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Bioinforma.ics Review of the Role of HSV-1 in a.zheimer’s Disea.e

a.va.ces in a.zheimer's Disea.e 2020年第3期9卷 57-75页

作者： Bria. T. Reiss Mea.e C. Eggleston a.a. C. Godbole julia a. marut Cecelia.M. McCa.n Jessica.a. Cottrell Tinchun Chu Sulie L. Cha.g Depa.tment of Biologica. Sciences Seton Hall University South Orange NJ USA Institute of Neuroimmune Pha.ma.ology Seton Hall University South Orange NJ USA

a.zheimer’s disea.e (a.) is a.neurodegenera.ive disea.e cha.a.terized by the progressive loss of cognitive functions in a.fected individua.s. Bra.n tissue pa.hology is a.socia.ed with the forma.ion of senile pla.ues which result from the over-production of a.yloid a.>β (Aβ), due to the cleavage of a membrane bound glycoprotein. It is unclear what causes AD and its associated pathologies, but age and genetic predisposition play an import role in the likelihood of disease development. Studies have shown that the reactivation of latent herpes simplex virus 1 (HSV-1) infection can lead to the neuropathy of acute herpes simplex encephalitis (HSE), which causes similar symptoms to AD. HSV-1 infection is a known risk factor for the development of AD, but no study has determined a definitive causal relationship. Using the Qiagen Ingenuity Pathway Analysis (IPA) tool, the inhibitory relationship between therapeutics for AD and HSV-1 were explored. Thirteen drugs developed to decrease Aβ buildup in AD and 32 drugs that act as HSV antivirals were retrieved from the data in the Qiagen Knowledge Base. These drugs were analyzed displayed as two separate networks. While many promising Aβ aggregation-targeting drugs have been discontinued due to lack of efficacy, HSV drugs could serve as potential therapeutics for those with AD. This review aims to describe new insights on how HSV-1 relates to the development of AD and highlight the mechanism of action of Aβa. style="font-fa.ily:Verda.a.

关键词： a.zheimer’s Disea.e a.yloid β Herpes Simplex Virus-1

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