Underlying mechanism by which estradiol enhances anti-viral responses
HSV-2 is one of the most dominant sexually transmitted infection (STI) worldwide, with global estimates of approximately 530 million individuals who are positive for HSV-2 [...]
HSV-2 is one of the most dominant sexually transmitted infection (STI) worldwide, with global estimates of approximately 530 million individuals who are positive for HSV-2. Rate of infection is higher in women, however, the cause for increased susceptibility has not been established. It has been shown that the hormonal microenvironment may be playing a role, as hormone treatment in animal models has shown to differentially prime immune responses to HSV-2. A recent study examining the role of estradiol in HSV-2 infection, led by MIRC graduate Varun Anipindi from Dr. Charu Kaushic’s lab, was published in PLoS Pathogens. The study showed, for the first time, a mechanism to describe how estradiol, a female sex hormone present during the menstrual cycle and found in oral contraceptives, can protect against sexually transmitted viral infections.
Using a mouse model of HSV-2 infection, Anipindi and collegues showed that estradiol primes dendritic cells in the vaginal tract to induce a Th17 response, which coincides with an increase in anti-viral Th1 responses. This pathway has important implications for addressing if some hormonal contraceptives may be better than others for women who are at higher risk for acquiring STIs. In addition, “We hope this raises awareness about the importance of vaccines administered by the mucosal route, and how this strategy can induce better protection,” says lead author Dr. Varun Anipindi. The study was highlighted as the Featured Research Article by PLoS Pathogens, selected by the Editors-in-Chief as being “a high-quality research article that is of particular importance and relevance to the pathogens community and general public”. Congratulations to Dr. Varun Anipindi and Dr. Charu Kaushic! Read More.
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