A patient with African trypanosomiasis suffers repeated waves of parasitaemia despite mounting a strong antibody response against the parasite each time. The molecular basis of this immune evasion is:

• A Intracellular survival within macrophages by blocking phagolysosome fusion
• B Antigenic variation by sequential switching of variant surface glycoprotein genes ✓
• C Molecular mimicry of host neural antigens
• D Shedding of complement receptors from the parasite surface

Explanation

Trypanosoma brucei is covered by a dense coat of a single variant surface glycoprotein (VSG). The parasite genome contains a large repertoire of VSG genes and pseudogenes, and it switches expression to a new VSG before antibodies clear the current population, producing successive waves of parasitaemia. This is the textbook example of antigenic variation. Unlike Leishmania, trypanosomes remain extracellular in blood, so intracellular survival does not apply.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.