How Does Herpes Affect The Nervous System – Herpes simplex virus type 1 (HSV-1) has been proposed as a possible infectious etiology of Alzheimer’s disease (AD) since the 1980s. Accumulating research thus far supports the association and possible causative role of HSV-1 in the development of AD. HSV-1 exhibits the neuropathological and behavioral changes of AD, such as amyloid-beta deposition, tau hyperphosphorylation, as well as memory and learning impairments in experimental settings. However, the neuroanatomical mechanisms of HSV-1 tropism in the brain have not been emphasized in detail. In this review, we propose that hippocampal vulnerability to HSV-1 infection plays a role in the development of AD and amnestic mild cognitive impairment (aMCI). Subsequently, this review is based on human studies linking HSV-1 to hippocampal-related brain disorders, namely AD and aMCI/MCI. Next, experimental models and clinical observations supporting the neurotropism or propensity of HSV-1 to infect the hippocampus are examined. Next, factors and mechanisms that predispose to HSV-1 infection of the hippocampus are discussed. In summary, the hippocampus contains high levels of viral cellular receptors, neural stem or progenitor cells (NSCs/NPCs), glucocorticoid receptors (GRs), and amyloid precursor proteins (APPs) that support HSV-1 infection, as well as against inadequate antiviral immunity. . HSV-1. Currently, established disease HSV-1 causes mucosal lesions and encephalitis; However, this review modifies that HSV-1 may induce and/or contribute to hippocampal-related brain disorders, particularly AD and aMCI/MCI.
Alzheimer’s disease (AD) is the leading neurodegenerative disease, accounting for approximately 60–80% of dementia worldwide (Q et al., 2009; Alzheimer’s Assoc., 2021). AD can progress from a long period of subtle memory loss called amnestic mild cognitive impairment (aMCI; the most common form of MCI) (Peterson et al., 2001). Although the etiology of AD is multifaceted, the hypothesis of an infectious cause in AD has emerged since the 1980s. Ball (1982) and Gannicliffe et al. (1986) first suggested that periodic reactivation of herpes simplex virus type-1 (HSV-1) in neurons could facilitate the development of AD. In subsequent decades, possible involvement of herpes viruses such as HSV-1, HSV-2, cytomegalovirus (CMV), human herpesvirus 6, 7, and 8 (HHV-6, -7, and -8), varicella. -zoster virus (VZV) and Epstein-Barr virus (EBV), investigated in AD and MCI (Polk et al., 2002; Strandberg et al., 2003; Carbone et al., 2014; Barnes et al., 2015). has been Agostini et al., 2016b; Tsai et al., 2017; Tzeng et al., 2018). According to reviews and meta-analyses (Steele and Eslick, 2015; Itzaki et al., 2016; Warren-Gash et al., 2019; Sait et al., 2021).
How Does Herpes Affect The Nervous System
HSV-1 is an enveloped, linear double-stranded DNA virus that infects more than 60% of the population worldwide (Luker et al., 2015; Herfouche et al., 2019; Khadr et al., 2019). Productive infection with HSV-1, either through primary infection or latent reactivation, results in lesions of the lips, cornea, or genital mucosa (Darugar et al., 1985; Scott et al., 1997; Ribes et al., 2001). HSV-1 also causes herpes simplex encephalitis (HSE), the most common form of infection-induced encephalitis ( Granerod et al., 2010 ; George et al., 2014 ). In pregnant mothers with genital herpes, HSV-1 vaginally can cause congenital herpes in the infant after delivery, resulting in mucosal lesions and central nervous system (CNS) infection (Whitley et al., 1991; Whitley et al., 2007).
A Novel Bioluminescent Herpes Simplex Virus 1 For In Vivo Monitoring Of Herpes Simplex Encephalitis
At the neuronal level, HSV-1 infection has been shown to induce tau hyperphosphorylation, amyloid-beta 40 and 42 (Aβ40/42) accumulation, oxidative stress, neuroinflammation, and apoptotic dysregulation, all of which are implicated in such pathophysiology. Neurodegenerative diseases. As in AD At the genetic level, HSV-1 life cycle gene products interact with AD susceptibility genes, such as presenilin 1 and 2 (PSEN1 and PSEN2), apolipoprotein E allele 4 (ApoE4) and the clusterin gene, to upregulate both. Viral infections and risk of AD. These molecular mechanisms of HSV-1-induced neuropathology in AD are reviewed in Harris and Harris (2018) and Duarte et al. (2019). Consequently, at the behavioral level, HSV-1 infection has been shown to cause memory and learning impairments reminiscent of AD (Beers et al., 1995; Armien et al., 2010; De Chiara et al., 2019).
Although the molecular mechanisms contributing to AD from HSV-1 have been extensively reviewed (Duarte et al., 2019; Marcocci et al., 2020), a neuroanatomical approach has not been considered in detail. Elucidation of the route and tropism of HSV-1 infection in the brain will increase understanding of the potential neurological health consequences of HSV-1 infection. This review, thus, examines which part of the brain is most affected by HSV-1. So far the literature suggests that it may be the hippocampus, which has a central role in learning and memory. Neuronal connections between the hippocampus and the entorhinal cortex, amygdala, olfactory bulb, and hypothalamus include the limbic system (Vilensky et al., 1982). In the mammalian hippocampus, lifelong neurogenesis has been observed in the subgranular zone of the dentate gyrus (DG), where neural stem or progenitor cells (NSCs/NPCs) are localized (Altman and Das, 1965; Erickson et al. , 1998). The hippocampus is sensitive to a variety of stressors, including chronic stress, aging, and microbial infections. As a result, hippocampal functions such as learning and memory will be compromised. Therefore, hippocampal dysfunction has been implicated in disorders characterized by memory impairment, such as depression, schizophrenia, dementia, aMCI/MCI, and AD, as reviewed in Small et al. (2011) and Anand and Dhikav (2012).
This review first discusses the potential role of HSV-1 in the development of AD and aMCI/MCI in humans. Next, this review describes the mechanisms of HSV-1 infection in neurons and a theoretical model of HSV-1 infection transmission, focusing on its neurotropism or propensity to target the hippocampus based on cell culture, animal, and human autopsy evidence. We suggest that hippocampal vulnerability to HSV-1 infection may also be an important factor initiating or facilitating the development of aMCI/MCI and AD. Next, factors and mechanisms influencing hippocampal susceptibility to HSV-1 infection are discussed.
HSE, either due to primary infection or viral reactivation, is known to have long-term neurological sequelae despite prompt antiviral treatment (Riancho et al., 2013; Armangue et al., 2018). Damage to the temporal lobe and limbic system (especially the hippocampus), as well as memory and behavior (eg, emotional instability and irritability) has often been observed in HSE survivors (Kapur et al., 1994; Capers-Lefebret al., 1996); Dagsdottir et al., 2014; Harris et al., 2020). Degeneration of similar brain regions and phenotypic abnormalities in HSE are similar to AD. This observation has led to the hypothesis that frequent and periodic HSV-1 reactivation may contribute to the development of AD, particularly in an elderly population with a weakened immune system (Ball, 1982; Esiri, 1982b; Gannicliffe et al., 1986). Therefore, this section will describe the association between HSV-1 and AD and memory impairment, which may also reflect prodromal AD in humans.
Shingles And Your Nerves
HSV-1 DNA has been detected in Aβ deposits in postmortem brain tissue of AD patients compared with non-AD controls ( Mori et al., 2004 ). The same study detected HSV-1 antigen in cortical neurons, providing the first evidence of possible HSV-1 reactivation in the AD brain (Morry et al., 2004). Another study showed that the majority of HSV-1 DNA was localized to Aβ plaques in the cortices of AD patients (Wozniak et al., 2009b). Furthermore, transcriptome analysis of brain samples from a cohort of AD patients revealed higher levels of HSV-1 latency-associated transcripts (LATs; transcripts from HSV-1 DNA) compared to older adults without AD (Readhead et al., 2018). These results suggest that HSV-1 can infect the brain and is associated with AD neuropathology.
Compared with age-matched healthy controls, individuals with AD and aMCI exhibit increased levels of HSV-1 IgG antibodies (Costa et al., 2017; Agostini et al., 2019; Pandey et al., 2019). associated with increased cortical volume (Mancuso et al., 2014a, b). Similarly, elevated antibody levels and increased avidity index against HSV-1 were observed in aMCI patients who did not develop AD compared to those who did not develop AD. In the same study, HSV-1-specific antibody titers were positively correlated with hippocampal and amygdala volumes (Agostini et al., 2016a). Other studies have also shown that aMCI patients exhibited higher HSV-1 IgG antibody levels and avidity index than healthy controls and AD patients (Kobayashi et al., 2013; Costa et al., 2020). Collectively, these results suggest that strong antibody responses against HSV-1 may prevent the progression of AD to AMCI, possibly through antibody neutralization of HSV-1 that protects the brain from HSV-1-induced neuropathology (Mancuso et al ., 2014a; Agostini) et al., 2016a; Costa et al., 2020).
When anti-HSV-1 immunity is insufficient to control HSV-1 infection, periodic HSV-1 reactivation and productive infections can occur. A nationwide retrospective cohort study in Taiwan found that individuals with recurrent HSV-1 infection had a 2.8-fold increased risk of developing AD compared with those without. More importantly, antiherpetic drugs reduced such risk by about 90% compared to placebo (Zheng et al., 2018). Another nationwide retrospective cohort study in Sweden involved HSV-1 or VZV infection and matched uninfected controls, with antiherpetic treatment added.
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