{"title":"免疫反应对寨卡病毒感染个体差异的贡献。","authors":"Erica L Mc Grath, Ping Wu","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Zika virus has emerged as a public health crisis and is associated with a number of neurological deficits; however, only subsets of individuals who contract a Zika virus infection develop severe symptoms. The mechanism underlying Zika virus-induced neuropathogenesis is still poorly understood. Recent studies have implicated the host immune response as a key regulator in Zika virus neuropathology. Specifically, immune responses generated from previous flavi virus infection may contribute to antibody-dependent enhancement of Zika virus infection. Innate immunity may also play an important role for the broad array of individual symptomatic differences. Therefore, host immunity may serve as a therapeutic target to reduce Zika-associated neuropathogenesis.</p>","PeriodicalId":72230,"journal":{"name":"Annals of public health and research","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9714954/pdf/nihms-1808883.pdf","citationCount":"0","resultStr":"{\"title\":\"Contributions of Immune Response to Individual Differences in Zika Virus Infection.\",\"authors\":\"Erica L Mc Grath, Ping Wu\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Zika virus has emerged as a public health crisis and is associated with a number of neurological deficits; however, only subsets of individuals who contract a Zika virus infection develop severe symptoms. The mechanism underlying Zika virus-induced neuropathogenesis is still poorly understood. Recent studies have implicated the host immune response as a key regulator in Zika virus neuropathology. Specifically, immune responses generated from previous flavi virus infection may contribute to antibody-dependent enhancement of Zika virus infection. Innate immunity may also play an important role for the broad array of individual symptomatic differences. Therefore, host immunity may serve as a therapeutic target to reduce Zika-associated neuropathogenesis.</p>\",\"PeriodicalId\":72230,\"journal\":{\"name\":\"Annals of public health and research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9714954/pdf/nihms-1808883.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annals of public health and research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2017/4/5 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of public health and research","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2017/4/5 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Contributions of Immune Response to Individual Differences in Zika Virus Infection.
Zika virus has emerged as a public health crisis and is associated with a number of neurological deficits; however, only subsets of individuals who contract a Zika virus infection develop severe symptoms. The mechanism underlying Zika virus-induced neuropathogenesis is still poorly understood. Recent studies have implicated the host immune response as a key regulator in Zika virus neuropathology. Specifically, immune responses generated from previous flavi virus infection may contribute to antibody-dependent enhancement of Zika virus infection. Innate immunity may also play an important role for the broad array of individual symptomatic differences. Therefore, host immunity may serve as a therapeutic target to reduce Zika-associated neuropathogenesis.