Topic 23 — HIV, Herpesvirus Infections and Antiviral Pharmacotherapy
3rd Year MBBS • Infection and Inflammation
A rapid connection of viral pathogenesis, clinical manifestations, diagnosis, antiviral targets, chickenpox epidemiology and key medico-legal principles.
1. THE TOPIC IN ONE CONNECTED FLOW
This topic connects two important viral patterns. HIV produces progressive immune failure by targeting CD4-positive cells, while herpesviruses establish lifelong latency with possible reactivation. Antiviral drugs work by blocking specific viral enzymes or entry steps, so understanding the viral life cycle directly explains both disease progression and treatment.
Primary infection → active replication → clinical illness → lifelong latency → later reactivation → recurrent disease.
Acyclovir → activation mainly in infected cells → viral DNA polymerase inhibition → reduced HSV/VZV replication; ganciclovir provides important anti-CMV activity, including in CMV retinitis.
2. KEY CLINICAL CONNECTIONS
Persistent viral replication → progressive CD4-cell loss → impaired cellular immunity → opportunistic disease.
CD4 count → degree of immune impairment; plasma HIV RNA → degree of viral replication.
Primary VZV infection → chickenpox → latency → later reactivation → herpes zoster.
Human reservoir + susceptible close contacts → efficient chickenpox spread in households and communities.
Acyclovir → viral thymidine kinase activation → DNA polymerase inhibition → reduced herpesvirus replication.
Predominant renal elimination → accumulation in renal impairment → increased toxicity risk.
NRTIs/NNRTIs → reverse transcriptase; integrase inhibitors → integration; protease inhibitors → maturation; entry inhibitors → viral entry.
Multiple targets together → stronger suppression → lower probability of resistant viral escape.
3. AIM HIGH-YIELD INTEGRATION REVIEW
Do not confuse CD4 count with viral load: CD4 reflects immune impairment, while plasma HIV RNA reflects active viral replication.