Herpes Simplex Virus 1 Induces Brain Inflammation and Multifocal Demyelination in the Cotton Rat Sigmodon hispidus

Boukhvalova, Marina S.; Mortensen, Emma; Mbaye, Aissatou; Lopez, Diego; Kastrukoff, Lorne F.; Blanco, Jorge C. G.

doi:10.1128/jvi.01161-19

Cited by 24 publications

(27 citation statements)

References 66 publications

(82 reference statements)

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“… 74 , 75 The main type of immunity that is activated is the innate immune response (the most rapid defense system for the host cell) to combat HSV-1 infection, 76 as demonstrated in hispid cotton rat ( Sigmodon hispidus) displaying brain inflammation and multifocal demyelination caused by HSV-1. 77 …”

Section: Hsv-1 and Enhanced Inflammation In Admentioning

confidence: 99%

Viral Involvement in Alzheimer’s Disease

Sait

Angeli

Doig

et al. 2021

ACS Chem. Neurosci.

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Alzheimer’s disease (AD) is characterized by the presence of β-amyloid plaques (Aβ) and neurofibrillary tangles (NFTs) in the brain. The prevalence of the disease is increasing and is expected to reach 141 million cases by 2050. Despite the risk factors associated with the disease, there is no known causative agent for AD. Clinical trials with many drugs have failed over the years, and no therapeutic has been approved for AD. There is increasing evidence that pathogens are found in the brains of AD patients and controls, such as human herpes simplex virus-1 (HSV-1). Given the lack of a human model, the route for pathogen entry into the brain remains open for scrutiny and may include entry via a disturbed blood–brain barrier or the olfactory nasal route. Many factors can contribute to the pathogenicity of HSV-1, such as the ability of HSV-1 to remain latent, tau protein phosphorylation, increased accumulation of Aβ in vivo and in vitro , and repeated cycle of reactivation if immunocompromised. Intriguingly, valacyclovir, a widely used drug for the treatment of HSV-1 and HSV-2 infection, has shown patient improvement in cognition compared to controls in AD clinical studies. We discuss the potential role of HSV-1 in AD pathogenesis and argue for further studies to investigate this relationship.

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Section: Hsv-1 and Enhanced Inflammation In Admentioning

confidence: 99%

Viral Involvement in Alzheimer’s Disease

Sait

Angeli

Doig

et al. 2021

ACS Chem. Neurosci.

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“…Regarding herpesviruses, the majority of which are ubiquitous viruses, they are known to infect and persist in several cell types, and the chronic infection that they cause may induce long lasting or chronic inflammation in several tissues. This facilitates the onset of a variety of inflammation-based diseases ranging from gastritis, inflammatory bowel diseases, autoimmune diseases, neurodegenerative diseases, and cancer [ 33 , 37 , 38 , 39 ]. Other completely different viruses such as hepatitis viruses may also cause diseases, to whose pathogenesis the inflammatory response strongly contributes.…”

Section: Targeting Upr or Prr Signaling To Mitigate Excessive Inflammmentioning

confidence: 99%

ER Stress, UPR Activation and the Inflammatory Response to Viral Infection

Cirone

2021

Viruses

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The response to invading pathogens such as viruses is orchestrated by pattern recognition receptor (PRR) and unfolded protein response (UPR) signaling, which intersects and converges in the activation of proinflammatory pathways and the release of cytokines and chemokines that harness the immune system in the attempt to clear microbial infection. Despite this protective intent, the inflammatory response, particularly during viral infection, may be too intense or last for too long, whereby it becomes the cause of organ or systemic diseases itself. This suggests that a better understanding of the mechanisms that regulate this complex process is needed in order to achieve better control of the side effects that inflammation may cause while potentiating its protective role. The use of specific inhibitors of the UPR sensors or PRRs or the downstream pathways activated by their signaling could offer the opportunity to reach this goal and improve the outcome of inflammation-based diseases associated with viral infections.

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“…Demyelinating lesions have also been associated with HSV-1-induced facial nerve paralysis [ 113 ]. A recent study demonstrated a direct association between infection with HSV-1 and multifocal brain demyelination in a murine model [ 114 ]. Moreover, in that study, demyelination was followed by remyelination, although it was incomplete and the presence of scars was observed.…”

Section: Hsv-1 and Demyelinationmentioning

confidence: 99%

The Role of Herpes Simplex Virus Type 1 Infection in Demyelination of the Central Nervous System

Bello-Morales

Andreu

Löpez‐Guerrero

2020

IJMS

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Herpes simplex type 1 (HSV-1) is a neurotropic virus that infects the peripheral and central nervous systems. After primary infection in epithelial cells, HSV-1 spreads retrogradely to the peripheral nervous system (PNS), where it establishes a latent infection in the trigeminal ganglia (TG). The virus can reactivate from the latent state, traveling anterogradely along the axon and replicating in the local surrounding tissue. Occasionally, HSV-1 may spread trans-synaptically from the TG to the brainstem, from where it may disseminate to higher areas of the central nervous system (CNS). It is not completely understood how HSV-1 reaches the CNS, although the most accepted idea is retrograde transport through the trigeminal or olfactory tracts. Once in the CNS, HSV-1 may induce demyelination, either as a direct trigger or as a risk factor, modulating processes such as remyelination, regulation of endogenous retroviruses, or molecular mimicry. In this review, we describe the current knowledge about the involvement of HSV-1 in demyelination, describing the pathways used by this herpesvirus to spread throughout the CNS and discussing the data that suggest its implication in demyelinating processes.

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Herpes Simplex Virus 1 Induces Brain Inflammation and Multifocal Demyelination in the Cotton Rat Sigmodon hispidus

Cited by 24 publications

References 66 publications

Viral Involvement in Alzheimer’s Disease

Viral Involvement in Alzheimer’s Disease

ER Stress, UPR Activation and the Inflammatory Response to Viral Infection

The Role of Herpes Simplex Virus Type 1 Infection in Demyelination of the Central Nervous System

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