Abstract
Cytomegalovirus (CMV) retinitis has become one of the most common manifestations of active CMV infection in patients with acquired immunodeficiency syndrome (AIDS). If left untreated, it results in complete loss of vision. At present, three systemic antiviral agents-ganciclovir, foscarnet, and cidofovir-are available for treatment of CMV retinitis. Unfortunately, reactivation of retinitis will occur with all three agents, and almost all patients eventually experience disease progression while receiving treatment. Therefore, our primary therapeutic challenge is to develop a means of preventing reactivation of CMV retinitis. Another challenge is to develop drugs that can be easily administered. Thus far, oral formulations have not succeeded in effectively meeting this challenge. Direct delivery of an antiviral agent into the vitreous of an infected eye, although easily performed and more effective in delaying time to progression, is unable to prevent or delay the progression of extraocular CMV disease. The ideal antiviral agent would have high central nervous system and tissue penetration, would suppress viral replication and mutation, would be administered orally, and would be inexpensive.

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