ArticleFrontiers in cellular and infection microbiology2025
Myeloid Cell Leukemia-1 knockout leads to increased viral propagation of Respiratory Syncytial Virus and influenza virus in mouse embryonic fibroblast cells and A549 cells: implications in cancer therapy.
Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Host mitochondrial apoptotic signatures in children with chronic conditions reveal viral modulation of MCL-1 in severe SARS-CoV-2 infection.Molecular biology reports · 2026Article
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3 authors.
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Abstract
Introduction: Respiratory Syncytial Virus (RSV) remains a significant global health burden, particularly affecting young children, elderly individuals, and immunocompromised patients. The antiapoptotic protein Myeloid Cell Leukemia-1 (Mcl-1) is rapidly upregulated following RSV infection; however, its functional significance in viral pathogenesis remains poorly defined. Methods: We investigated the role of Mcl-1 during RSV infection using Mcl-1 knockout mouse embryonic fibroblasts (ΔMcl-1 MEFs) and human alveolar epithelial (A549) cells subjected to small interfering RNA (siRNA)-mediated Mcl-1 knockdown. Viral replication was quantified by plaque assays, and phenotypic effects were assessed through syncytia formation and apoptosis assays. To assess broader implications, influenza A virus replication was also evaluated in ΔMcl-1 MEFs and Mcl-1-silenced A549 cells. Results: RSV replication was significantly enhanced in ΔMcl-1 MEFs compared to wild-type (WT) controls, with increased viral titers, larger syncytia formation, and elevated apoptosis during the late stages of infection. Consistent results were observed in A549 cells following Mcl-1 knockdown, where RSV titers increased by more than 3 log₁₀. Influenza A virus replication was also markedly elevated in ΔMcl-1 MEFs and siRNA-treated A549 cells, suggesting that Mcl-1 exerts a broad antiviral effect across multiple respiratory viruses. Discussion: These findings indicate that Mcl-1 upregulation during RSV and influenza virus infection functions as a critical host antiviral defense mechanism, rather than a viral evasion strategy. Clinically, our results raise concerns regarding therapies that target Mcl-1, such as certain anticancer treatments, which may inadvertently increase susceptibility to severe viral infections. Careful monitoring and potential prophylactic antiviral interventions may be warranted in patients receiving Mcl-1 inhibitor therapies.
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