Abstract
The skin is an active immune organ that functions as the first and largest site of defense to the outside environment. Serving as the primary interface between host and pathogen, the skin’s early immune responses to viral invaders often determine the course and severity of infection. We review the current literature pertaining to the mechanisms of cutaneous viral invasion for classical skin-tropic, oncogenic, and vector-borne skin viruses. We discuss the skin’s evolved mechanisms for innate immune viral defense against these invading pathogens, as well as unique strategies utilized by the viruses to escape immune detection. We additionally explore the roles that demographic and environmental factors, such as age, biological sex, and the cutaneous microbiome, play in altering the host immune response to viral threats.
Highlights
The skin is a dynamic barrier organ that establishes a clear boundary between the host and the outside world
We provide an overview of viral entry mechanisms by various viruses with differing infection propensities, i.e. classically skin-tropic and oncogenic skin viruses, as well as vector-introduced skin viruses. We review how these viruses uniquely interact with different aspects of the cutaneous innate immune system, and we further explore some evolved viral mechanisms that directly interfere with the host innate immune response
Absence of natural killer (NK) cells resulted in a diminished CD4+ and CD8+ T cell responses, and the presence of NK cells alone were identified to be able to rescue dysmorphic CD8+ T cells to mount an effective CD8+ T cell response even in the absence of CD4+ T helper cells [30]. These findings propose a potential role of NK cells to mediate and bridge innate and adaptive immune responses
Summary
The skin is a dynamic barrier organ that establishes a clear boundary between the host and the outside world. Responses by the cutaneous innate immune system and its effectors play essential roles in early destruction of pathogens as well as establishment of an immune barrier to prevent systemic infection. This is accomplished via phagocytic cells (i.e. macrophages, neutrophils, and dendritic cells), leukocytes (i.e. natural killer (NK) cells, mast cells, basophils, and eosinophils), as well as epidermal keratinocytes. In immunocompromised and neonatal patients, HSV has the potential to disseminate and cause severe morbidity and mortality [3] In both primary and reactivated infections, viral entry and replication largely occur in the epidermis, where keratinocytes are the predominant cell type. Toll-like receptor (TLR) 2 senses viral gB and gH/gL and activates the nuclear factor kB (NF-kB) pathway to induce expression of pro-inflammatory cytokines (e.g. tumor necrosis factor (TNF)-a, interleukin (IL)-6 and IL-12) and chemokines (e.g. CC chemokine ligand 2 (CCL2)) [12,13,14,15]
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