Aciclovir
(Redirected from Zovirax)
Antiviral medication used to treat herpes simplex virus infections
Aciclovir, also known as acyclovir, is an antiviral drug primarily used for the treatment of herpes simplex virus infections, including genital herpes, cold sores, and shingles. It is also used in the management of varicella zoster virus infections, such as chickenpox. Aciclovir is a synthetic purine nucleoside analogue derived from guanine.
Mechanism of Action[edit | edit source]
Aciclovir works by inhibiting the replication of viral DNA. It is selectively activated by the viral enzyme thymidine kinase, which phosphorylates aciclovir to its monophosphate form. Cellular enzymes then convert it to aciclovir triphosphate, which competitively inhibits viral DNA polymerase and incorporates into viral DNA, leading to chain termination.
Pharmacokinetics[edit | edit source]
Aciclovir is available in various forms, including oral tablets, topical creams, and intravenous formulations. The bioavailability of oral aciclovir is relatively low, ranging from 10% to 20%. It is widely distributed in body tissues and fluids, including the cerebrospinal fluid. Aciclovir is primarily excreted by the kidneys.
Clinical Uses[edit | edit source]
Aciclovir is used to treat:
- Herpes simplex virus infections, including genital herpes and cold sores.
- Varicella zoster virus infections, such as chickenpox and shingles.
- Prophylaxis in immunocompromised patients to prevent herpes virus infections.
Side Effects[edit | edit source]
Common side effects of aciclovir include nausea, diarrhea, headache, and dizziness. Intravenous administration can lead to more serious side effects such as renal dysfunction and neurological effects.
Synthesis[edit | edit source]
Aciclovir is synthesized from guanine derivatives. The synthesis involves the conversion of guanine to a nucleoside analogue through a series of chemical reactions, including the introduction of an acyclic side chain.
Resistance[edit | edit source]
Resistance to aciclovir can occur, particularly in immunocompromised patients. Resistance is usually due to mutations in the viral thymidine kinase or DNA polymerase genes, leading to reduced drug activation or binding.
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