Ultrastructural and Functional Characterization of Mitochondrial Dynamics Induced by Human Respiratory Syncytial Virus Infection in HEp-2 Cells

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 responsibl...

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Vydáno v:Viruses Ročník 15; číslo 7; s. 1518
Hlavní autoři: Lara-Hernandez, Ignacio, Muñoz-Escalante, Juan Carlos, Bernal-Silva, Sofía, Noyola, Daniel E., Wong-Chew, Rosa María, Comas-García, Andreu, Comas-Garcia, Mauricio
Médium: Journal Article
Jazyk:angličtina
Vydáno: Switzerland MDPI AG 07.07.2023
MDPI
Témata:
Analysis
Antiviral agents
Antiviral drugs
Apoptosis
Cristae
Development and progression
Diagnosis
energy
Evaluation
Genetic regulation
Genotype & phenotype
Hepatitis
Human orthopneumovirus
human respiratory syncytial virus
Immune response
Infections
Kinases
Mitochondria
mitochondrial alterations
Organelles
Pathogenesis
phenotype
Phenotypes
Physiological aspects
Proteins
PTEN-induced putative kinase
Respiratory syncytial virus
Respiratory syncytial virus infection
respiratory system
Respiratory tract diseases
Sodium
Structure
therapeutics
Transmission electron microscopy
ultrastructural characterization
Viral infections
Viruses
Mexico
Grand Island
United States > US
mitochondrial alterations
ultrastructural characterization
human respiratory syncytial virus
ISSN:1999-4915, 1999-4915
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Shrnutí: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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ISSN:1999-4915
1999-4915
DOI:10.3390/v15071518