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Host cellular transcriptional response to respiratory syncytial virus infection in HEp-2 cells: insights from cDNA microarray and quantitative PCR analyses
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Host cellular transcriptional response to respiratory syncytial virus infection in HEp-2 cells: insights from cDNA microarray and quantitative PCR analyses
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Journal Article
Host cellular transcriptional response to respiratory syncytial virus infection in HEp-2 cells: insights from cDNA microarray and quantitative PCR analyses
2025
Overview
Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections in young children and elderly, worldwide and poses significant risks to immunocompromised individuals. 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). HEp-2 cells were infected with RSV at a multiplicity of infection of 1, and total RNA was isolated 24 hours post-infection for gene expression profiling. Radiolabeled cDNA probes from RSV-infected and mock-infected cells 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. The proinflammatory cytokine 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.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Arrays
/ Cancer
/ Cellular and Infection Microbiology
/ host transcriptomic response
/ Host-Pathogen Interactions - genetics
/ Humans
/ Oligonucleotide Array Sequence Analysis
/ Real-Time Polymerase Chain Reaction
/ Respiratory Syncytial Virus Infections - genetics
/ Respiratory Syncytial Virus Infections - virology
/ Respiratory Syncytial Virus, Human - physiology
/ Vimentin
/ Viruses
