Abstract
The entry of herpes simplex virus into cells was once thought to be a general process. It is now understood that the virus is able to use multiple mechanisms for entry and spread, including the use of receptors and co-receptors that have been determined to be cell-type specific. This is certainly true for ocular cell types, which is important as the virus may use different mechanisms to gain access to multiple anatomic structures in close proximity, leading to various ocular diseases. There are some patterns that may be utilized by the virus in the eye and elsewhere, including surfing along filopodia in moving from cell to cell. There are common themes as well as intriguing differences in the entry mechanisms of herpes simplex virus into ocular cells. We discuss these issues in the context of conjunctivitis, keratitis, acute retinal necrosis, and other ocular diseases.
ACKNOWLEDGMENTs
This work was supported by NIH grants AI057860 (D.S.), AI081869 (D.S.) and a Core Grant EY01792. D.S. is a recipient of the Lew Wasserman Merit award from Research to Prevent Blindness (RPB). A.V.F is supported by an RPB Medical Student Eye Research Fellowship.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.