{"title":"Herpesvirus initiation of dementias and autoimmune diseases.","authors":"Kevin Roe","doi":"10.1007/s13365-025-01265-8","DOIUrl":null,"url":null,"abstract":"<p><p>Several viral, bacterial, fungal, and protozoan parasite pathogens are capable of causing either active and/or latent chronic infections, particularly if they are highly immuno-evasive. The nine human herpesviruses are among the most evasive pathogens. They can remain latent for decades, but can periodically reactivate into active chronic infections after various triggers: medical treatments causing intentional or unintentional immune system suppression, other pathogen infections, malnutrition, stress, or unusual host cell signaling. Various neurological disorders including dementias and severe autoimmune diseases have been linked to highly prevalent human herpesvirus infections including herpes simplex type 1 and 2, varicella-zoster virus, Epstein-Barr virus, human cytomegalovirus, and herpesviruses 6A, 6B, 7 and 8. For example, dementias including Alzheimer's disease have been extensively linked to herpes simplex type 1 and 2, and herpesvirus 6A and 7, but other herpesviruses may be indirectly involved in dementias. For instance, recent evidence strongly suggests dementias can result from reactivated varicella-zoster herpes virus infections, whereas effective vaccinations against varicella-zoster herpes virus reactivations to avoid shingles have also shown significant reductions in dementia probabilities for vaccinated individuals. This raises questions about how various herpesviruses can initiate or enable neurological diseases including dementias and autoimmune diseases, and how their infections and particularly their reactivations from latency can initiate these diseases.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":" ","pages":"305-332"},"PeriodicalIF":1.9000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of NeuroVirology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s13365-025-01265-8","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/7/7 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Several viral, bacterial, fungal, and protozoan parasite pathogens are capable of causing either active and/or latent chronic infections, particularly if they are highly immuno-evasive. The nine human herpesviruses are among the most evasive pathogens. They can remain latent for decades, but can periodically reactivate into active chronic infections after various triggers: medical treatments causing intentional or unintentional immune system suppression, other pathogen infections, malnutrition, stress, or unusual host cell signaling. Various neurological disorders including dementias and severe autoimmune diseases have been linked to highly prevalent human herpesvirus infections including herpes simplex type 1 and 2, varicella-zoster virus, Epstein-Barr virus, human cytomegalovirus, and herpesviruses 6A, 6B, 7 and 8. For example, dementias including Alzheimer's disease have been extensively linked to herpes simplex type 1 and 2, and herpesvirus 6A and 7, but other herpesviruses may be indirectly involved in dementias. For instance, recent evidence strongly suggests dementias can result from reactivated varicella-zoster herpes virus infections, whereas effective vaccinations against varicella-zoster herpes virus reactivations to avoid shingles have also shown significant reductions in dementia probabilities for vaccinated individuals. This raises questions about how various herpesviruses can initiate or enable neurological diseases including dementias and autoimmune diseases, and how their infections and particularly their reactivations from latency can initiate these diseases.
期刊介绍:
The Journal of NeuroVirology (JNV) provides a unique platform for the publication of high-quality basic science and clinical studies on the molecular biology and pathogenesis of viral infections of the nervous system, and for reporting on the development of novel therapeutic strategies using neurotropic viral vectors. The Journal also emphasizes publication of non-viral infections that affect the central nervous system. The Journal publishes original research articles, reviews, case reports, coverage of various scientific meetings, along with supplements and special issues on selected subjects.
The Journal is currently accepting submissions of original work from the following basic and clinical research areas: Aging & Neurodegeneration, Apoptosis, CNS Signal Transduction, Emerging CNS Infections, Molecular Virology, Neural-Immune Interaction, Novel Diagnostics, Novel Therapeutics, Stem Cell Biology, Transmissable Encephalopathies/Prion, Vaccine Development, Viral Genomics, Viral Neurooncology, Viral Neurochemistry, Viral Neuroimmunology, Viral Neuropharmacology.