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Author: Dr Fiona Larsen MB ChB, Dept of Dermatology Greenlane Hospital, Auckland, New Zealand, 2004.
Aciclovir is the most widely prescribed antiviral drug in the world. It was first available on prescription in 1983.
Aciclovir is a synthetic compound with a similar molecular structure to purine nucleoside. It has been shown to stop the growth of herpes simplex virus (HSV), Varicella zoster virus (VZV) (the cause of chickenpox and shingles), Epstein-Barr virus (EBV, the cause of infectious mononucleosis), and to a lesser extent cytomegalovirus (CMV).
Aciclovir is used in the treatment of:
Aciclovir is also available as a cold-sore cream for the lips and face, and as an ophthalmic ointment for eye infections. It should be applied at the first sign of recurrent infection, often a tingling feeling. It is then rubbed into the affected area every four hours during waking hours for 5 days. It is not suitable to use inside the mouth or other mucous membranes.
Best results are achieved if the treatment begins within 48 hours of the onset of the rash. Oral aciclovir 800 mg five times a day for 7 days accelerates the rate of healing of blisters. In zoster infections, it also reduces the severity and duration of pain and may prevent post-herpetic neuralgia.
Intravenous aciclovir achieves higher blood levels compared to oral aciclovir. It is recommended for severe infections:
Intravenous aciclovir is given over 1 hour every 8 hours for 7 days in a dose of 5 mg/kg for HSV and 10 mg/kg for VZV.
To become effective, aciclovir must first be changed to aciclovir monophosphate by an enzyme that is only found in viruses, called thymidine kinase (TK). It is then converted to its active triphosphate form by human enzymes found inside the cells.
CMV does not produce thymidine kinase so the antiviral activity of aciclovir in CMV infections is poor.
Aciclovir triphosphate (AT) is the active form of the drug. It reduces the production of viral DNA by competing with a natural compound, deoxyguanosine triphosphate, for the viral DNA polymerase enzyme. Incorporation of AT into the viral DNA completely prevents the synthesis of new DNA.
Viral DNA polymerase binds 10–30 times more strongly to AT than the cellular DNA polymerase. This means aciclovir is not toxic.
Unfortunately, only about 15–20% of the dose of aciclovir is absorbed through the gut wall, which means it must be taken frequently as it only active for two or three hours in the bloodstream.
Side effects are uncommon from aciclovir but include nausea or vomiting, diarrhoea, headache, fever, confusion, lymphadenopathy, generalised muscle aches and itchy skin.
Aciclovir should be used with caution in patients with kidney disease. The dose should be reduced to prevent the accumulation of the drug and to decrease the risk that the drug will damage the kidneys or the nervous system. Aciclovir can also cause abnormal liver function blood tests, and rarely, a lowering of the white cell count.
A pregnancy registry of more than 1000 women who received aciclovir before or during early pregnancy showed no increased rates of miscarriage or birth defects in offspring. However, as with any medicine, it should only be given in pregnancy if the benefits are believed to outweigh the risk.
Valaciclovir is a prodrug of aciclovir and has better bioavailability. It can also be used to treat HSV and HZV. It is used to prevent CMV infection following an organ transplant. Usual doses are:
Famciclovir is used for HSV and HZV. The usual doses are:
If you are not based in New Zealand, we suggest you refer to your national drug approval agency for further information about medicines (eg, the Australian Therapeutic Goods Administration and the US Food and Drug Administration) or a national or state-approved formulary (eg, the New Zealand Formulary and New Zealand Formulary for Children and the British National Formulary and British National Formulary for Children).
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