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Viruses
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Innate and Adaptive Immunity to Cutaneous Virus Infection
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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 11403

Special Issue Editor

Dr. Christopher C. Norbury

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

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Published Papers (7 papers)

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Research

Jump to: Review

14 pages, 518 KiB  
Article
Herald Patch as the Only Evidence of Pityriasis Rosea: Clinical, Laboratory and Pathogenetic Features
by Francesco Drago, Astrid Herzum, Serena Varesano, Gaetano Serviddio, Francesco Broccolo and Giulia Ciccarese
Viruses 2025, 17(1), 119; https://doi.org/10.3390/v17010119 - 16 Jan 2025
Viewed by 513
Abstract
Pityriasis rosea (PR) is a self-limited exanthem associated with the endogenous systemic reactivation of human herpesvirus (HHV)-6 and HHV-7. The disease typically begins with a single erythematous patch on the trunk (herald patch), followed by a secondary eruption of smaller papulosquamous lesions. Rarely, [...] Read more.
Pityriasis rosea (PR) is a self-limited exanthem associated with the endogenous systemic reactivation of human herpesvirus (HHV)-6 and HHV-7. The disease typically begins with a single erythematous patch on the trunk (herald patch), followed by a secondary eruption of smaller papulosquamous lesions. Rarely, the herald patch may be the only cutaneous manifestation of PR. The present work aimed to examine the clinical and laboratory features of the PR cases characterized by the herald patch as the sole cutaneous manifestation and to compare them with the classic form of PR. An observational, retrospective study was conducted on patients presenting with herald patch as the only sign of PR (cases) and on a series of age- and sex-matched patients who presented with a typical PR pattern (controls). The records of the patients were extracted from a PR registry, which collected data on patients with PR diagnosed from 2003 to 2023 by at least two dermatologists from the same study team. Nineteen patients (eleven males, eight females) with a mean age of 27.1 years presented the herald patch as the only cutaneous manifestation of PR. Nineteen age- and sex-matched patients were considered controls. In the cases, the exanthem duration was shorter than in controls, and the mean HHV-6 and HHV-7 DNA plasma load was lower than in controls. This rare variant of PR might be considered an abortive form of the exanthem that occurs when the HHV-6/7 reactivation from latency is contrasted by a more robust immunological response than in classic PR. Full article
(This article belongs to the Special Issue Innate and Adaptive Immunity to Cutaneous Virus Infection)
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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 1672
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)
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Review

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17 pages, 1871 KiB  
Review
Breaching the Barrier: Investigating Initial Herpes Simplex Viral Infection and Spread in Human Skin and Mucosa
by Hafsa Rana, Naomi R. Truong, Dona R. Sirimanne and Anthony L. Cunningham
Viruses 2024, 16(11), 1790; https://doi.org/10.3390/v16111790 - 18 Nov 2024
Viewed by 1230
Abstract
Herpes simplex virus (HSV) is sexually transmitted via the anogenital mucosa where it initially infects epidermal keratinocytes and mononuclear phagocytes (MNPs). It then spreads to the dorsal root ganglion via sensory nerve endings, to remain latent for life with periodic reactivation. Currently, there [...] Read more.
Herpes simplex virus (HSV) is sexually transmitted via the anogenital mucosa where it initially infects epidermal keratinocytes and mononuclear phagocytes (MNPs). It then spreads to the dorsal root ganglion via sensory nerve endings, to remain latent for life with periodic reactivation. Currently, there is no cure or vaccine. Initial or recurrent HSV infection can produce serious complications and mediate acquisition of HIV. This review outlines the initial events after the HSV infection of human anogenital mucosa to determine the optimal window to target the virus before it becomes latent. After infection, HSV spreads rapidly within the mid-layers of epidermal keratinocytes in the explanted human inner foreskin. Infected cells produce chemokines, which modulate nectin-1 distribution on the surface of adjacent keratinocytes, facilitating viral spread. Epidermal Langerhans cells and dendritic cells become infected with HSV followed by a “viral relay” to dermal MNPs, which then present viral antigen to T cells in the dermis or lymph nodes. These data indicate the need for interruption of spread within 24 h by diffusible vaccine-induced mediators such as antiviral cytokines from resident immune cells or antibodies. Intradermal/mucosal vaccines would need to target the relevant dermal MNPs to induce HSV-specific CD4+ and CD8+ T cells. Full article
(This article belongs to the Special Issue Innate and Adaptive Immunity to Cutaneous Virus Infection)
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11 pages, 1194 KiB  
Review
Local Power: The Role of Tissue-Resident Immunity in Human Genital Herpes Simplex Virus Reactivation
by Jia Zhu and Maurine D. Miner
Viruses 2024, 16(7), 1019; https://doi.org/10.3390/v16071019 - 25 Jun 2024
Viewed by 1692
Abstract
From established latency, human herpes virus type 2 (HSV-2) frequently reactivates into the genital tract, resulting in symptomatic ulcers or subclinical shedding. Tissue-resident memory (TRM) CD8+ T cells that accumulate and persist in the genital skin at the local site of [...] Read more.
From established latency, human herpes virus type 2 (HSV-2) frequently reactivates into the genital tract, resulting in symptomatic ulcers or subclinical shedding. Tissue-resident memory (TRM) CD8+ T cells that accumulate and persist in the genital skin at the local site of recrudescence are the “first responders” to viral reactivation, performing immunosurveillance and containment and aborting the ability of the virus to induce clinical lesions. This review describes the unique spatiotemporal characteristics, transcriptional signatures, and noncatalytic effector functions of TRM CD8+ T cells in the tissue context of human HSV-2 infection. We highlight recent insights into the intricate overlaps between intrinsic resistance, innate defense, and adaptive immunity in the tissue microenvironment and discuss how rapid virus–host dynamics at the skin and mucosal level influence clinical outcomes of genital herpes diseases. Full article
(This article belongs to the Special Issue Innate and Adaptive Immunity to Cutaneous Virus Infection)
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19 pages, 380 KiB  
Review
Vaccinia Virus: Mechanisms Supporting Immune Evasion and Successful Long-Term Protective Immunity
by Joy Hsu, Suyon Kim and Niroshana Anandasabapathy
Viruses 2024, 16(6), 870; https://doi.org/10.3390/v16060870 - 29 May 2024
Viewed by 1851
Abstract
Vaccinia virus is the most successful vaccine in human history and functions as a protective vaccine against smallpox and monkeypox, highlighting the importance of ongoing research into vaccinia due to its genetic similarity to other emergent poxviruses. Moreover, vaccinia’s ability to accommodate large [...] Read more.
Vaccinia virus is the most successful vaccine in human history and functions as a protective vaccine against smallpox and monkeypox, highlighting the importance of ongoing research into vaccinia due to its genetic similarity to other emergent poxviruses. Moreover, vaccinia’s ability to accommodate large genetic insertions makes it promising for vaccine development and potential therapeutic applications, such as oncolytic agents. Thus, understanding how superior immunity is generated by vaccinia is crucial for designing other effective and safe vaccine strategies. During vaccinia inoculation by scarification, the skin serves as a primary site for the virus–host interaction, with various cell types playing distinct roles. During this process, hematopoietic cells undergo abortive infections, while non-hematopoietic cells support the full viral life cycle. This differential permissiveness to viral replication influences subsequent innate and adaptive immune responses. Dendritic cells (DCs), key immune sentinels in peripheral tissues such as skin, are pivotal in generating T cell memory during vaccinia immunization. DCs residing in the skin capture viral antigens and migrate to the draining lymph nodes (dLN), where they undergo maturation and present processed antigens to T cells. Notably, CD8+ T cells are particularly significant in viral clearance and the establishment of long-term protective immunity. Here, we will discuss vaccinia virus, its continued relevance to public health, and viral strategies permissive to immune escape. We will also discuss key events and populations leading to long-term protective immunity and remaining key gaps. Full article
(This article belongs to the Special Issue Innate and Adaptive Immunity to Cutaneous Virus Infection)
21 pages, 1496 KiB  
Review
The Dynamic Relationship between Dengue Virus and the Human Cutaneous Innate Immune Response
by Michelle M. Martí, Priscila M. S. Castanha and Simon M. Barratt-Boyes
Viruses 2024, 16(5), 727; https://doi.org/10.3390/v16050727 - 4 May 2024
Cited by 1 | Viewed by 2461
Abstract
Dengue virus (DENV) is a continuing global threat that puts half of the world’s population at risk for infection. This mosquito-transmitted virus is endemic in over 100 countries. When a mosquito takes a bloodmeal, virus is deposited into the epidermal and dermal layers [...] Read more.
Dengue virus (DENV) is a continuing global threat that puts half of the world’s population at risk for infection. This mosquito-transmitted virus is endemic in over 100 countries. When a mosquito takes a bloodmeal, virus is deposited into the epidermal and dermal layers of human skin, infecting a variety of permissive cells, including keratinocytes, Langerhans cells, macrophages, dermal dendritic cells, fibroblasts, and mast cells. In response to infection, the skin deploys an array of defense mechanisms to inhibit viral replication and prevent dissemination. Antimicrobial peptides, pattern recognition receptors, and cytokines induce a signaling cascade to increase transcription and translation of pro-inflammatory and antiviral genes. Paradoxically, this inflammatory environment recruits skin-resident mononuclear cells that become infected and migrate out of the skin, spreading virus throughout the host. The details of the viral–host interactions in the cutaneous microenvironment remain unclear, partly due to the limited body of research focusing on DENV in human skin. This review will summarize the functional role of human skin, the cutaneous innate immune response to DENV, the contribution of the arthropod vector, and the models used to study DENV interactions in the cutaneous environment. Full article
(This article belongs to the Special Issue Innate and Adaptive Immunity to Cutaneous Virus Infection)
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18 pages, 2409 KiB  
Review
T Cell Surveillance during Cutaneous Viral Infections
by Luxin Pei and Heather D. Hickman
Viruses 2024, 16(5), 679; https://doi.org/10.3390/v16050679 - 26 Apr 2024
Viewed by 1443
Abstract
The skin is a complex tissue that provides a strong physical barrier against invading pathogens. Despite this, many viruses can access the skin and successfully replicate in either the epidermal keratinocytes or dermal immune cells. In this review, we provide an overview of [...] Read more.
The skin is a complex tissue that provides a strong physical barrier against invading pathogens. Despite this, many viruses can access the skin and successfully replicate in either the epidermal keratinocytes or dermal immune cells. In this review, we provide an overview of the antiviral T cell biology responding to cutaneous viral infections and how these responses differ depending on the cellular targets of infection. Much of our mechanistic understanding of T cell surveillance of cutaneous infection has been gained from murine models of poxvirus and herpesvirus infection. However, we also discuss other viral infections, including flaviviruses and papillomaviruses, in which the cutaneous T cell response has been less extensively studied. In addition to the mechanisms of successful T cell control of cutaneous viral infection, we highlight knowledge gaps and future directions with possible impact on human health. Full article
(This article belongs to the Special Issue Innate and Adaptive Immunity to Cutaneous Virus Infection)
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