Oseltamivir (Tamiflu) inhibits viral neuraminidase. What is the consequence if neuraminidase is NOT inhibited?

• A Viral RNA polymerase cannot complete replication without neuraminidase cofactor activity
• B New virions remain bound to sialic acid on the surface of infected cells and cannot spread to infect new cells ✓
• C Hemagglutinin cannot undergo the conformational change needed for membrane fusion and entry
• D M2 proton channel function is impaired, preventing viral uncoating in the endosome

Explanation

Influenza neuraminidase cleaves sialic acid (N-acetylneuraminic acid) residues on the surface of infected cells and on budding virions. This cleavage releases newly formed virions from the host cell membrane and prevents viral self-aggregation. Without neuraminidase activity, newly assembled virions remain tethered to hemagglutinin-bound sialic acid on the cell surface, clumping together and failing to spread to neighboring cells. Oseltamivir and zanamivir mimic the transition state of this reaction, competitively blocking the active site. M2 channel blockade is the mechanism of amantadine/rimantadine (active only against Influenza A).

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.