The immune response to herpes simplex virus |
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| Affiliation: | 1. Department of Neurosurgery, Juntendo University Nerima Hospital, Tokyo, Japan;2. Medical Technology Innovation Center, Juntendo University, Tokyo, Japan;3. Departments of Clinical Virology, Tamil Nadu, India;1. Departments of Biostatistics, Tamil Nadu, India;2. Departments of Hepatology, Christian Medical College, Vellore, Tamil Nadu, India;1. Leibniz Institute on Aging – Fritz-Lipmann Institute (FLI), Beutenbergstr. 11, 07745 Jena, Germany;2. Faculty of Biology and Pharmacy, Friedrich Schiller University Jena, Fürstengraben 1, 07743 Jena, Germany;1. Department of Microbiology, University of Washington, 960 Republican Street, Seattle, WA 98109, USA;3. From the Departments of Neurobiology, Neurology, and Pathology, The University of Chicago, Chicago, Illinois 60637 and;4. the Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, United Kingdom |
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| Abstract: | Several host immune mechanisms are activated in the course of a herpes simplex virus infection. These include natural resistance mechanisms (natural killer cells and interferon), antiviral antibodies and effector CD4 and CD8 T lymphocytes. An important mechanism in the control of viral replication in epidermal cells involves the recruitment and activation of macrophages by CD4 T cells. In some instances, the action of CD4 T cells can lead to immune pathology following infection of the eye (stromal ketatitis) or central nervous system (demyelination). Despite the efficiency of the immune response in countering infection, the virus has evolved strategies to subvert the action of antibodies and complement and the detection of infected cells by cytotoxic T lymphocytes. |
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