{"doi":"10.1002/ctm2.1414","title":"Infant respiratory syncytial virus infection and childhood asthma: A shift in the paradigm?","abstract":"The idea that some non-respiratory viruses can impact health years after the initial infection is well established.1 For example, someone acutely infected with hepatitis B or human papillomavirus can develop a chronic infection that may result in cirrhosis or cervical cancer, respectively, decades later. Whether RNA respiratory viruses (e.g. respiratory syncytial virus [RSV], influenza virus, parainfluenza virus, metapneumovirus, rhinovirus and coronavirus) result in chronic morbidity has been more difficult to study and establish. This is in part because —unlike hepatitis B or human papilloma virus— most RNA respiratory viruses don't become chronic infections, generally cause a mild disease, and don't lead to persistent symptoms in most infected individuals. Thus, despite the recognized global burden associated with RNA respiratory viruses, acute respiratory infections due to these infectious agents have been traditionally thought of as a transient illness with no important long-term effects.2, 3 However, emerging evidence of potentially causal associations between RNA respiratory viruses and the onset of chronic lung diseases (e.g. severe acute respiratory syndrome coronavirus 2 and post coronavirus disease [post-COVID] conditions or human rhinovirus C and childhood asthma) has shifted this paradigm, suggesting that these infectious agents are not merely “in-and-out” and may cause more than an acute self-limited disease.4, 5 This is of significant importance in understanding host risk factors, identifying viral strains resulting in chronic disease, and in considering prevention of long-term complications. Respiratory syncytial virus is the most common etiology of lower respiratory tract infections (LRTIs) in infants worldwide, although it usually causes asymptomatic or mild disease in the majority of infants.3 The potential association between infant RSV LRTIs and childhood asthma was first described in 1959.6 Since then, numerous observational studies and meta-analyses have repeatedly demonstrated that children with an early-life RSV LRTI are at a higher risk of childhood asthma.7-10 However, an RSV LRTI is not an exposure, it is a clinical phenotype. In addition, because RSV LRTIs and childhood asthma share many clinical features (such as wheezing) and could have a shared genetic risk, an RSV LRTI in infancy may just represent the first acute asthma expression in a genetically predisposed child.7, 11, 12 To address this issue, we designed a prospective birth cohort of ∼2000 unselected, healthy term children to test the association of infant RSV infection (and not solely infant RSV LRTI) with childhood asthma.13 This study design has the advantage of avoiding confounding by a shared genetic origin, as we have found no evidence of genetic risk for infant RSV infection.14 Furthermore, this study design gives us the opportunity to study the group of children not infected with RSV in infancy to understand the impact of delaying the infant RSV infection on childhood asthma risk. In contrast, studies focusing on children with an infant RSV LRTI compare this group to those without an infant RSV LRTI, although the latter is a heterogenous group that includes children not infected with RSV in infancy and those who had milder RSV infections in the first year of life. In our study, using molecular and serologic testing to establish RSV infection or no infection during infancy, we found that ∼54% of children are infected with RSV in infancy, which is consistent with other studies.15, 16 Importantly, children without an infant RSV infection had a ∼26% lower risk of childhood asthma than those with an infant RSV infection. In exploratory analyses, infant RSV infection was more strongly associated with development of a non-atopic asthma phenotype. Last, leveraging the population-based study design that included children infected and not infected with RSV in infancy, we estimated that ∼15% cases of childhood asthma could be prevented by de","journal":"Clinical and Translational Medicine","year":2023,"id":375546,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":4,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9608,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2023-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":275878,"name":"Tina V. Hartert","orcid":"0000-0001-7470-1166","position":1,"is_corresponding":false},{"id":388231,"name":"Christian Rosas‐Salazar","orcid":"0000-0001-6644-5780","position":0,"is_corresponding":true}],"reference_count":29,"raw_metadata":null,"created_at":"2026-07-19T01:16:23.381203Z","pmid":"37700493","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}