BRIEF RESEARCH REPORT article
Front. Cell. Infect. Microbiol.
Sec. Virus and Host
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1613386
This article is part of the Research TopicPerspectives in Virus and Host: 2025View all 6 articles
Host Cellular Transcriptional Response to Respiratory Syncytial Virus Infection in HEp-2 Cells: Insights from cDNA Microarray and Quantitative PCR Analyses
Provisionally accepted
Manoj Kumar Pastey1*
Christopher Lupfer2- 1Oregon State University, Corvallis, United States
- 2Missouri State University, Springfield, Illinois, United States
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Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections in young children, elderly and immunocompromised, To elucidate host-virus interactions at the transcriptional level, we analyzed differential gene expression in HEp-2 cells infected with RSV using cDNA microarray analysis complemented by quantitative PCR (qPCR). Radiolabeled cDNA probes from RSV-infected were hybridized to Atlas® Human Cancer cDNA arrays, and differential gene expression was quantified by densitometry. We identified 12 host genes that were significantly upregulated in RSV-infected cells from the cDNA microarray (≥2-fold increase, P<0.01), confirmed by qPCR, encompassing functional categories including cell cycle regulation, cytoskeletal organization, apoptosis modulation, immune evasion, and inflammation. Notably, the cyclin-dependent kinase inhibitor CDKN1A was induced ~14-fold, suggesting RSV triggers a host cell cycle arrest. The intermediate filament protein, vimentin was up ~6-fold, consistent with cytoskeletal rearrangements observed during viral syncytium formation. Anti-apoptotic MCL1 increased ~11-fold, while pro-apoptotic caspase-4 showed a more modest 1.6-fold rise, indicating a complex regulation of cell death pathways. We also observed marked upregulation of a fibronectin receptor subunit (~24-fold) and complement regulatory protein CD59 (~2-fold), highlighting potential mechanisms of enhanced cell-cell fusion and viral immune evasion. Interleukin-6 was elevated ~7-fold, underscoring the inflammatory response to RSV. These findings provide a global snapshot of the host transcriptomic response to RSV infection and yield insights into how RSV modulates host cellular machinery to favor viral replication and spread. Understanding these host-virus interactions may unveil novel targets for antiviral therapy and inform strategies to mitigate RSV disease pathogenesis.
Keywords: respiratory syncytial virus, Host-virus interactions, Gene Expression, host transcriptomic response, Microarray
Received: 17 Apr 2025; Accepted: 04 Jun 2025.
Copyright: © 2025 Pastey and Lupfer. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Manoj Kumar Pastey, Oregon State University, Corvallis, United States
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