This is an antiviral gating module, not a specific disease and not a drug target. It is the antiviral analog of the antibacterial intracellular_pathogen_persistence module: both encode a pharmacologic constraint on what therapy can achieve rather than an enzyme a drug inhibits. Disorder entries for latency-establishing viral infections reference nodes via conforms_to (e.g., "viral_latency_reservoir_persistence#Antiviral Suppression Without Eradication of the Reservoir"), and their suppressive treatments — which point at a polymerase/integrase/protease target-module node via target_mechanisms for their molecular action — are gated by this module's explanation of why that action cannot cure. Key conformance / treatment-gating target: "Antiviral Suppression Without Eradication of the Reservoir" (the node that distinguishes "an antiviral is used" from "the infection is cured" — replication inhibitors cannot clear an archived, non-replicating genome, mandating lifelong therapy and motivating the functional-cure / reservoir-elimination research frontier). Worked "suppression ≠ cure" conformers are Acquired_Immunodeficiency_Syndrome (integrated proviral reservoir in resting CD4+ T cells) and Hepatitis_B (nuclear cccDNA), to be contrasted with Hepatitis_C, which is curable because it establishes no such reservoir. See projects/ANTIVIRAL.md.
Establishment of a Latent or Archival Viral Genome
trigger
After initial infection, latency-establishing viruses deposit their genome in a stable, transcriptionally quiescent form that persists independently of active replication. The molecular form varies by virus family: HIV and other retroviruses integrate a provirus into the host chromosome of long-lived resting memory CD4+ T cells; hepatitis B converts its relaxed-circular DNA into a covalently closed circular DNA (cccDNA) episome in the hepatocyte nucleus; herpes simplex virus establishes a non-replicating latent infection in sensory neurons. In each case the archived genome is laid down early, is indistinguishable from the host's own nucleic acid to the immune system, and serves as the durable template from which infectious virus can later be regenerated. This is the trigger node of the module — the event that creates a reservoir no replication-targeting drug can reach.
Downstream
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Antiviral Suppression Without Eradication of the Reservoir
Once a latent or episomal genome is established, replication-targeting antivirals can suppress active virus but cannot clear the archived reservoir.
Antiviral Suppression Without Eradication of the Reservoir
intrinsic resistance
Direct-acting antivirals act on the replicating virus — the polymerase, protease, integrase, or assembly machinery engaged only during active replication. The latent reservoir is, by definition, not replicating: the integrated provirus is transcriptionally silent, the cccDNA episome is a stable template rather than a replicating intermediate, and the latent neuronal HSV genome makes no infectious particles. Consequently suppressive therapy drives plasma viremia to undetectable levels and arrests disease progression but leaves the archived genome intact, so it cannot cure the infection. This is the gating principle that distinguishes suppression from eradication and mandates indefinite (often lifelong) therapy; it is the canonical conformance / treatment-gating target of the module and the reason the "functional cure" and reservoir-elimination strategies (e.g. "shock-and-kill", cccDNA-directed agents) are an active frontier rather than standard care.
Downstream
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Reactivation and Viral Rebound on Treatment Interruption
Because the archived reservoir survives suppression, stopping therapy allows the latent genome to resume replication and viremia to rebound.
Reactivation and Viral Rebound on Treatment Interruption
adaptive escape
The persistence of a suppressed-but-not-eradicated reservoir has a direct clinical consequence: when suppressive therapy is interrupted, the archived genome exits latency and reignites productive infection. For HIV, a small fraction of the latent reservoir produces infectious virus that rekindles systemic infection within weeks of stopping ART; for hepatitis B, the stable cccDNA reactivates the virus when nucleos(t)ide analogs are withdrawn; for herpes simplex virus, the latent neuronal genome periodically reactivates to cause recurrent peripheral disease, which is why no drug eradicates the virus. This rebound is the escape consequence that closes the loop of the module and operationalizes "suppression is not cure": it is the reason therapy must be continued indefinitely and the endpoint that any curative or functional-cure strategy must abolish.