Aciclovir

Antiviral medication used to treat herpes simplex virus infections

2D structure of Aciclovir

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

Comparison of guanosine and aciclovir structures

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

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

Aciclovir tablets

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

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

Synthesis of Aciclovir

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

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.

Related Pages

• Herpes simplex virus
• Varicella zoster virus
• Antiviral drug