Differential expression of cytokines and elevated levels of MALAT1 - Long non-coding RNA in response to non-structural proteins of human respiratory syncytial virus.

Autor: Dudek I; Department of Molecular Virology, Institute of Microbiology, Faculty of Biology, University of Warsaw, Warsaw, Poland. Electronic address: ji.dudek@uw.edu.pl., Czerkies M; Department of Biosystems and Soft Matter, Institute of Fundamental Technological Research, Polish Academy of Sciences, Warsaw, Poland., Kwiatek A; Department of Molecular Virology, Institute of Microbiology, Faculty of Biology, University of Warsaw, Warsaw, Poland. Electronic address: a.kwiatek2@uw.edu.pl.
Jazyk: angličtina
Zdroj: Virology [Virology] 2024 Sep; Vol. 597, pp. 110127. Date of Electronic Publication: 2024 Jun 01.
DOI: 10.1016/j.virol.2024.110127
Abstrakt: Human Respiratory Syncytial Virus (hRSV), a prevalent respiratory pathogen affecting various age groups, can trigger prolonged and intense inflammation in humans. The severity and outcome of hRSV infection correlate with elevated levels of pro-inflammatory agents, yet the underlying reasons for this immune system overstimulation remain elusive. We focused on the impact of hRSV non-structural proteins, NS1 and NS2, on immune response within epithelial cells. Available data indicates that these proteins impair the interferon pathway. We reinforce that NS1 and NS2 induce heightened secretion of the pro-inflammatory cytokines IL-6 and CXCL8. We also indicate that hRSV non-structural proteins provoke differential gene expression of human host FosB and long non-coding RNAs (MALAT1, RP11-510N19.5). It suggests an impact of NS molecules beyond IFN pathways. Thus, new light is shed on the interplay between hRSV and host cells, uncovering unexplored avenues of viral interference, especially the NS2 role in cytokine expression and immune modulation.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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