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Genetic Insights into Host-Viral Response and Pathogenesis 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: 20 September 2024 | Viewed by 795

Special Issue Editor

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Guest Editor
Department of Chemical, Pharmaceutical and Agricultural Sciences (DOCPAS), University of Ferrara, Via Fossato di Mortara 64/A, 44121 Ferrara, Italy
Interests: herpes simplex; in vitro molecular studies; virus-host interaction pathways
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Special Issue Information

Dear Colleagues,

Numerous evidence shows that genetics play a leading role in influencing the course of many infectious diseases, and determine the probability of developing a disease. The clearance of the microbial agent, which is capable of influencing organ susceptibility and/or the effectiveness of the immune response, is strictly dependent on genetic factors. For this reason, it is important to understand how, at the molecular level, viruses can dynamically influence chromatin remodeling to allow for the regulation of gene expression and other processes that require access to cellular DNA, and how these host–pathogen interactions can influence the genetic diversity of both organisms. Infections are perhaps one of the main selective pressures acting on humans. Knowledge of the virus–host molecular interactions and the identification of the key factors that modify the cellular genome, gene expression and epigenetic modifications are essential for understanding the fate of infections, viral diseases and their pathogenesis. However, not much is known about these interactions; as such, further exploration is required as it could provide new perspectives for prevention of infections, drug-treatments and vaccine development.

This Special Issue, ‘Genetic Insights into Host-Viral Response and Pathogenesis 2.0’ aims to collate original articles, reviews, as well as short communications, that focus on host–virus interaction, and the molecular and genetic mechanisms of host–virus response and pathogenesis.

Prof. Dr. Peggy Marconi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • viruses
  • host–virus interaction
  • genetics
  • molecular aspects
  • epigenetics
  • immunity
  • prevention
  • drug-treatments
  • vaccine development

Published Papers (1 paper)

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21 pages, 3783 KiB  
Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1)
by Anna Caproni, Chiara Nordi, Riccardo Fontana, Martina Facchini, Sara Melija, Mariangela Pappadà, Mattia Buratto and Peggy Marconi
Int. J. Mol. Sci. 2024, 25(9), 4608; https://doi.org/10.3390/ijms25094608 - 23 Apr 2024
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Although Herpes simplex virus type 1 (HSV-1) has been deeply studied, significant gaps remain in the fundamental understanding of HSV-host interactions: our work focused on studying the Infected Cell Protein 27 (ICP27) as an inhibitor of the Absent-in-melanoma-2 (AIM 2) inflammasome pathway, leading [...] Read more.
Although Herpes simplex virus type 1 (HSV-1) has been deeply studied, significant gaps remain in the fundamental understanding of HSV-host interactions: our work focused on studying the Infected Cell Protein 27 (ICP27) as an inhibitor of the Absent-in-melanoma-2 (AIM 2) inflammasome pathway, leading to reduced pro-inflammatory cytokines that influence the activation of a protective innate immune response to infection. To assess the inhibition of the inflammasome by the ICP27, hTert-immortalized Retinal Pigment Epithelial cells (hTert-RPE 1) infected with HSV-1 wild type were compared to HSV-1 lacking functional ICP27 (HSV-1∆ICP27) infected cells. The activation of the inflammasome by HSV-1∆ICP27 was demonstrated by quantifying the gene and protein expression of the inflammasome constituents using real-time PCR and Western blot. The detection of the cleavage of the pro-caspase-1 into the active form was performed by using a bioluminescent assay, while the quantification of interleukins 1β (IL-1β) and 18 (IL-18)released in the supernatant was quantified using an ELISA assay. The data showed that the presence of the ICP27 expressed by HSV-1 induces, in contrast to HSV-1∆ICP27 vector, a significant downregulation of AIM 2 inflammasome constituent proteins and, consequently, the release of pro-inflammatory interleukins into the extracellular environment reducing an effective response in counteracting infection. Full article
(This article belongs to the Special Issue Genetic Insights into Host-Viral Response and Pathogenesis 2.0)
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