An Atlas of Antiviral Therapeutic Outcomes: How Viral Biology Shapes the Reach of Treatment

Antiviral inhibition does not produce a single therapeutic endpoint: some infections can be cured after finite treatment, others require durable suppression, and others remain difficult to influence because the actionable phase is brief or anatomically inaccessible. These different outcomes reflect the biological state that preserves infection or permits return, the time during which a drug-sensitive process remains causally important, the anatomical space in which consequential virus or viral material resides, and the capacity of viral populations to evolve under therapeutic pressure. Here, we examine these relationships across curable, suppressible, latent, acute, neuroinvasive, and post-acute viral infections. Comparisons among HCV, HIV-1, HBV, HSV, influenza, RSV, dengue, SARS-CoV-2, Ebola virus, CHIKV, and other systems show how persistence architecture, diagnostic timing, tissue pharmacology, host context, and resistance can determine whether antiviral activity translates into virological cure, durable suppression, recurrence control, prevention, or incomplete therapeutic control. Human challenge studies, clinical programs with discordant outcomes, and resistance studies further illustrate where mechanistic activity and therapeutic sufficiency diverge. Across these examples, antiviral outcome depends ultimately on whether treatment can intercept the biological state that determines the subsequent fate of infection.