What is the primary mechanism by which acyclovir works as an antiviral agent?

Acyclovir is an antiviral medication primarily used to treat infections caused by certain types of viruses, particularly the herpes simplex virus. Its mechanism of action is centered on its structural similarity to guanosine, which allows it to act as a guanosine analog.

Once inside the infected cell, acyclovir is phosphorylated by the virally encoded enzyme thymidine kinase to its monophosphate form. Further phosphorylation by host cell kinases then converts it to the triphosphate form. This active triphosphate form competes with the natural nucleotide (deoxyguanosine triphosphate) for incorporation into viral DNA during replication. When acyclovir triphosphate is integrated into the growing DNA strand, it effectively terminates DNA chain elongation due to its structure lacking the necessary components for further elongation.

This mechanism renders acyclovir particularly effective against viruses that rely on synthesizing their own DNA, as it disrupts the viral replication process. This is why recognizing acyclovir's role as a chain-terminating guanosine analog is key to understanding how it inhibits viral replication. Other mechanisms, such as inhibition of RNA polymerase or blocking protein synthesis, are not relevant to acyclovir's action,