Affiliations 

  • 1 School of Pharmacy, University of Nottingham Malaysia, Semenyih, Malaysia
  • 2 School of Medicine, International Medical University, Kuala Lumpur, Malaysia; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; Taiwan International Graduate Program in Molecular Medicine, National Yang Ming Chiao Tung University and Academia Sinica, Taipei, Taiwan
  • 3 School of Medicine, International Medical University, Kuala Lumpur, Malaysia
  • 4 School of Medicine, International Medical University, Kuala Lumpur, Malaysia; Institute for Research, Development and Innovation (IRDI), International Medical University, Kuala Lumpur, Malaysia
  • 5 Faculty of Medicine and Health Sciences, University Tunku Abdul Rahman, Sg Long, Malaysia
  • 6 Programme in Emerging Infectious Diseases, Duke-NUS Medical School, 169857, Singapore; Infectious Diseases Translational Research Programme, Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
  • 7 Programme in Emerging Infectious Diseases, Duke-NUS Medical School, 169857, Singapore
  • 8 Institute for Research, Development and Innovation (IRDI), International Medical University, Kuala Lumpur, Malaysia; AGTC Genomics, Bukit Jalil, Kuala Lumpur 57000, Malaysia
  • 9 School of Pharmacy, University of Nottingham Malaysia, Semenyih, Malaysia; School of Medicine, International Medical University, Kuala Lumpur, Malaysia. Electronic address: kenny.voon@nottingham.edu.my
Microbes Infect, 2024;26(1-2):105243.
PMID: 38380604 DOI: 10.1016/j.micinf.2023.105243

Abstract

Pteropine orthoreovirus (PRV) causes respiratory tract infections in humans. Despite its emergence as a zoonotic and respiratory virus, little is known about its cell tropism, which hampers progress in fully understanding its pathogenesis in humans. Hek293 cells are most susceptible to PRV infection, while HeLa cells are the least. Human cytokeratin 1 (CK1) was identified as the protein that interacts with PRV. The immunofluorescence assay and qPCR results revealed prior treatment with anti-CK1 may provide Hek293 cells protection against PRV. The KRT1-knockout Hek293 cells were less susceptible to PRV infection. Further study into the pathogenesis of PRV in humans is needed.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.