Abstract
Notable among the many communicable agents known to infect the human cornea is the human adenovirus, with less than ten adenoviruses having corneal tropism out of more than 100 known types. The syndrome of epidemic keratoconjunctivitis (EKC), caused principally by human adenovirus, presents acutely with epithelial keratitis, and later with stromal keratitis that can be chronic and recurrent. In this review, we discuss the current state of knowledge regarding the molecular biology of adenovirus infection of corneal stromal cells, among which the fibroblast-like keratocyte is the most predominant, in order to elucidate basic pathophysiologic mechanisms of stromal keratitis in the human patient with EKC.
Highlights
Over half of all conjunctivitis cases are caused by adenovirus [1,3,4], and in an undetermined but significant proportion of these cases, the cornea is infected
Menon and coworkers demonstrated that the epidemic keratoconjunctivitis (EKC)-causing human adenovirus species D type 37 (HAdV-D37), but not the highly similar but non-EKC-associated Human adenoviruses (HAdV)-D19, induced ectodomain release of corneal epithelial MUC16, reducing barrier function to infection [62]
The epithelial keratitis induced by viral cytopathic effect resolves within days, but stromal keratitis in the form of subepithelial infiltrates (SEI) ensues [52], typically appearing at 14–21 days pi
Summary
The cornea is the transparent window of the eye. The cornea is a mucosal surface and frequently encounters external infectious agents, whether airborne, through hand-to-eye contact, on fomites or contact lenses, or due to trauma. The cornea is the most anterior eye tissue and, from front to back (Figure 1A), is composed of corneal epithelium, epithelial basement membrane, Bowman’s layer, stroma, Descemet’s membrane, and the single-cell layer-thick corneal endothelium. The corneal epithelium, like other epithelial surfaces, expresses membrane-associated mucins (MAMs), and viruses must first negotiate a MAM-rich glycocalyx in order to infect corneal epithelial cells. MUC16 expressed by corneal epithelial cells has been shown to directly impact adenovirus tropism for the eye. Menon and coworkers demonstrated that the EKC-causing human adenovirus species D type 37 (HAdV-D37), but not the highly similar but non-EKC-associated HAdV-D19, induced ectodomain release of corneal epithelial MUC16, reducing barrier function to infection [62]. In a subset of infected eyes, after the epithelium has healed (C), the level of the corneal epithelial basement membrane. Make up the greatup majority of majority cells in the fibroblasts and myofibroblasts [82].keratocytes
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