Modification of Cellular Response by HSV

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 4916

Special Issue Editor


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Guest Editor
Department of Nanobiology and Biomaterials, Military Institute of Hygiene and Epidemiology, 01-163 Warsaw, Poland
Interests: herpes simplex type 1 and 2; viral encephalitis; apoptosis; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Cells have an innate capacity to activate effective antiviral countermeasures that can limit viral replication and viral dissemination. Among these antiviral responses, cell death and autophagy are common host defense mechanisms against viral infection that eliminates virus-infected cells before the production of progeny virions. Herpesviruses have a long history of co-evolution with the host species, and they can successfully survive in the host for life, as in the case of alphaherpesviruses. Therefore,  herpesviruses have evolved various strategies to suppress apoptosis and autophagy by encoding anti-apoptotic factors or regulating apoptotic  and autophagic signaling pathways, which promote viral propagation and evasion of the host defense. However, evading cell-death-based defenses may also lead to virus-related pathogenesis and excessive destruction of tissues.

For this Special Issue, we invite the submission of original research papers and review articles spanning the entire spectrum of cellular antiherpes viral mechanisms in different animal species from both the virus and host perspectives. Also welcome are articles that present strategies for future antiviral development considering the complexity of host–virus interactions and usefulness of existing treatments targeting apoptosis and autophagy.

Dr. Malgorzata Krzyzowska
Guest Editor

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Keywords

  • herpesviruses
  • apoptosis
  • autophagy
  • latency
  • pathogenesis

Published Papers (2 papers)

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Research

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21 pages, 8944 KiB  
Article
Equid Alphaherpesvirus 1 (EHV-1) Influences Morphology and Function of Neuronal Mitochondria In Vitro
by Marcin Chodkowski, Anna Słońska, Karolina Gregorczyk-Zboroch, Zuzanna Nowak-Zyczynska, Anna Golke, Małgorzata Krzyżowska, Marcin W. Bańbura and Joanna Cymerys
Pathogens 2022, 11(8), 876; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11080876 - 03 Aug 2022
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Abstract
Mitochondria are key cellular organelles responsible for many essential functions, including ATP production, ion homeostasis and apoptosis induction. Recent studies indicate their significant role during viral infection. In the present study, we examined the effects of equine herpesvirus type 1 (EHV-1) infection on [...] Read more.
Mitochondria are key cellular organelles responsible for many essential functions, including ATP production, ion homeostasis and apoptosis induction. Recent studies indicate their significant role during viral infection. In the present study, we examined the effects of equine herpesvirus type 1 (EHV-1) infection on the morphology and mitochondrial function in primary murine neurons in vitro. We used three EHV-1 strains: two non-neuropathogenic (Jan-E and Rac-H) and one neuropathogenic (EHV-1 26). The organization of the mitochondrial network during EHV-1 infection was assessed by immunofluorescence. To access mitochondrial function, we analyzed reactive oxygen species (ROS) production, mitophagy, mitochondrial inner-membrane potential, mitochondrial mass, and mitochondrial genes’ expression. Changes in mitochondria morphology during infection suggested importance of their perinuclear localization for EHV-1 replication. Despite these changes, mitochondrial functions were preserved. For all tested EHV-1 strains, the similarities in the increased fold expression were detected only for COX18, Sod2, and Tspo. For non-neuropathogenic strains (Jan-E and Rac-H), we detected mainly changes in the expression of genes related to mitochondrial morphology and transport. The results indicate that mitochondria play an important role during EHV-1 replication in cultured neurons and undergo specific morphological and functional modifications. Full article
(This article belongs to the Special Issue Modification of Cellular Response by HSV)
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Review

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14 pages, 1571 KiB  
Review
Role of Microglia in Herpesvirus-Related Neuroinflammation and Neurodegeneration
by Magdalena Patrycy, Marcin Chodkowski and Malgorzata Krzyzowska
Pathogens 2022, 11(7), 809; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11070809 - 19 Jul 2022
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Abstract
Neuroinflammation is defined as an inflammatory state within the central nervous system (CNS). Microglia conprise the resident tissue macrophages of the neuronal tissue. Upon viral infection of the CNS, microglia become activated and start to produce inflammatory mediators important for clearance of the [...] Read more.
Neuroinflammation is defined as an inflammatory state within the central nervous system (CNS). Microglia conprise the resident tissue macrophages of the neuronal tissue. Upon viral infection of the CNS, microglia become activated and start to produce inflammatory mediators important for clearance of the virus, but an excessive neuroinflammation can harm nearby neuronal cells. Herpesviruses express several molecular mechanisms, which can modulate apoptosis of infected neurons, astrocytes and microglia but also divert immune response initiated by the infected cells. In this review we also describe the link between virus-related neuroinflammation, and development of neurodegenerative diseases. Full article
(This article belongs to the Special Issue Modification of Cellular Response by HSV)
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