Viral Infections

Disease / Phenomenon

Viral infections occur when a virus enters host cells and redirects their machinery to replicate itself. Because viruses are obligate intracellular parasites carrying minimal genetic material of their own, nearly every step of their life cycle depends on host proteins — a dependency that shapes both disease mechanisms and therapeutic strategy. Outcomes range enormously: some infections are cleared silently, others cause acute illness such as influenza or COVID-19, some establish latency and reactivate later like herpesviruses and varicella zoster, and some persist chronically, as with hepatitis B and C or HIV, driving long-term tissue damage and cancer risk. Much of the symptom burden reflects the immune response rather than direct viral cytopathology.

Infection proceeds through attachment to specific receptors, entry, uncoating, genome replication, protein synthesis, assembly, and release. Host defense begins with pattern recognition receptors — TLR3, TLR7, RIG-I, MDA5, and cGAS-STING — detecting viral nucleic acids and triggering type I and III interferon responses through IRF3 and IRF7, which induce hundreds of interferon-stimulated genes. Natural killer cells and cytotoxic T lymphocytes eliminate infected cells while B cells generate neutralizing antibody. Viruses counter with interferon antagonists and immune evasion, and excessive cytokine release can itself cause organ injury. This page maps these processes to pathways and biomarkers.