Respiratory Syncytial Virus Infection in Homeless Populations, Washington, USA

Boonyaratanakornkit, Jim; Ekici, Seda; Magaret, Amalia; Gustafson, Kathryn E.; Scott, Emily; Haglund, Micaela; Kuypers, Jane; Pergamit, Ronald; Lynch, John B.; Chu, Helen Y.

doi:10.3201/eid2507.181261

Cited by 11 publications

(13 citation statements)

References 13 publications

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“…With the more recent identification of group 2 and group 3 innate lymphoid cell subsets, or ILC2 and ILC3, that mimic IL-13 producing T helper (TH2) and TH17 cells in cytokine production, respectively, we chose to examine these innate lymphoid cell populations for their contributions to viral-induced asthma exacerbation. We further chose Respiratory Syncytial Virus-A2 (RSV-A2) for our studies as the RSV-specific response generates substantial TSLP, IL-25 and IL-33 and mucus production [6,7,14], and this virus has been well characterized for exacerbating OVA-induced inflammation previously [15][16][17][18][19][20]. Clinical data also suggests that asthmatic individuals are at greater risk of respiratory complication from community-acquired RSV infections in comparison to otherwise healthy counterparts [18,21,22].…”

Section: Introductionmentioning

confidence: 99%

Neutralization of IL-33 modifies the type 2 and type 3 inflammatory signature of viral induced asthma exacerbation

et al. 2021

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Background Respiratory viral infections are one of the leading causes of need for emergency care and hospitalizations in asthmatic individuals, and airway-secreted cytokines are released within hours of viral infection to initiate these exacerbations. IL-33, specifically, contributes to these allergic exacerbations by amplifying type 2 inflammation. We hypothesized that blocking IL-33 in RSV-induced exacerbation would significantly reduce allergic inflammation. Methods Sensitized BALB/c mice were challenged with aerosolized ovalbumin (OVA) to establish allergic inflammation, followed by RSV-A2 infection to yield four treatment groups: saline only (Saline), RSV-infected alone (RSV), OVA alone (OVA), and OVA-treated with RSV infection (OVA-RSV). Lung outcomes included lung mRNA and protein markers of allergic inflammation, histology for mucus cell metaplasia and lung immune cell influx by cytospin and flow cytometry. Results While thymic stromal lymphopoietin (TSLP) and IL-33 were detected 6 h after RSV infection in the OVA-RSV mice, IL-23 protein was uniquely upregulated in RSV-infected mice alone. OVA-RSV animals varied from RSV- or OVA-treated mice as they had increased lung eosinophils, neutrophils, group 2 innate lymphoid cells (ILC2) and group 3 innate lymphoid cells (ILC3) detectable as early as 6 h after RSV infection. Neutralized IL-33 significantly reduced ILC2 and eosinophils, and the prototypical allergic proteins, IL-5, IL-13, CCL17 and CCL22 in OVA-RSV mice. Numbers of neutrophils and ILC3 were also reduced with anti-IL-33 treatment in both RSV and OVA-RSV treated animals as well. Conclusions Taken together, our findings indicate a broad reduction in allergic-proinflammatory events mediated by IL-33 neutralization in RSV-induced asthma exacerbation.

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Section: Introductionmentioning

confidence: 99%

Neutralization of IL-33 modifies the type 2 and type 3 inflammatory signature of viral induced asthma exacerbation

et al. 2021

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“…Limited data describing RSV infections among PEH suggests that homelessness is a risk factor for hospitalization with RSV infection 14 . If targeted treatments for RSV become available, providing access to testing for RSV will be a key step in ensuring timely access to antivirals for patients in this vulnerable group.…”

Section: Discussionmentioning

confidence: 99%

“…Limited data describing RSV infections among PEH suggests that homelessness is a risk factor for hospitalization with RSV infection. 14 If targeted treatments for RSV become available, providing access to testing for RSV will be a key step in ensuring timely access to antivirals for patients in this vulnerable group. Our data showed substantial overlap in the seasonal peaks and clinical presentations of RSV and influenza, suggesting that rapid, accurate testing will be necessary because clinical diagnosis is not sufficient to ascertain the cause of acute respiratory disease.…”

Section: Discussionmentioning

confidence: 99%

Respiratory syncytial virus and other respiratory virus infections in residents of homeless shelters – King County, Washington, 2019–2021

McCulloch

Rogers

Wang

et al. 2023

Influenza Resp Viruses

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Respiratory syncytial virus (RSV) causes disproportionate morbidity and mortality in vulnerable populations. We tested residents of homeless shelters in Seattle, Washington for RSV in a repeated cross-sectional study as part of community surveillance for respiratory viruses. Of 15 364 specimens tested, 35 had RSV detected, compared to 77 with influenza. The most common symptoms for both RSV and influenza were cough and rhinorrhea. Many individuals with RSV (39%) and influenza (58%) reported that their illness significantly impacted their ability to perform their regular activities. RSV and influenza demonstrated similar clinical presentations and burden of illness in vulnerable populations living in congregate settings.

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“…With the more recent identi cation of group 2 and group 3 innate lymphoid cell subsets, or ILC2 and ILC3, that mimic IL-13 producing T helper (TH2) and TH17 cells in cytokine production, respectively, we chose to examine these innate lymphoid cell populations for their contributions to viral-induced asthma exacerbation. We further chose Respiratory Syncytial Virus-A2 (RSV-A2) for our studies as the RSV-speci c response generates substantial TSLP, IL-25 and IL-33 and mucus production (6,7,14), and this virus has been well characterized for exacerbating OVA-induced in ammation previously (15)(16)(17)(18)(19)(20). Clinical data also suggests that asthmatic individuals are at greater risk of respiratory complication from community-acquired RSV infections in comparison to otherwise healthy counterparts (18,21,22).…”

Section: Introductionmentioning

confidence: 99%

Neutralization of IL-33 Modifies the Type 2 and Type 3 Inflammatory Signature of Viral Induced Asthma Exacerbation.

Warren

Poole

Sweeter

et al. 2021

Preprint

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Background: Respiratory viral infections are one of the leading causes of need for emergency care and hospitalizations in asthmatic individuals, and airway-secreted cytokines are released within hours of viral infection to initiate these exacerbations. IL-33, specifically, contributes to these allergic exacerbations by amplifying type 2 inflammation. We hypothesized that blocking IL-33 in RSV-induced exacerbation would significantly reduce allergic inflammation. Methods: Sensitized BALB/c mice were challenged with aerosolized ovalbumin (OVA) to establish allergic inflammation, followed by RSV-A2 infection to yield four treatment groups: Saline only (Saline), RSV-infected alone (RSV), OVA alone (OVA), and OVA-treated with RSV infection (OVA-RSV). Lung outcomes included lung mRNA and protein markers of allergic inflammation, histology for mucus cell metaplasia and lung immune cell influx by cytospin and flow cytometry. Results: While thymic stromal lymphopoietin (TSLP) and IL-33 were detected 6 hours after RSV infection in the OVA-RSV mice, IL-23 protein was uniquely upregulated in RSV-infected mice alone. OVA-RSV animals varied from RSV- or OVA-treated mice as they had increased lung eosinophils, neutrophils, group 2 innate lymphoid cells (ILC2) and group 3 innate lymphoid cells (ILC3) detectable as early as 6 hours after RSV infection. Neutralized IL-33 significantly reduced ILC2 and eosinophils, and the prototypical allergic proteins, IL-5, IL-13, CCL17 and CCL22 in OVA-RSV mice. Numbers of neutrophils and ILC3 were also reduced with anti-IL-33 treatment in both RSV and OVA-RSV treated animals as well. Conclusions: Taken together, our findings indicate a broad reduction in allergic-proinflammatory events mediated by IL-33 in RSV-induced asthma exacerbation.

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Respiratory Syncytial Virus Infection in Homeless Populations, Washington, USA

Cited by 11 publications

References 13 publications

Neutralization of IL-33 modifies the type 2 and type 3 inflammatory signature of viral induced asthma exacerbation

Neutralization of IL-33 modifies the type 2 and type 3 inflammatory signature of viral induced asthma exacerbation

Respiratory syncytial virus and other respiratory virus infections in residents of homeless shelters – King County, Washington, 2019–2021

Neutralization of IL-33 Modifies the Type 2 and Type 3 Inflammatory Signature of Viral Induced Asthma Exacerbation.

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