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Human respiratory syncytial virus (hRSV) is the leading cause of acute lower respiratory tract infections in children under five years of age and older adults worldwide. During hRSV infection, host cells undergo changes in endomembrane organelles, including mitochondria. This organelle is responsible for energy production in the cell and plays an important role in the antiviral response. The present study focuses on characterizing the ultrastructural and functional changes during hRSV infection using thin-section transmission electron microscopy and RT-qPCR. Here we report that hRSV infection alters mitochondrial morphodynamics by regulating the expression of key genes in the antiviral response process, such as Mfn1, VDAC2, and PINK1. Our results suggest that hRSV alters mitochondrial morphology during infection, producing a mitochondrial phenotype with shortened cristae, swollen matrix, and damaged membrane. We also observed that hRSV infection modulates the expression of the aforementioned genes, possibly as an evasion mechanism in the face of cellular antiviral response. Taken together, these results advance our knowledge of the ultrastructural alterations associated with hRSV infection and might guide future therapeutic efforts to develop effective antiviral drugs for hRSV treatment.

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Zika virus (ZIKV) infections have been associated with severe clinical outcomes, including neurological manifestations, especially in newborns with intrauterine infection. However, no licensed vaccines or specific antiviral agents are available yet. Therefore, safe and low-cost therapy is required, especially for pregnant women. In this sense, metformin, an FDA-approved drug used to treat gestational diabetes, has previously exhibited an effect anti-ZIKA in vitro in HUVEC cells by activating AMPK. In this study, we evaluated metformin treatment during in vitro ZIKV infection in a permissive trophoblast cell line JEG3. Our results demonstrate that metformin impacts viral replication and protein synthesis and reverts the cytoskeletal changes promoted by ZIKV infection. Beyond this, lipid droplet formation is reduced, which is associated with the lipogenic activation of infection. Taken together, our findings indicate that metformin has potential as an antiviral agent against in vitro ZIKV infection in trophoblastic cells.