{'fraction_non_alphanumeric': 0.032441200324412, 'fraction_numerical': 0.009732360097323601, 'mean_word_length': 5.529100529100529, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Microglial activation during HSV‐1 infection is increased by vitamin E deficiency

Previous studies from our laboratory have shown that dietary a‐tocopherol (VE) is critical to regulating the cytokine and chemokine response in the brain to herpes simplex virus (HSV) infection. Microglial cells have been identified as a source of pro‐inflammatory cytokine production during HSV‐1 infection in both humans and mice. During HSV‐1 infection, microglia from BALB/c mice produce a vigorous, but not protective response to HSV‐1. In VE deficient (VE‐D) mice, the pro‐inflammatory response was even more robust than in the VE adequate (VE‐A) mice. In this study, we determined that VE‐D mice have increased proliferation and activation of microglia and increased numbers of infiltrating macrophage following HSV‐1 infection compared to VE‐A mice. Administration of U‐83836E, a lazaroid compound that is a potent inhibitor of membrane lipid peroxidation with anti‐oxidant properties similar to VE, alters the response of microglia in both VE‐A and VE‐D mice infected with HSV‐1. These data suggest that oxidative stress during HSV‐1 infection alters microglial responses and that VE deficiency acts synergistically to amplify this response.