Why has the epidemiology of RSV changed during the COVID-19 pandemic?

نویسندگان

چکیده

The coronavirus disease 2019 (COVID-19) pandemic has drastically perturbed the epidemiology of Respiratory Syncytial Virus (RSV) respiratory tract infections in children. reasons for this are not clear. In article, we review current literature and critically discuss different theories to explain why RSV changed during COVID-19 pandemic. Proposed mechanisms include decreased viral immunity vulnerable age groups caused by prolonged lack circulation early pandemic, potential Severe Acute Syndrome Corona 2 (SARS-CoV-2)-induced immune dysregulation, interactions between SARS-CoV-2 RSV, modifications health-seeking behaviors as well heath systems factors. Research genomics phylogeny, more robust immunology research is needed guide prevention health care resource planning. a leading cause acute young children, with an estimated 30 million cases, 3·6 hospital admissions 100,000 deaths each year, worldwide.1Li Y. Wang X. Blau D.M. et al.Global, regional, national burden estimates lower due syncytial virus children younger than 5 years 2019: systematic analysis.Lancet. 2022; 399: 2047-2064Summary Full Text PDF PubMed Google Scholar Infants six months at higher risk severe disease, particularly those born prematurely, chronic lung or congenital heart neurological conditions immunodeficiency. Yet, healthy term-born infants contribute highest morbidity burden, about one two percent who need hospitalization across jurisdictions.2Wildenbeest J.G. Billard M.N. Zuurbier R.P. al.The Europe: prospective birth cohort study.Lancet Respir Med. 2023; 11: 341-353Summary Scopus (7) typically causes bronchiolitis, characterized distress, cough varying degrees hypoxia airway congestion older might also present apnea infants.3Dalziel S.R. Haskell L. O'Brien S. al.Bronchiolitis.Lancet. 400: 392-406Summary (15) Newborns relatively protected against maternal antibodies transferred via placenta.4Abu-Raya B. Reicherz F. 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Another theory multiple resulted level viruses, including increase co-infections super-infections.38Piret Boivin Viral interference viruses.Emerg 28: 273-281Crossref (40) Regarding both additive subtractive effects, supported observations from experimental models, and/or data.38Piret Indeed, could enhance suppress replication another hosts, through structural functional mucosa, as, example, induction interferon responses.38Piret case available models do support co-infection enhances cytopathogenicity bronchial epithelium model.39Dee Schultz Haney Bissett Magill C. Murcia P.R. Influenza A trigger response blocks syndrome tract.J 227: 1396-1406Crossref Scholar,40Fage Hénaut Carbonneau Piret A(H1N1)pdm09 but interferes sequential nasal epithelial cells.Viruses. 14: 395Crossref Moreover, triggered weaker anti-viral responses cultures interferon-stimulated genes.39Dee Generally, studies prevalence which does prior concurrent led disease.41Agathis N.T. 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Information healthcare providers.https://www.cdc.gov/coronavirus/2019-ncov/hcp/pediatric-hcp.htmlDate addition, parents never infants, propensity seeking once began resurge. deteriorated resources heightened tendency pivot centers consultation, fueled media coverage crises last resurged. gaps care, compounded provider burnouts, document general. This, career workers similarly less illness child, stress further. behavior crisis whether persisted now requires urgent studies. unclear sustainably approach society delaying “normalization” COVID-19. All questions certainly orient effective solutions stabilized frazzled systems. More warranted understand since social contacts adults. Robust interplay phylogenic, Understanding help predict anticipate upcoming season(s). possibility worth investigating, contradiction Zealand Australia. Although virulence, fully understanding will crucial next seasons.

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ژورنال

عنوان ژورنال: EClinicalMedicine

سال: 2023

ISSN: ['2589-5370']

DOI: https://doi.org/10.1016/j.eclinm.2023.102089