Summary auto-generated
This study examined how herpes simplex virus type 2 (HSV-2) suppresses the immune response by analyzing virus-specific antibody-producing B cells in infected mice using an immunospot assay. Female BALB/c and NMRI mice received primary and secondary infections with HSV-1 or HSV-2 at various doses and timepoints. Results showed that HSV-1 induced robust IgM and IgG antibody-secreting B cell responses starting at day 5 post-infection, whereas HSV-2 induced very low numbers of antibody-producing cells that appeared late. Secondary HSV-1 infections at day 8 showed minimal splenic B cell responses despite normal humoral antibody booster reactions, suggesting extrasplenic antibody production. However, secondary infections at days 21-35 induced strong splenic B cell responses. HSV-2-induced suppression persisted for over 40 days but eventually waned, indicating that antigen presentation and memory cell generation remained intact. The findings suggest HSV-2 suppression operates through multiple mechanisms affecting B cell activation and proliferation, possibly involving macrophage dysfunction or defective T helper cell responses.
Key findings
- HSV-2 induced significantly fewer IgM and IgG antibody-secreting B cells compared to HSV-1, with delayed kinetics
- HSV-2-induced immunosuppression lasted over 40 days but eventually resolved, indicating preserved immune memory
- Secondary HSV-1 infections at day 8 showed minimal splenic B cell responses despite normal humoral antibody responses, suggesting extrasplenic antibody production during early suppression
- By days 21-35, secondary infections generated strong splenic B cell responses with predominantly IgG-secreting cells
- The suppression mechanism likely involves macrophage dysfunction and possible defects in T helper cell proliferation rather than antigen presentation or memory cell impairment
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Abstract
The mechanism of herpes simplex virus (HSV)-2-induced immunosuppression was analysed by determination of the number of IgM and IgG antibody-secreting B cells in female BALB/c mice using an immunospot assay. Primary HSV-1 or -2 as well as homologous or heterologous booster infections at different times were performed. In accordance with earlier results on humoral antibody generation, in contrast to HSV-1, HSV-2 induced only very low numbers of antibody-producing B cells in dose-response experiments. They appeared late after infection compared to HSV-1. Despite a homologous humoral booster reaction against HSV-1 at day 8 no IgM- or IgG-secreting cells in the spleen could be detected. This non-reactivity of the spleen had vanished 10 days later, when secondary reactions of B cells could be observed. Secondary infections with a high homologous dose of HSV-2 after a low primary dose produced only a low booster response of IgG-secreting B cells. Suppression of humoral antibody production induced by HSV-2 (high dose) waned after more than 50 days, indicating that the HSV-2-induced suppression did not impair antigen presentation or memory cell generation.