Dementia and cognitive impairment in adults as sequels of HSV-1-related encephalitis: a review

Abstract

ABSTRACT. Considering the variety of mechanisms of Herpes simplex virus (HSV-1) contamination and its broad invasive potential of the nervous system, a life-long latent infection is established. Infected adult individuals may be susceptible to viral reactivation when under the influence of multiple stressors, especially regarding immunocompromised patients. This guides a series of neuroinflammatory events on the cerebral cortex, culminating, rarely, in encephalitis and cytotoxic / vasogenic brain edema. A sum of studies of such processes provides an explanation, even though not yet completely clarified, on how the clinical evolution to cognitive impairment and dementia might be enabled. In addition, it is of extreme importance to recognize the current dementia and cognitive deficit worldwide panorama. The aim of this literature review is to elucidate the available data upon the pathophysiology of HSV-1 infection as well as to describe the clinical panorama of the referred afflictions.

Disrupting Neurons and Glial Cells Oneness in the Brain—The Possible Causal Role of Herpes Simplex Virus Type 1 (HSV-1) in Alzheimer’s Disease

“…Interestingly, the virus exploits molecular strategies to evade host cell death through suppression of both host cell death pathways for the benefit of viral replication [ 228 ]; yet, the entry and spread of HSV-1 in the CNS leads to severe and long-term brain damage. Neuroanatomical HSV-1 tropism not only comprises TG or DRG, but also cingulate gyrus, orbitofrontal, insular, and mesial temporal lobe regions of the cerebral cortex [ 3 ], including, in particular, the hippocampus, which exhibits a high level of HSV-1 receptors [ 266 ]. AD is considered hippocampal-related brain disorder, and cerebral cortex regions that are damaged during HSE correspond to areas in which changes are observed in AD patients’ brains [ 3 ].…”

“…Neuroanatomical HSV-1 tropism not only comprises TG or DRG, but also cingulate gyrus, orbitofrontal, insular, and mesial temporal lobe regions of the cerebral cortex [ 3 ], including, in particular, the hippocampus, which exhibits a high level of HSV-1 receptors [ 266 ]. AD is considered hippocampal-related brain disorder, and cerebral cortex regions that are damaged during HSE correspond to areas in which changes are observed in AD patients’ brains [ 3 ].…”

“…As mentioned by Itzhaki, R. [ 1 ], Alzheimer’s disease (AD) is considered as a multifactorial ailment, partly exerted by genetic or environmental factors; however, the neuropathological processes that lead to the disease are still not fully understood. In recent years, many studies advocate the relationship between HSV-1 infection and various neuropsychiatric and neurodegenerative diseases [ 2 , 3 ].…”

B cells going viral in theCNS: Dynamics, complexities, and functions of B cells responding to viral encephalitis

“…Reactivation generally leads to lesions at peripheral mucosal sites innervated by affected neurons. However, HSV encephalitis, while rare, causes serious neurological disease 8,9 . Notable RNA viruses include members of the insect borne Togaviridae , Bunyaviridae , and Flaviviridae families, as well as the zoonotic Rhabdoviridae family 5 .…”

“…However, HSV encephalitis, while rare, causes serious neurological disease. 8 , 9 Notable RNA viruses include members of the insect borne Togaviridae , Bunyaviridae , and Flaviviridae families, as well as the zoonotic Rhabdoviridae family. 5 30%‐50% of encephalitis survivor afflicted by the Japanese encephalitis virus (JEV) (Flavivirus) will suffer long‐term neurological impairment.…”