Evaluation of the cervicovaginal environment in asymptomatic Human T-cell lymphotropic virus type 1 infected women

ABSTRACT Introduction: Human T-cell lymphotropic virus type 1 (HTLV-1) is sexually transmitted and causes persistent infection. This virus induces activation of the immune system and production of inflammatory cytokines. This study aimed to assess the cytokine profile and cytopathological findings in the cervicovaginal fluid of asymptomatic HTLV-1-infected women. Methods: HTLV-1-infected and uninfected women were selected at the Centro de Atendimento ao Portador de HTLV in Salvador-Brazil. None of the included HTLV-1-infected women reported any HTLV-1-associated diseases. All volunteers underwent gynecological examination to collect cervicovaginal fluid. Cytokine quantification was performed using the Cytometric Bead Array (CBA) Human Th1/Th2/Th17 kit. Light microscopy was used to evaluate cervicovaginal cytopathology. In addition, proviral load in cervicovaginal fluid and peripheral blood was measured by real-time quantitative polymerase chain reaction. Results: 112 women (63 HTLV-1-infected and 49 uninfected) were evaluated. No differences were found with respect to cytopathological cervicovaginal findings between the groups. IL-2, TNF, IL-4, IL-10, and IL-17 levels were significantly higher in cervicovaginal fluid of the HTLV-1-infected women than in uninfected women (p < 0.05). Conversely, IFN-γ was found to be lower in the HTLV-1-infected women (p < 0.001) compared to uninfected individuals. Cervicovaginal proviral load was detectable in 53% of the HTLV-1-infected women and was found to be consistently lower than the proviral load in peripheral blood. Conclusions: HTLV-1 infection induces immune activation in cervicovaginal environment, characterized by elevated concentrations of Th1, Th2, and IL17 in the cervicovaginal fluid.

Immunogenicity of soluble haemagglutinin-lipopolysaccharide complex of classical vibrio cholerae.

Soluble haemagglutinin-lipopolysaccharide complexes were found to be good antigens since it elicited high levels of the antibodies in the intestine especially of the IgA class. These specific antibodies sustained for a long period of time at the significantly high levels (longer than 6 months). The enteric memory primed by the antigens in the intestinal tract were longer than 3 months. Pools of intestinal fluids obtained from mice immunized with single dose of SH-LPS at 1 week, 1 month and 3 months after the antigen stimulation conferred protection against the homologous challenge. Better protection was found in the corresponding specimens collected from mice which received antigen booster at 3 months after the first stimulation. Multiple oral doses of the antigens (three doses at weekly intervals) did not have any advantage over the single dose immunization. The intestinal fluids obtained from the former group conferred similar degree of protection as those from the latter though the serum specimens offered higher PD50. The protection against cholera does not correlate with the levels of vibriocidal antibody in the body fluids which seems to confirm the hypothesis that the mechanism of protection against cholera by intestinal antibody is by reducing or preventing the attachment of the vibrios to the epithelium either via agglutinating process or via masking of the vibrio adhesive sites.