Poster Presentation: HOOKWORM–SARS-CoV-2 COINFECTION: TRANSCRIPTOMIC MODULATION IN HAMSTERS

Abstract

Background: Helminth infections are known to modulate host immune responses and may influence the clinical severity of viral infections such as COVID-19. However, the molecular mechanisms underlying helminth–SARS-CoV-2 coinfection remain poorly understood.

Aim: To evaluate the impact of hookworm (Ancylostoma ceylanicum) infection on lung and intestinal transcriptomic responses following SARS-CoV-2 infection in a Syrian hamster model.

Methods: Syrian hamsters were divided into four groups: naïve, hookworm-only (HW), SARS-CoV-2-only (CoV), and coinfected (HW+CoV). Hookworm infection was established prior to SARS-CoV-2 challenge. Clinical outcomes, viral titers, and tissue-specific transcriptomic profiles were assessed using RNA sequencing and differential gene expression analysis.

Results: Both CoV and HW+CoV groups exhibited comparable weight loss and viral titers, indicating no effect of hookworm infection on viral replication. Transcriptomic analysis revealed significant modulation of host responses in coinfected animals. In the lung, coinfection was associated with upregulation of B-cell and immunoglobulin-related genes (including JCHAIN) and downregulation of inflammatory pathways such as TLR signaling and severity-associated markers (CHI3L1, HMOX1), suggesting attenuation of hyperinflammation. In contrast, the intestine demonstrated increased expression of inflammatory genes (e.g., FOLR2, PLA2G4F) and reversal of interferon suppression, indicating enhanced local immune activation.

Conclusion: Hookworm coinfection reprograms host immune responses during SARS-CoV-2 infection, promoting protective immunomodulation in the lung while enhancing inflammatory responses in the intestine, without affecting viral load.