To view this page ensure that Adobe Flash Player version 11.1.0 or greater is installed.
Topical Ganciclovir in Herpetic Eye Disease
Khalid F Tabbara
The Eye Center and The Eye Foundation for Research in Ophthalmology, Riyadh, Saudi Arabia; Department of Ophthalmology, College of Medicine, King Saud University,
Riyadh, Saudi Arabia; The Wilmer Ophthalmological Institute of The Johns Hopkins University School of Medicine, Baltimore, Maryland, US.
Abstract Herpetic keratitis is a common cause of ocular morbidity and corneal blindness. The disease has a worldwide distribution. There are different types
of Herpes virus with variable ocular and adnexal manifestations. Herpes virus stays dormant in the nerve ganglia following a primary infection.
Topical antiviral agents include acyclovir and ganciclovir. Both agents may be used for the treatment and prophylaxis of herpetic keratitis. Antiviral
prophylaxis is of crucial importance in the prevention of recurrent keratitis in patients with penetrating keratoplasty for herpes induced corneal
scars. Recurrent herpetic keratitis in such patients frequently eventuate in the rejection of the graft. This article reviews topical ganciclovir
0.15% gel in the therapy and prophylaxis of herpetic keratitis.
Keywords Acyclovir, antiviral therapy, corneal epithelial keratitis, ganciclovir, herpes virus, herpes virus 1, herpes virus 2, herpetic keratitis,
Disclosure: Khalid F Tabbara has nothing to declare in relation to this article. No funding was received in the publication of this article.
Acknowlegements: This Study was presented in part at the Annual meeting of the American Academy of Ophthalmology (AAO), 14–17 November 2015, Sands Expo and
Convention Centre, Las Vegas, Nevada, US.
Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any noncommercial use, distribution, adaptation, and
reproduction provided the original author(s) and source are given appropriate credit.
Received: February 4, 2016 Accepted: March 8, 2016 Citation: US Ophthalmic Review, 2016;9(1):25–9
Correspondence: Khalid F Tabbara, The Eye Center, 241 Makkah Road, PO Box 55307, Riyadh 11534, Saudi Arabia. E: firstname.lastname@example.org
Herpetic keratitis is the most common cause of corneal blindness, and is
considered to be a major indication for penetrating keratoplasty (PKP). 1
Herpetic keratitis is caused by human herpes virus (HHV). Table 1 shows
the herpes viruses that may cause disease in man. 2–5
Certain viral infections have been eradicated by vaccination, and
others are controlled by public health measures. The resilience of
viruses has led to the emergence of new viruses and the evolution of
old viruses causing potentially blinding diseases of the eye. HHV type 1
(HHV-1) is endemic worldwide and humans are the only known natural
reservoir for the virus. By age 60, approximately 95% of individuals are
infected by HHV-1. HHV-1 is transmitted by direct contact with infected
secretions such as saliva or tears or coming in contact with cutaneous
lesions infected by HHV-1.There are approximately one million cases of
new ocular herpetic infections annually worldwide.
Patients make an average of four visits to the ophthalmologist for the first
episode and six visits for recurring episodes of herpetic keratitis. 6–10 It is
estimated that close to two-thirds of all cases of primary herpes infections
are asymptomatic. Initial exposure to HHV leads to primary infection.
The virus becomes latent in the nerve ganglia and approximately 98% of
patients with herpes infection shed HHV-1 genome in tears or saliva. 11
Following a primary infection, the virus stays latent in the sensory and
TOU CH MED ICA L MEDIA
autonomic neurons of ganglia (trigeminal ganglion, ciliary ganglion, superior
cervical ganglion). The recurrences (secondary infection) of herpetic
lesions are the result of reactivation of the virus. 6,12,13 The reactivation
leads to shedding of the virus or recurrence of the disease. There are
risk factors both genetic and environmental that lead to reactivation. The
clinical manifestations depend on the site of latency. Infection with HHV is
determined by local susceptibility, general host immunity, the virus strain,
and genetic predisposition. 14 The site of viral latency determines the future
of reactivation and clinical manifestations of the disease. Latency of HHV in
the trigeminal ganglion may lead to recurrence of herpetic keratitis. There
are 25 different types of neurons in the trigeminal ganglion.
Latency in the superior cervical ganglion may lead to reactivation and
recurrence of herpetic intraocular inflammation and anterior uveitis. 12,13
Latency in the ciliary ganglion may lead to recurrent intraocular
inflammation. Alpha adrenergic compounds and estradiol may lead
to the reactivation of HHV from the neurons of the trigeminal ganglia.
Infection of the autonomic nervous system and latency in the superior
cervical ganglion may lead to uveitis but not keratitis. On the other hand,
latency in the lateral geniculate body may lead to acute retinal necrosis.
Systemic and intravitreal administration of ganciclovir have been
recommended for the treatment of cytomegalovirus and retinitis and for