Influenza viruses pose significant global health threats, causing widespread morbidity and mortality due to their genetic variability and rapid evolution. Traditional experimental models, such as immortalized cell lines and animal models, often fall short of accurately replicating the complex interactions between influenza viruses and the human immune system. Recent advancements, including reconstituted human airway epithelia, lung-on-a-chip models, and human airway organoids, provide more accurate representations of human respiratory physiology and immune responses. These alternatives enable in-depth investigations into viral propagation, host immune responses, and tissue damage. While each model has its unique advantages and limitations, integrating them could offer a more comprehensive understanding of influenza pathogenesis. This knowledge can drive the development and evaluation of more effective vaccines and therapeutic interventions, enhancing preparedness for future influenza outbreaks.
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http://dx.doi.org/10.1016/j.coviro.2025.101452 | DOI Listing |
Proc Natl Acad Sci U S A
March 2025
State Key Laboratory for Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730000, People's Republic of China.
6-methyladnosine (mA) modification is present in both positive- and negative-strand RNA of influenza A virus (IAV) and affects the replication and pathogenicity of IAV. However, little is known about the regulatory mechanism of mA in IAV RNA. In the present study, we identified the mA methylation of the viral RNA of different IAV subtypes and confirmed that mA modification promotes the polymerase activity and replication of IAV.
View Article and Find Full Text PDFImmun Inflamm Dis
March 2025
Pandemic Preparedness, Infection, and Advanced Research Center, The University of Tokyo, Tokyo, Japan.
Background: COVID-19, caused by SARS-CoV-2, was first documented in Japan in January 2020. We previously reported an increased risk of rhinovirus infections among children during the early phase of the COVID-19 pandemic. Here, we assessed the impact of COVID-19 on respiratory virus infections after SARS-CoV-2 spread nationwide.
View Article and Find Full Text PDFPLoS Negl Trop Dis
March 2025
CSIR Institute of Genomics and Integrative Biology (CSIR-IGIB), New Delhi, India.
Background: COVID-19 pandemic had unprecedented global impact on health and society, highlighting the need for a detailed understanding of SARS-CoV-2 evolution in response to host and environmental factors. This study investigates the evolution of SARS-CoV-2 via mutation dynamics, focusing on distinct age cohorts, geographical location, and vaccination status within the Indian population, one of the nations most affected by COVID-19.
Methodology: Comprehensive dataset, across diverse time points during the Alpha, Delta, and Omicron variant waves, captured essential phases of the pandemic's footprint in India.
Pediatr Infect Dis J
March 2025
Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee.
Background: Respiratory syncytial virus (RSV) is a major cause of severe respiratory infections in infants, especially under 5 years of age. Several studies have reported that interactions between RSV and bacteria like Streptococcus pneumoniae (SP), Moraxella catarrhalis (MC), Haemophilus influenzae (HI) and Staphylococcus aureus (SA) may influence their pathogenicity and the clinical outcome of infection. However, existing knowledge about RSV-bacterial interactions in infants comes primarily from cross-sectional studies, which cannot evaluate the influence of infection sequence on these interactions.
View Article and Find Full Text PDFHost-specific factors, including genetic background and sex, shape viral adaptation and influence virulence, yet their interactions and quantitative effects remain poorly understood. Additionally, multiple infections, where a host is infected with viruses from more than one source, are hypothesized to enhance viral diversity and increase virulence, but their impact in vertebrate hosts remains largely unexplored. We experimentally adapted influenza A virus (IAV) to male and female BALB/c and C57BL/6 mice under single and multiple infection conditions.
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