Respiratory Syncytial Virus Infection in Adults

Falsey, Ann R.

doi:10.1055/s-2007-976489

Cited by 187 publications

(173 citation statements)

References 109 publications

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“…RSV appears in epidemics [Waris, 1991]. Immunity after infection is low and reinfections are common among both children and adults [Henderson et al, 1979;Falsey and Walsh, 2000].…”

Section: Introductionmentioning

confidence: 99%

Molecular epidemiology and genetic variability of respiratory syncytial virus (RSV) in Stockholm, 2002–2003

Östlund¹,

Lindell²,

Stenler³

et al. 2007

Journal of Medical Virology

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The epidemiology and genetic variability of circulating respiratory syncytial virus (RSV) strains in Stockholm during the season 2002-2003 were studied in consecutive RSV isolates derived from respiratory samples and diagnosed in the laboratory. Two hundred thirty-four viruses were sequenced. The samples were mainly from children under 1 year old (79%). The phylogeny of the N-terminal part of the G gene was studied after amplification and sequencing. One hundred fifty-two viruses belonged to subgroup B and 82 to subgroup A. The subgroup A viruses could be further divided into genotypes GA2 (25) and GA5 (57) and the subgroup B viruses into GB3 (137) and SAB1 (15) strains. These strains clustered with subgroup A and subgroup B strains from Kenya from the same period, as well as with strains from Great Britain from 1995 to 1998. The dominance of subgroup B strains in Stockholm during 2002-2003 is in agreement with findings from other parts of the world during the same years. Only two genotypes of subgroup A, GA2 and GA5, were circulating during this time, and GA2 has been circulating in Sweden for more than 20 years. Consecutive strains from the same individual displayed no variability in the sequenced region, which was also true of strains that had been passaged in cell cultures.

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“…RSV appears in epidemics [Waris, 1991]. Immunity after infection is low and reinfections are common among both children and adults [Henderson et al, 1979;Falsey and Walsh, 2000].…”

Section: Introductionmentioning

confidence: 99%

Molecular epidemiology and genetic variability of respiratory syncytial virus (RSV) in Stockholm, 2002–2003

Östlund¹,

Lindell²,

Stenler³

et al. 2007

Journal of Medical Virology

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“…Clinically, the role of RSV infection in COPD has become better defined, with several groups demonstrating that the inflammatory process is augmented in the presence of such infection (67,68). One of these groups has suggested that persistence of infection may be particularly important in progression of the underlying obstructive process (67), although this remains controversial (69). It is evident that viral infection could account for the inflammatory response previously described as typical of an AE-COPD.…”

Section: Virusesmentioning

confidence: 99%

“…The therapy for RSV is largely supportive, although aerosolized ribavirin has been licensed for use in infants (69). This agent is a guanosine analog with broad antiviral properties (69).…”

Section: Pathogen-specific Therapymentioning

confidence: 99%

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Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Martínez

2007

Proceedings of the American Thoracic Society

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Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the natural history of this chronic lung disorder. These events can be caused by a large number of infectious and noninfectious agents and are associated with an increased local and systemic inflammatory response. Their frequency and severity have been linked to progressive deterioration in lung function and health status. Infectious pathogens ranging from viral to atypical and typical bacteria have been implicated in the majority of episodes. Most therapeutic regimens to date have emphasized broad, nonspecific approaches to bronchoconstriction and pulmonary inflammation. Increasingly, therapy that targets specific etiologic pathogens has been advocated. These include clinical and laboratory-based methods to identify bacterial infections. Further additional investigation has suggested specific pathogens within this broad class. As specific antiviral therapies become available, better diagnostic approaches to identify specific pathogens will be required. Furthermore, prophylactic therapy for at-risk individuals during high-risk times may become a standard therapeutic approach. As such, the future will likely include aggressive diagnostic algorithms based on the combination of clinical syndromes and rapid laboratory modalities to identify specific causative bacteria or viruses.

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“…Respiratory syncytial virus (RSV) is the most common cause of hospitalization in children under the age of 2 years (Wright and Piedimonte 2011). In addition, RSV adversely affects the elderly and immunocompromised individuals, causing severe lower respiratory tract infection and pneumonia (Falsey 2007). This virus first replicates in epithelial cells of the upper respiratory tract and then migrates throughout the lungs, where it induces pulmonary inflammation, epithelial cell necrosis, and mucus plugging leading to airway obstruction and lung hyperinflation (Simoes 2008; Wright and Piedimonte 2011).…”

Section: Introductionmentioning

confidence: 99%

Nanoparticles increase human bronchial epithelial cell susceptibility to respiratory syncytial virus infection via nerve growth factor-induced autophagy

et al. 2017

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Cytotoxic and neuroinflammatory effects of TiO2 nanoparticles (TiO2‐NP) in human airways are mediated by nerve growth factor (NGF), which is also implicated in the pathophysiology of respiratory syncytial virus (RSV) infection. We tested the hypothesis that exposure to TiO2‐NP results in increased susceptibility to RSV infection and exacerbation of airway inflammation via NGF‐mediated induction of autophagy in lower respiratory tract cells. Human primary bronchial epithelial cells were exposed to TiO2‐NP for 24 h prior to infection with recombinant red RSV (rrRSV). Expression of NGF and its TrkA and p75NTR receptors was measured by real‐time PCR and fluorescence‐activated cell sorting (FACS). Autophagy was assessed by beclin‐1 expression analysis. Cell death was studied by FACS after annexin V/propidium iodide staining. rrRSV infection efficiency more than doubled in human bronchial cells pre‐exposed to TiO2‐NP compared to controls. NGF and its TrkA receptor were upregulated in RSV‐infected bronchial cells pre‐exposed to TiO2‐NP compared to controls exposed to either rrRSV or TiO2‐NP alone. Silencing NGF gene expression with siRNA significantly inhibited rrRSV infection. rrRSV‐infected cells pre‐exposed to TiO2‐NP also showed increase in necrotic cell death and reduction in apoptosis, together with 4.3‐fold increase in expression of the early autophagosomal gene beclin‐1. Pharmacological inhibition of beclin‐1 by wortmannin resulted in increased apoptotic rate along with lower viral load. This study shows that TiO2‐NP exposure enhances the infectivity of RSV in human bronchial epithelial cells by upregulating the NGF/TrkA axis. The mechanism of this interaction involves induction of autophagy promoting viral replication and necrotic cell death.

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Respiratory Syncytial Virus Infection in Adults

Cited by 187 publications

References 109 publications

Molecular epidemiology and genetic variability of respiratory syncytial virus (RSV) in Stockholm, 2002–2003

Molecular epidemiology and genetic variability of respiratory syncytial virus (RSV) in Stockholm, 2002–2003

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Nanoparticles increase human bronchial epithelial cell susceptibility to respiratory syncytial virus infection via nerve growth factor-induced autophagy

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