Innate and Adaptive Immunity to Cutaneous Virus Infection

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 1046

Special Issue Editor


E-Mail Website
Guest Editor
Penn State College of Medicine, Department of Microbiology and Immunology, Hershey, PA 17033, USA
Interests: cutaneous virus infection; interferons; keratinocytes; gamma delta T cells; monocytes; macrophages; dendritic cells

Special Issue Information

Dear Colleagues,

The skin is the largest contiguous organ in the body, and, as the organ with the largest environmentally exposed surface area, is a crucial defensive barrier against the invasion of pathogens. A number of viruses infect through microabrasions in the epidermal barrier, while others are transmitted by insect vectors into the skin. The diversity of cutaneous virus infections is increased by a division into two general strategies: There are viruses that cause, and try to partially evade, a large inflammatory and adaptive immune response while spreading elsewhere in the body. These viruses can produce a virulent reaction in the skin, damaging the barrier function and potentially allowing secondary infections. Conversely, there are viruses that attempt to infect the outermost layer of the epidermis and remain as immunologically silent as possible.  These viruses often remain latent in the skin, but can then induce tumor formation at a much later time point. The local cutaneous immune system must be specialized to respond to each mode of transmission and infection, while minimizing damage to the barrier function of the skin. Skin pathologies will often reduce the effectiveness of cutaneous antiviral responses, promoting virus growth as well as spread and reducing barrier function; however, while many studies have focused on responses to cutaneous virus infections, we feel that a Special Issue dedicated to these responses may reveal common, as well as virus-specific, components of the cutaneous antiviral response.

In this Special Issue, we welcome the submission of a wide range of articles, including original research, short communications, and reviews, that focus on the innate, primary, or memory adaptive immune response to cutaneous virus infections. Articles could focus on cell-type specializations in the skin, novel effector mechanisms displayed in the skin, the recognition and elimination of virus-induced cutaneous tumors, and mechanisms deployed to avoid damage to the skin barrier function.

Dr. Christopher C. Norbury
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. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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.

Keywords

  • cutaneous/skin
  • virus
  • interferon
  • T cell
  • dendritic cell
  • monocyte
  • keratinocyte
  • poxvirus
  • herpes simplex virus
  • papilloma virus
  • merkel cell polyomavirus
  • antimicrobial peptides

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

30 pages, 7305 KiB  
Article
γδ T Cells Mediate a Requisite Portion of a Wound Healing Response Triggered by Cutaneous Poxvirus Infection
by Irene E. Reider, Eugene Lin, Tracy E. Krouse, Nikhil J. Parekh, Amanda M. Nelson and Christopher C. Norbury
Viruses 2024, 16(3), 425; https://doi.org/10.3390/v16030425 - 10 Mar 2024
Viewed by 800
Abstract
Infection at barrier sites, e.g., skin, activates local immune defenses that limit pathogen spread, while preserving tissue integrity. Phenotypically distinct γδ T cell populations reside in skin, where they shape immunity to cutaneous infection prior to onset of an adaptive immune response by [...] Read more.
Infection at barrier sites, e.g., skin, activates local immune defenses that limit pathogen spread, while preserving tissue integrity. Phenotypically distinct γδ T cell populations reside in skin, where they shape immunity to cutaneous infection prior to onset of an adaptive immune response by conventional αβ CD4+ (TCD4+) and CD8+ (TCD8+) T cells. To examine the mechanisms used by γδ T cells to control cutaneous virus replication and tissue pathology, we examined γδ T cells after infection with vaccinia virus (VACV). Resident γδ T cells expanded and combined with recruited γδ T cells to control pathology after VACV infection. However, γδ T cells did not play a role in control of local virus replication or blockade of systemic virus spread. We identified a unique wound healing signature that has features common to, but also features that antagonize, the sterile cutaneous wound healing response. Tissue repair generally occurs after clearance of a pathogen, but viral wound healing started prior to the peak of virus replication in the skin. γδ T cells contributed to wound healing through induction of multiple cytokines/growth factors required for efficient wound closure. Therefore, γδ T cells modulate the wound healing response following cutaneous virus infection, maintaining skin barrier function to prevent secondary bacterial infection. Full article
(This article belongs to the Special Issue Innate and Adaptive Immunity to Cutaneous Virus Infection)
Show Figures

Figure 1

Back to TopTop