Corneal latency and transmission of herpes simplex virus-1

Abstract

The transmission of herpes simplex virus (HSV)-1 by corneal transplantation has rarely been reported. It is believed that these cases have resulted either from reactivated virus traveling from the trigeminal ganglion to the cornea or from latent HSV-1 in the donor cornea itself. Studies of long-term viral presence in corneal tissue have sought to determine whether there is evidence of true non-neuronal latency, although there are problems in its definition. Recent studies provide new insights into neuronal latency, while similar HSV-1 gene regulation in the cornea may implicate corneal latency in pathophysiology and as a potential risk for transplant recipients. This issue has led to concerns over eye banking, which currently screens for other infectious agents but not HSV-1. Here we review the literature regarding corneal latency and the transmission of HSV-1.

Figure 1. Herpes simplex virus ocular infection, neuronal spread, latency and reactivation

The HSV virion is shown. The spikes on the envelope represent glycoproteins required for entry and spread. The icosahedral nucleocapsid contains viral DNA. HSV may initially infect the eye or (more commonly) oral mucosa, leading to retrograde spread of the virus along sensory nerves to a sensory ganglion, where it develops a lifelong latent infection. Latency-associated transcripts are expressed in high amounts during latency. Reactivation from latency can lead to ocular infection via anterograde viral spread. The virus may also develop latency in the cornea with local reactivations or occasional migrate to the CNS. HSV: Herpes simplex virus; LAT: Latency-associated transcripts.