Epidemiologic, Experimental, and Clinical Links between Respiratory Syncytial Virus Infection and Asthma

Mohapatra, Shyam S.; Boyapalle, Sandhya

doi:10.1128/cmr.00054-07

Cited by 109 publications

(89 citation statements)

References 138 publications

(126 reference statements)

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“…A wide range of epidemiological studies support the observation that infants with recurrent RSV infection are more prone than others to develop asthmatic bronchitis and bronchial asthma some years later (Mohapatra and Boyapalle, 2008;Stensballe et al, 2009).…”

Section: Introductionmentioning

confidence: 84%

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Li¹,

Wu²,

Li³

et al. 2012

Genet. Mol. Res.

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ABSTRACT. We examined the underlying neural-endocrine mechanisms of asthma associated with respiratory syncytial virus infection. Thirty Sprague-Dawley rats were randomly divided into control group, respiratory syncytial virus (RSV) group, and anti-nerve growth factor (NGF) IgG group. An RSV infection model was established by nasal drip once a week. In the anti-NGF antibody intervention group, each rat was given an intraperitoneal injection of anti-NGF IgG 3 h before RSV infection. Optical microscopy and transmission electron microscopy were used to observe the structural changes in adrenal medulla cells. Changes in adrenaline and norepinephrine in serum were detected by ELISA. NGF expression was assayed by immunohistochemistry. Expression differences in synaptophysin mRNA were detected by RT-PCR. Transmission electron microscopy displayed widened adrenal medulla intercellular spaces, reduced chromaffin particle concentration, and increased mitochondria in the RSV infection group. At the same time, NGF expression was increased in the RSV infection group significantly. In addition, the adrenaline concentration was significantly Mechanisms of respiratory syncytial virus-associated asthma decreased compared with the control and anti-NGF antibody groups. Synaptophysin mRNA expression was significantly increased in the RSV infection and anti-NGF antibody groups. However, compared with the RSV infection group, synaptophysin mRNA expression was significantly decreased in the anti-NGF antibody group. We conclude that RSV infection could induce adrenal medulla cell differentiation to nerve cells by over-expression of NGF, resulting in the decreased endocrine function found in asthma progression.

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Section: Introductionmentioning

confidence: 84%

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Li¹,

Wu²,

Li³

et al. 2012

Genet. Mol. Res.

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“…RSVinduced lower respiratory tract infection (LRTI), a complication of RSV infection of immunologically naïve children, represents the more clinically significant of these diseases. In the United States alone, LRTI accounts for 120,000 hospitalizations annually and is associated with postinfectious sequelae of recurrent episodic wheezing (36,43,44). Despite the fact that nearly 100% of U.S. children are infected by RSV before the age of 3, there is no efficacious vaccine or treatment (51).…”

mentioning

confidence: 99%

RelA Ser276 Phosphorylation-Coupled Lys310 Acetylation Controls Transcriptional Elongation of Inflammatory Cytokines in Respiratory Syncytial Virus Infection

Brasier

Tian

Jamaluddin

et al. 2011

J Virol

135

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Respiratory syncytial virus (RSV) is a negative-sense single-stranded RNA virus responsible for lower respiratory tract infections (LRTIs) in humans. In experimental models of RSV LRTI, the actions of the nuclear factor B (NF-B) transcription factor mediate inflammation and pathology. We have shown that RSV replication induces a mitogen-and-stress-related kinase 1 (MSK-1) pathway that activates NF-B RelA transcriptional activity by a process involving serine phosphorylation at serine (Ser) residue 276. In this study, we examined the mechanism by which phospho-Ser276 RelA mediates expression of the NF-B-dependent gene network. RelA-deficient mouse embryonic fibroblasts (

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“…Approximately 2 to 3% of infected infants and an increasing number of elderly patients develop significant morbidity and mortality from RSV infection (4,54,59,62). Although the mechanism is unclear, early, severe RSV infection is a risk factor for recurrent wheezing and asthma (42,45). In infants, RSV can cause bronchiolitis, leading to severe respiratory illness requiring hospitalization (ϳ120,000 cases/year in the United States) (4,54,59).…”

mentioning

confidence: 99%

Genomewide Association Analysis of Respiratory Syncytial Virus Infection in Mice

Stark

Barmada

Winterberg

et al. 2010

J Virol

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Respiratory syncytial virus (RSV) is the major cause of lower respiratory tract infection in infants, with about half being infected in their first year of life. Yet only 2 to 3% of infants are hospitalized for RSV infection, suggesting that individual susceptibility contributes to disease severity. Previously, we determined that AKR/J (susceptible) mice developed high lung RSV titers and showed delayed weight recovery, whereas C57BL/6J (resistant) mice demonstrated low lung RSV titers and rapid weight recovery. In addition, we have reported that gene-targeted mice lacking the cystic fibrosis transmembrane conductance regulator (Cftr; ATP-binding cassette subfamily C, member 7) are susceptible to RSV infection. For this report, recombinant backcross and F2 progeny derived from C57BL/6J and AKR/J mice were infected with RSV, their lung titers were measured, and quantitative trait locus (QTL) analysis was performed. A major QTL, designated Rsvs1, was identified on proximal mouse chromosome 6 in both recombinant populations. Microarray analysis comparing lung transcripts of the parental strains during infection identified several candidate genes that mapped to the Rsvs1 interval, including Cftr. These findings add to our understanding of individual RSV susceptibility and strongly support a modifier role for CFTR in RSV infection, a significant cause of respiratory morbidity in infants with cystic fibrosis.A major cause of lower respiratory tract infection during infancy and childhood, respiratory syncytial virus (RSV) produces annual epidemics in which Ͼ50% of infants are infected during their first RSV season, and nearly all children are infected by 2 to 3 years of age (25,32). Approximately 2 to 3% of infected infants and an increasing number of elderly patients develop significant morbidity and mortality from RSV infection (4,54,59,62). Although the mechanism is unclear, early, severe RSV infection is a risk factor for recurrent wheezing and asthma (42, 45). In infants, RSV can cause bronchiolitis, leading to severe respiratory illness requiring hospitalization (ϳ120,000 cases/year in the United States) (4, 54, 59). Severe RSV infections are more likely to occur in patients that are immunocompromised or in infants born prematurely. Outside of these high-risk groups, it is not clear why only a small percentage of children develop severe illness.While almost every child becomes infected with RSV, the gene-environment interactions that predispose children to develop severe RSV infection are unknown. Previous studies of children have suggested several candidate genes associated with severe RSV infection, including polymorphisms in surfactant-associated proteins A and D (34, 36, 49) and several cytokines (21,23,26,27,50). However, these genetic differences explain only a part of the variable response to RSV infection, making it difficult to assess the specific role(s) of these genes in disease severity. Severity of RSV infection is likely to be a complex trait and involves differences that control the initial infect...

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Epidemiologic, Experimental, and Clinical Links between Respiratory Syncytial Virus Infection and Asthma

Cited by 109 publications

References 138 publications

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

RelA Ser276 Phosphorylation-Coupled Lys310 Acetylation Controls Transcriptional Elongation of Inflammatory Cytokines in Respiratory Syncytial Virus Infection

Genomewide Association Analysis of Respiratory Syncytial Virus Infection in Mice

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