Journal
CRITICAL REVIEWS IN MICROBIOLOGY
Volume 45, Issue 5-6, Pages 581-594Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/1040841X.2019.1660615
Keywords
HSV-1; Microglia; CNS diseases; inflammation; innate immunity
Categories
Funding
- National Natural Science Foundation of China [81603341, 81573471]
- Science and Technology Program of Guangzhou, China [201604020178]
- Key Projects of Biological Industry Science & Technology of Guangzhou China [201504291048224]
- Foundation of key Laboratory of the Ministry of Education [2016RF01]
- Science & Technology Plan Program of Guangdong Province China [2015A050502028]
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Microglia, as brain-resident macrophages, are the first line of defense against brain invading pathogens. Further, their dysfunction has been recognized to be closely associated with mounting CNS diseases. Of note, chronic HSV-1 infection leads to the persistent activation of microglia, which elicit a comprehensive response by generating certain factors with neurotoxic and neuroprotective effects. CNS infection with HSV-1 results in herpes simplex encephalitis and herpes simplex keratitis. Microglial immune response plays a crucial role in the development of these diseases. Moreover, HSV-1 infection is strongly associated with several CNS diseases, especially Alzheimer's disease and schizophrenia. These CNS diseases can be effectively ameliorated by eliciting an appropriate immune response, such as inhibition of microglial proliferation and activation. Therefore, it is crucial to reassess the positive and negative roles of microglia in HSV-1 CNS infection for a more comprehensive and detailed understanding of the relationship between microglia and CNS diseases. Hence, the present review focuses on the dual roles of microglia in mediating HSV-1 CNS infection, as well as on the strategy of targeting microglia to ameliorate CNS diseases. Further research in this field can help comprehensively elucidate the dual role of the microglial immune response in HSV-1 CNS infection, providing a theoretical basis for identifying therapeutic targets against overactive microglia in CNS diseases and HSV-1 infection.
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