Vidarabine (adenine arabinoside, Vira-A) is an adenine nucleoside analogue containing arabinose in place of ri-bose. It is obtained from cultures of Streptomyces an-tibioticus and has activity against HSV-1, HSV-2, VZV, CMV, HBV, poxviruses, hepadnaviruses, rhabdoviruses, and certain RNA tumor viruses.
Vidarabine’s specific mechanism of action is not fully understood. Cellular enzymes convert this drug to a triphosphate that inhibits DNA polymerase activity. Vidarabine triphosphate competes with deoxyadeno-sine triphosphate (dATP) for access to DNA poly-merase and also acts as a chain terminator. Although vidarabine is incorporated into host DNA to some ex-tent, viral DNA polymerase is much more susceptible to inhibition by vidarabine. Vidarabine also inhibits ri-bonucleoside reductase and other enzymes. Resistance occurs as a result of DNA polymerase mutation.
Vidarabine is administered only as a topical ophthalmic ointment. It has relatively limited solubility and is not significantly absorbed after application to the eye. Within the tissues, it is rapidly deaminated to its princi-pal metabolite, arabinosyl hypoxanthine, which retains some degree of antiviral activity.
The principal use of vidarabine is in the treatment of HSV keratoconjunctivitis. It is also used to treat super-ficial keratitis in patients unresponsive or hypersensi-tive to topical idoxuridine.
The most commonly observed side effects associated with vidarabine are lacrimation, burning, irritation, pain, and photophobia. Vidarabine has oncogenic and mutagenic potential; however, the risk of systemic ef-fects is low because of its limited absorption. It should not be used in conjunction with ophthalmic cortico-steroids, since these drugs increase the spread of HSV infection and may produce side effects such as in-creased intraocular pressure, glaucoma, and cataracts.
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