Association between knowledge, risk behaviours, and testing for sexually transmitted infections among men who have sex with men: findings from a large online survey in the United Kingdom.

OBJECTIVES: In the UK, men who have sex with men (MSM) bear a disproportionate sexually transmitted infection (STI) burden. We investigated MSM's STI knowledge; whether their STI testing behaviour met national guidelines (annually if sexually active; 3-monthly if engaging in STI risk behaviours); and the relationship between STI testing in the last 3 months, STI knowledge and STI risk behaviours by HIV status. METHODS: Sexually active (in the last year) men aged > 15 years who were UK residents and were recruited from gay-orientated online dating platforms completed an anonymous online survey about STI knowledge, STI risk behaviours, and STI testing (March-May 2017). This included 11 true statements about STIs. Respondents scored 1 for each statement they 'knew', with those scoring < 6 overall treated as having 'poor' STI knowledge. Descriptive and multivariable analyses were conducted, separately by HIV status, to test our hypothesis and calculate adjusted odds ratios (AORs) with 95% confidence intervals (CIs). RESULTS: Compared to HIV-positive men (n = 489), the proportion of HIV-negative/unknown-status men (n = 3157) with 'poor' STI knowledge was significantly higher (46.4% versus 22.9% for HIV-positive men) and the proportion with STI testing in the last 12 months was lower (71.6% versus 87.2%, respectively). In the last 3 months, 56.9% of HIV-negative/unknown-status and 74.1% of HIV-positive men reported STI risk behaviours, of whom 45.8% and 55.1%, respectively, had been tested for STIs during this time. Among HIV-negative/unknown-status men, those reporting STI risk behaviours were more likely (AOR 1.52; 95% CI 1.26-1.84) and those with poor STI knowledge less likely (AOR 0.73; 95% CI 0.61-0.89) to have been tested during the last 3 months. However, neither factor was independently associated with 3-monthly testing among HIV-positive men. CONCLUSIONS: Improving STI knowledge, especially among HIV-negative/unknown-status men, and promoting frequent STI testing among men engaging in STI risk behaviours are vital to address the poor sexual health of MSM

The role of IL-4 in adult acquired and congenital toxoplasmosis

The course of Toxoplasma gondii infection was studied in IL-4-deficient mice from three genetic backgrounds and their wild-type counterparts following peroral inoculation of tissue cysts. Survival rates were significantly reduced in disease-susceptible C57 BL6 mice and F1 (C57BL6× 129Sv) mice deficient in IL-4 compared with wild-type controls. In contrast, this difference was not observed in T. gondii-resistant BALBc mice. However, brain tissue cyst burdens in IL-4-deficient mice were either equivalent to (C57BL6 and BALBc mice) or significantly less (B6129 mice) than similarly infected wild-type mice. Thus strain-specific differences in the course of T. gondii were demonstrated in the absence of IL-4. The course of T. gondii infection was also compared between B6129 IL-4-deficient mice and their wild-type counterparts following peroral challenge with 20 tissue cysts on day 12 of pregnancy. Age-matched non-pregnant IL-4−/− and IL-4+/+ mice were also infected to assess the role of IL-4 on T. gondii infection during pregnancy. Disease phenotypes, as measured by mortality, were reversed if infections were initiated during pregnancy compared with non-pregnant infection. Thus significant mortality occurred immediately post partum in IL-4+/+ mothers, while all IL-4−/− mothers survived. Cyst burdens 28 days p.i. were significantly lower in IL-4−/− mothers than IL-4+/+ mothers and both IL-4−/− and IL-4+/+ non-pregnant mice. Congenital disease transmission as measured by foetal death or vertical disease transmission was independent of the presence or absence of IL-4. These studies demonstrate a role for IL-4 in pregnancy-induced immunosuppression and the associated increased susceptibility to T. gondii infection

Innate immunity to Toxoplasma gondii is influenced by gender and is associated with differences in interleukin-12 and gamma interferon production.

Given that differences between the sexes in relative susceptibility to parasitic infections have been noted, this study further elucidates the mechanisms responsible by demonstrating that male SCID mice are more resistant than female mice to infection with Toxoplasma gondii and that this difference correlates with enhanced innate immune responses in these animals. Male SCID mice exhibited longer survival times, lower parasite burdens, and less severe pathological changes postinfection. An immunological basis for these differences is demonstrated in that these animals produced interleukin-12 more rapidly and exhibited higher levels of gamma interferon earlier postinfection

Different roles for interleukin-4 during the course of Toxoplasma gondii infection

The course of Toxoplasma gondii infection from initiation of disease perorally until day 28 postinfection was compared between interleukin-4 (IL-4) gene knockout (IL-4-/-) mice and their wild-type (IL-4+/+) counterparts on a disease-susceptible genetic background. The rate of mortality was significantly greater in mice deficient in Il-4 than in the immunocompetent controls. Although levels of T. gondii-specific spleen cell proliferation measured in vitro were similar between groups at all time points examined throughout infection, the quantities of cytokines released into the culture supernatant differed. Culture supernatants from spleen cells derived from IL-4-deficient mice contained significantly more gamma interferon than those derived from IL-4+/+ mice at day 7 postinfection. Conversely, IL-10 production was significantly greater from the spleen cells derived from wild-type mice at day 28 postinfection. Splenocytes from both groups of mice had a marked inhibition of proliferation in response to soluble tachyzoite antigen as well as reduced proliferation in response to concanavalin A between days 7 and 14 postinfection and marked proliferation on days 21 and 28 postinfection. At day 28 postinfection, histological examination of the brains indicated that IL-4+/+ mice had more severe pathological changes and more cysts than IL-4-/- mice. In addition, although many nonencysted single organisms were present in IL-4+/+ mice within both necrotic lesions and microglial nodules, few nonencysted parasites were found, and no necrotic lesions were present in IL-4-deficient animals. These results suggest that the observed reduction in mortality during the early acute phases of infection may be due to the down-regulatory effects of Il-4 or associated Th2-derived products on proinflammatory cytokines such as gamma interferon. However, the long-term effects of IL-4 are detrimental, possibly because of the ability of this cytokine to inhibit proinflammatory antiparasitic products. This may explain the increased parasite multiplication with cysts observed in the brains of IL-4+/+ mice

A protective role for IL-6 during early infection with Toxoplasma gondii

IL-6 deficient mice were found to be signifcantly more susceptible to peroral infection with Toxoplasma gondii than their wild-type counterparts as measured by survival, brain cyst burdens and brain pathology at 28 days postinfection. The physical manifestations of disease, such as weight loss, were not observed in IL-6 deficient animals until at least seven days later than such changes occurred in wild-type mice. During this early stage of infection IL-6+/+ but not IL-6-/- mice mounted a peripheral blood neutrophilia. Furthermore, between 6-8 days post-infection there was a significant increase in plasma IFN-gamma levels in wild-type but not IL-6 deficient mice. Not until days 18-23 post-infection, concurrent with the majority of deaths in IL-6-/- mice, were plasma IFN-gamma levels substantially and significantly raised in IL-6-/- mice. At this time not only were these plasma IFN-gamma levels 20-fold higher than background but eight-fold greater than peak (6-8 clays post-infection) IFN-gamma levels in IL-6+/+ mice. IFN-gamma dependent parasite specific IgG2a levels were also significantly higher in IL-6-/- mice over this period and thereafter Overall the evidence suggests that in the absence of IL-6 mice are unable to initiate a rapid proinflammatory response against T. gondii, which allows increased parasite growth. Increased mortality in IL-6-/- mice may be directly due to this increased parasite burden and the excessive inflammatory response this induces three weeks post-infection

Novel and improved method for the synthesis of 2-mercaptobenzimidazole derivatives

International audience2-mercaptobenzimidazole derivatives were synthesized by reaction of o-phenylenediamines with N-aminorhodanine. This reaction represent a new synthesis of 2-mercaptobenzazole. The structure of the obtained products was established by spectroscopic data. © 2016, Oriental Scientific Publishing Company. All rights reserved