Review reveals mechanisms of viral latency, reactivation, and immunopathology in herpetic stromal keratitis, highlighting challenges in preventing corneal blindness.
Herpes simplex virus (HSV) infects epithelial cells and establishes lifelong latency in neuronal nuclei of the regional ganglion. Although active replication of HSV can be treated effectively with anti-HSV drugs, control of the reactivated HSV in the regional ganglion is a difficult task: Reactivated HSV in the trigeminal ganglion (TG) comes down via axon and infect the cornea Some patients eventually develop vision threatening herpetic stromal keratitis (HSK) that is the second leading cause of corneal blindness after trauma. Corneal herpes continues to cause blindness in developed countries. In this review, we describe initial attachment of HSV, entry and infection at peripheral epithelial cells, establishment of latency in neuron, reactivation and egress, corneal infection and immunopathology of HSK. We also discuss prevention and treatment of the disease.
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Kozaburo Hayashi (2020) studied this question.
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