Hepatitis E virus (HEV) infection during pregnancy is associated with particularly high mortality. Which immunological mechanism is most important in HEV-associated fulminant hepatic failure in pregnancy?
- A HEV ORF3 protein interacting with progesterone-driven immunological shifts altering Th1/Th2 balance and CD8+ T cell activity ✓
- B Cross-reactive anti-HEV IgM antibodies causing type II hypersensitivity to liver antigens
- C Pre-existing anti-HBs antibodies cross-reacting with HEV capsid protein
- D HEV superinfection on chronic HBV-infected liver causing additive necrosis
Explanation
HEV infection in the third trimester of pregnancy carries a case fatality rate of 15–25% (compared to <1% in non-pregnant adults). The exact mechanism is not fully elucidated but involves the pregnancy-associated shift toward Th2 immunity and progesterone-mediated immunological tolerance. These changes appear to alter antiviral immune control of HEV, allowing higher viral replication and enhanced immunopathology when immune responses are mounted. HEV ORF3 protein has been shown to interact with progesterone receptor membrane component (PGRMC) on hepatocytes, modulating cell survival. Vertical transmission to the neonate also occurs. Anti-HEV IgM does not cause liver damage by type II hypersensitivity; the mechanism is T cell-mediated immunopathology in the context of altered pregnancy immunity.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.