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The role of acyclovir in the prevention of CMV infections in immunocompromised patients is also generally accepted, but its use in diseases caused by other herpes viruses such as EBV and HHV-6 has not been supported in clinical investigations to date.

Acyclovir zovirax (acyclovir) selectively inhibits DNA replication of herpes viruses, with low host cell toxicity. The antiviral is preferentially activated in infected cells; initial phosphorylation occurs via viral thymidine kinase, and acyclovir triphosphate (the active derivative obtained from the monophosphate via host cell enzymes) inhibits viral DNA polymerase more readily than the cellular enzyme, thus preventing viral replication.

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Use of oral acyclovir is effective but controversial in the treatment of otherwise healthy individuals with varicella (chickenpox), and in some countries it has been recommended for use only in cases which may be potentially severe. The development of rash and pain associated with herpes zoster (shingles) is attenuated with oral or intravenous aciclovir therapy, ocular involvement is prevented, and post-herpetic neuralgia appears to be decreased. Similarly, in a few patients with zoster ophthalmicus, oral acyclovir has reduced the frequency and severity of long term ocular complications and post-herpetic neuralgia, and herpes zoster oticus is improved with intravenous aciclovir.

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The in vivo activity of aciclovir was demonstrated in animal models of HSV ocular, cutaneous, genital, CNS and neonatal infections. Initiation of aciclovir administration within 24 hours of viral challenge can reduce the establishment of viral latency following primary infection, but eradication of established latent virus has not been achieved.

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Orally or intravenously administered aciclovir is distributed to a wide range of tissues and fluids, crosses the placenta and accumulates in breast milk. Plasma protein binding is 9 to 33%, and is independent of plasma aciclovir concentrations. Drug interactions appear to be scarce. Area under the plasma concentration-time curve values and elimination half-life are increased when acyclovir and probenecid are coadministered.

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Combination of aciclovir with various antiviral compounds has resulted in synergistic or additive antiviral activity in vitro against HSV, VZV and CMV. Although part of the latent HSV reservoir is eradicated by acyclovir in ganglionic or tissue cultures and replication is readily interrupted, reversion to latency occurs after several days of exposure.

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Double-blind placebo-controlled studies in immunocompetent patients have demonstrated the efficacy of intravenous (5 mg/kg 3 times daily), oral (200mg 5 times daily) and topical (applied 4 to 6 times daily) acyclovir 200mg initiated within 4 days of the first symptoms of HSV perigenital infection. The duration of viral shedding and time to complete healing of lesions are significantly reduced, particularly in the primary episode.

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In descending order of susceptibility, the viruses against which acyclovir exhibits in vitro antiviral activity are HSV-1 and 2, VZV, EBV, human herpesvirus 6 (HHV-6) and CMV. The in vitro activity of acyclovir cream was generally similar to or greater than that of most other antiviral agents tested against HSV and VZV; ganciclovir, idoxuridine and vidarabine are more potent than aciclovir against CMV; ganciclovir and foscarnet appear to be more potent against HHV-6; and aciclovir appears to have greater activity than penciclovir against EBV.

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Complete suppression of recurrence for 5 years has been achieved in 20% of patients on Acyclovir prophylaxis (800 to 1600 mg/day). Two well-controlled trials have demonstrated a clear advantage for oral ACYCLOVIR tablets over oral inosine pranobex in the suppression of recurrent genital HSV infection.

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Crowns and veneers can often be used for to improve appearance and to repair teeth with great results. If a tooth is lost through an accident or is too badly damaged to be saved with a crown or veneer, a bridge may be the treatment.

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Can be an alternative to amalgam (metal) fillings. They are made of a plastic material and are tooth-coloured rather than silver.

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These are artificial teeth which are secured firmly in the mouth and can be used to replace a single missing tooth or several teeth

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Although Epstein-Barr virus (EBV) appears to have only minimal thymidine kinase activity, EBV DNA polymerase is very susceptible to inhibition by aciclovir triphosphate. Since cytomegalovirus (CMV) does not code for thymidine kinase, and CMV DNA polymerase is poorly inhibited by aciclovir triphosphate formed by cellular enzymes, CMV is less susceptible to aciclovir than are herpes simplex virus (HSV), varicella zoster virus (VZV) and EBV.

Dr. Christy Donovan