Virus meets host
The evidence connects viral RNA structure, mitophagy, entry co-factors, iron-linked receptor abundance, infected-cell trafficking, and Dicer–Ago2 antiviral RNAi.
Identifying viral structures and host pathways that govern entry, survival, susceptibility, spread, and restriction.
The evidence connects viral RNA structure, mitophagy, entry co-factors, iron-linked receptor abundance, infected-cell trafficking, and Dicer–Ago2 antiviral RNAi.
PRRSV infectious clones, porcine epithelial systems, newborn piglets, sow–colostrum–neonate transmission, avian macrophages, and SPF chickens.
Clone rescue, gene silencing, receptor blocking, signaling and endocytosis perturbation, iron manipulation, animal challenge, cell tracking, small-RNA mapping, and nucleic-acid intervention.
Targets appear in viral RNA, entry machinery, host metabolism, stress control, cell trafficking, and sequence-specific RNA defense.
Independent editorial synthesis · reviewed 7 September 2026
ORCID 0000-0002-2349-0028 · NJAU College of Veterinary Medicine
Six papers selected for conceptual importance and temporal coverage. They are examples, not a substitute for the complete reconciled bibliography.
In PRRSV infectious-clone experiments, the proximal 5′-UTR stem-loop structure—not a fixed primary sequence—was consistently required for infectivity.
Official bibliography role: Correspondence AuthorTGEV-induced DJ-1-associated mitophagy limited oxidative stress and apoptosis in porcine cells; the net effect in animals was not established.
Verified paper role: Correspondence AuthorEGFR acted with APN and entry-linked signaling as a TGEV co-factor; it was not proposed as a replacement for the known receptor.
Official bibliography role: Correspondence AuthorHigh apical TfR1 and iron deficiency increased PEDV susceptibility in neonatal and cell models, identifying an age-linked entry mechanism rather than a treatment recommendation.
Official bibliography role: Correspondence AuthorThe study supports infected T-cell movement from sow intestine through blood and mammary tissue into colostrum, without estimating its population-level share of transmission.
Official bibliography role: Correspondence AuthorWild-type avian coronavirus and influenza infection generated Dicer–Ago2 antiviral vsiRNAs; the proposed therapeutic-vaccine route remains experimental.
Official bibliography role: Participating authorsThese overlapping themes are an editorial synthesis of the publication record. They do not claim sole scientific ownership, clinical validation, regulatory approval, or independent replication. Titles and bibliographic facts come from the reconciled record; explanatory summaries are constrained to the cited evidence.