of chronic diarrhea associated with HIV infection.
The hypothesis that failure of hosts infected with Trypanosoma brucei to express type 1 hypersensitivity is related to this parasite's ability to down-regulate IgE production, and not to an innate lack of allergenicity of T. brucei antigens, was tested by studying anaphylaxis-induced changes in net epithelial ion transport in rats. Transport changes were quantified electrophysiologically in vitro, as a change in transmural short-circuit current when sensitized intestine was challenged with homologous antigen. Rats injected parenterally with trypanosome antigen elicited intestinal anaphylaxis in response to antigenic challenge, whereas the intestine of rats infected with T. brucei failed to respond. Infection with T. brucei also suppressed the anaphylactic response in rats sensitized to and challenged with ovalbumin and T. spiralis-derived antigens. In these cases suppression was related to the ability of T. brucei to block production of IgE, and not to the physiological failure of the epithelial response. However, in rats sensitized by infection with T. spiralis, neither the anaphylactic response nor IgE production were inhibited by T. brucei. Furthermore, intestinal mastocytosis normally associated with trichinosis was unaffected by the trypanosome infection. Results support the conclusion that the failure to express anaphylaxis in T. brucei-infected rats is due to the inhibition of IgE production and not to the lack of allergenicity of trypanosome antigens.
Sera of vervet monkeys experimentally infected with T. b. rhodesiense were examined using a double antibody sandwich ELISA and Procyclic Agglutination Trypanosomiasis Test (PATT) for the presence of circulating trypanosomal antigens and anti-procyclic surface antibodies, respectively. Trypanosomal antigens were detected at 7 days post infection and remained at a detectable level thereafter during the infection. Antigens were not detected in sera prior to experimental infection or at 26 days after trypanocidal drug treatment. Although both the PATT and the sandwich ELISA results correlated with the infection status of the animals, the sandwich ELISA gave a better indication of the disease progression than the PATT, especially during trypanocidal drug therapy. The results illustrate the potential utility of the double antibody sandwich ELISA for diagnosis of African sleeping sickness.
Blood-cerebrospinal fluid (CSF) barrier damage in 11 vervet monkeys was estimated before infection and during the early and late phases of Trypanosoma rhodesiense disease, using the method given by Tibbling, Link and Ohman (1977). Of the 11, only one monkey showed signs of barrier impairment that ranged from a slight (12.6) to total barrier impairment (285); the latter occurring just before the height of clinical encephalitis. The barrier reverted to normal after melarsoprol treatment at 1.8 mg/kg X 4. Between the two extremes of barrier impairment, there were periods of remission during which time the barrier reverted to normal. This monkey however continued to suffer epileptic fits for a period of three months, a condition that started soon after the treatment.
Explore the source record for details and available documents.
Uncoated procyclic culture forms of African trypanosomes were used in immunofluorescence and simple agglutination assays to detect antibodies in the sera of vervet monkeys infected with T. b. rhodesiense. Antibodies to procyclic surface antigens were found in sera from animals with active, untreated infections or sera taken soon after treatment with trypanocidal drugs. The antibodies were detectable within 7 days of infection. No specific antibodies were detected in sera prior to infection or long after drug cure. The results indicate that antigens expressed on the surface of procyclic culture forms of T. brucei spp. are useful for the detection of antibodies produced in response to infection with T. b. rhodesiense and may allow the development of a simple immunodiagnostic test for African sleeping sickness. In addition, the use of a form of the trypanosome of a different differentiation state from the infecting organism illustrates the utility of this approach for detection of antibodies to common antigens.
Explore the source record for details and available documents.
Explore the source record for details and available documents.