中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (2): 211-221.doi: 10.4103/1673-5374.226380

• 综述:退行性病与再生 • 上一篇    下一篇

嗜神经性人疱疹病毒单纯疱疹病毒1型和人疱疹病毒6型对神经退行性疾病病理的贡献

  

  • 收稿日期:2018-01-16 出版日期:2018-02-15 发布日期:2018-02-15

Contributions of neurotropic human herpesviruses herpes simplex virus 1 and human herpesvirus 6 to neurodegenerative disease pathology

Jessica M. Hogestyn1, David J. Mock2, Margot Mayer-Proschel1, 2   

  1. 1 Department of Neuroscience, University of Rochester, Rochester, NY, USA
    2 Department of Biomedical Genetics, University of Rochester, Rochester, NY, USA
  • Received:2018-01-16 Online:2018-02-15 Published:2018-02-15
  • Contact: Margot Mayer-Proschel, Ph.D.,Margot_mayer-proschel@urmc.rochester.edu.

摘要:

orcid:0000-0001-6490-2933(Margot Mayer-Proschel)

Abstract:

Human herpesviruses (HVs) have developed ingenious mechanisms that enable them to traverse the defenses of the central nervous system (CNS). The ability of HVs to enter a state of latency, a defining characteristic of this viral family, allows them to persist in the human host indefinitely. As such, HVs represent the most frequently detected pathogens in the brain. Under constant immune pressure, these infections are largely asymptomatic in healthy hosts. However, many neurotropic HVs have been directly connected with CNS pathology in the context of other stressors and genetic risk factors. In this review, we discuss the potential mechanisms by which neurotropic HVs contribute to neurodegenerative disease (NDD) pathology by highlighting two prominent members of the HV family, herpes simplex virus 1 (HSV-1) and human herpesvirus 6 (HHV-6). We (i) introduce the infectious pathways and replicative cycles of HSV-1 and HHV-6 and then (ii) review the clinical evidence supporting associations between these viruses and the NDDs Alzheimer’s disease (AD) and multiple sclerosis (MS), respectively. We then (iii) highlight and discuss potential mechanisms by which these viruses exert negative effects on neurons and glia. Finally, we (iv) discuss how these viruses could interact with other disease-modifying factors to contribute to the initiation and/or progression of NDDs.

Key words:  herpes simplex virus 1, human herpesvirus 6, central nervous system, neurodegeneration, demyelination, Alzheimer’s disease, multiple sclerosis, viral latency, viral reactivation