Herpesviruses in brains in Alzheimer's and Parkinson's diseases

Hemling, Niina; Röyttä, Matias; Rinne, Juha O.; Pöllänen, Paju; Broberg, Eeva; Tapio, Virpi; Vahlberg, Tero; Hukkanen, Veijo

doi:10.1002/ana.10662

Cited by 110 publications

(95 citation statements)

References 19 publications

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“…HSV-induced encephalitis has been the most common cause of sporadic, fatal encephalitis, and two-thirds of cases are likely due to viral reactivation from latency (13,27). In addition, HSV has been suspected to be involved in a number of neurological disorders, such as epilepsy, multiple sclerosis, Alzheimer's disease, Parkinson's disease, and autism (1,2,9,11,12,21).…”

mentioning

confidence: 99%

“…Subsequent studies led to the assumption that latent HSV genomes in the CNS were defective for reactivation (20,22,25). This long-standing concept and the lack of an assay impaired studies on HSV reactivation from the CNS for more than two decades, even though HSV was suspected of being involved in neurological diseases, such as epilepsy, multiple sclerosis, Alzheimer's disease, and Parkinson's disease (1,9,11,12,21). Our current findings of efficient reactivation of latent HSV from mouse CNS strongly argue against this concept and are consistent with investigations showing no obvious qualitative differences in the latent infections of ganglia and the CNS (3,6,7,20,22,24).…”

mentioning

confidence: 99%

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Efficient Reactivation of Latent Herpes Simplex Virus from Mouse Central Nervous System Tissues

Chen

Yao

Huang

et al. 2006

J Virol

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For decades, numerous ex vivo studies have documented that latent herpes simplex virus (HSV) reactivates efficiently from ganglia, but rarely from the central nervous systems (CNS), of mice when assayed by mincing tissues before explant culture, despite the presence of viral genomes in both sites. Here we show that 88% of mouse brain stems reactivated latent virus when they were dissociated into cell suspensions before ex vivo explant culture. The efficient reactivation of HSV from the mouse CNS was demonstrated with more than one viral strain, viral serotype, and mouse strain, further indicating that the CNS can be an authentic latency site for HSV with the potential to cause recurrent disease.

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mentioning

confidence: 99%

mentioning

confidence: 99%

Efficient Reactivation of Latent Herpes Simplex Virus from Mouse Central Nervous System Tissues

Chen

Yao

Huang

et al. 2006

J Virol

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“…[92][93][94] While patients rarely exhibit signs of encephalitis, many postmortem studies find a high prevalence of HSV-1 in the brain. [95][96][97][98] Strikingly, Alzheimer disease brains contain a high localization of HSV-1 DNA within amyloid plaques, 72% in AD patients, whereas only 24% of the DNA associates with plaques in agematched non-AD patients, who accumulate plaques at a much lower rate. 7 Furthermore, animal models and acute HSV-1 encephaltitis patients show that the virus targets brain regions overlapping with AD: frontal and temporal cortices and the hippocampus.…”

Section: Hsv-1-associated Autophagy Dysfunction: a Risk Factor For Nementioning

confidence: 99%

Autophagy interaction with herpes simplex virus type-1 infection

O’Connell

Liang

2016

Autophagy

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More than 50% of the U.S. population is infected with herpes simplex virus type-I (HSV-1) and global infectious estimates are nearly 90%. HSV-1 is normally seen as a harmless virus but debilitating diseases can arise, including encephalitis and ocular diseases. HSV-1 is unique in that it can undermine host defenses and establish lifelong infection in neurons. Viral reactivation from latency may allow HSV-1 to lay siege to the brain (Herpes encephalitis). Recent advances maintain that HSV-1 proteins act to suppress and/or control the lysosome-dependent degradation pathway of macroautophagy (hereafter autophagy) and consequently, in neurons, may be coupled with the advancement of HSV-1-associated pathogenesis. Furthermore, increasing evidence suggests that HSV-1 infection may constitute a gradual risk factor for neurodegenerative disorders. The relationship between HSV-1 infection and autophagy manipulation combined with neuropathogenesis may be intimately intertwined demanding further investigation.

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“…In each selected clinical study (Table 2), a correlation can be made between an adverse or high-risk association, a low-risk or protective effect, or no association relative to the ApoE genotype. For example, hepatitis B (Percy et al, 2003), multiple sclerosis (Minagar et al, 2004), Huntington's disease (Saft et al, 2004), and Parkinson's disease (Hemling et al, 2003) are conditions in which, to date, no association or risk factor involvement has been proven to exist between any ApoE genotype and disease severity or protection. While it is assumed that these diseases are not related to the presence or absence of specific ApoE alleles, in any clinical condition, subsets of clinical patients and more stringent definitions might identify an association.…”

Section: Chemistry and Genetics Of Human Apoementioning

confidence: 99%

Apolipoprotein E alleles can contribute to the pathogenesis of numerous clinical conditions including HSV-1 corneal disease

Hill

Bhattacharjee

Neumann

2007

Experimental Eye Research

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Apolipoprotein E (ApoE) alleles have been reported to affect the clinical outcome of numerous cardiovascular, neurodegenerative, and viral infectious diseases, including atherosclerosis, Alzheimer's disease (AD), hepatitis C, and HIV. The major alleles of ApoE are ε 2, ε 3, and ε 4. ApoE genotypes have been hypothesized to regulate many biological functions, resulting in significant changes in the onset and/or outcome (severity and duration) of several clinical conditions. Based on genetic analyses in human and animal studies using knockout (ApoE −/−) mice and mice transgenic for human ε 3 and ε 4, we present evidence that strongly suggests that the ApoE alleles can regulate the pathogenesis of ocular herpes simplex virus type 1 (HSV-1) infections. This review will summarize the major studies that support this hypothesis. Significant gender based differences in HSV-1 pathogenesis have also been reported, suggesting that hormonal regulation combined with ApoE genotype plays a significant role in HSV-1 pathogenesis. Identification of specific mechanisms in ocular HSV-1 infections related to the ApoE alleles and gender could lead to therapeutic intervention based on the properties of the apoE isoforms. While many clinical investigations have been reported and, to a lesser extent, transgenic mouse studies have been conducted, no specific mechanisms of how ApoE induces or alters clinical disease are known.

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Herpesviruses in brains in Alzheimer's and Parkinson's diseases

Cited by 110 publications

References 19 publications

Efficient Reactivation of Latent Herpes Simplex Virus from Mouse Central Nervous System Tissues

Efficient Reactivation of Latent Herpes Simplex Virus from Mouse Central Nervous System Tissues

Autophagy interaction with herpes simplex virus type-1 infection

Apolipoprotein E alleles can contribute to the pathogenesis of numerous clinical conditions including HSV-1 corneal disease

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