Pathophysiology
Clinical meaning
Antiviral agents target specific stages of the viral replication cycle. Unlike bacteria, viruses are obligate intracellular parasites that hijack host cell machinery. The viral life cycle includes attachment (binding to host cell receptors), penetration (entry via fusion or endocytosis), uncoating (release of viral genome), replication (genome copying using viral or host polymerases), assembly (packaging new virions), and release (budding or cell lysis). Antiviral drugs exploit differences between viral and host processes: nucleoside/nucleotide analogs (acyclovir, tenofovir, sofosbuvir) mimic natural nucleotides and incorporate into growing viral DNA/RNA chains causing premature termination; protease inhibitors (ritonavir, simeprevir) block viral polyprotein cleavage essential for producing functional viral proteins; neuraminidase inhibitors (oseltamivir) prevent influenza virion release from host cells; integrase inhibitors (dolutegravir) block HIV proviral DNA integration into the host genome. Resistance develops through mutations in viral enzymes that reduce drug binding affinity, making combination therapy and appropriate prescribing critical.