Tolerogenic Lung Allograft Microenvironment Suppresses Pathogenic Tissue Remodeling Following Respiratory Virus Infection in Mice.

Tolerance after lung transplantation is associated with the induction of Foxp3 regulatory T cell-enriched bronchus-associated lymphoid tissue, which suppresses local and systemic alloimmune responses. How this tolerogenic graft environment shapes responses to respiratory viral infections, a known contributor to adverse outcomes after lung transplantation, remains unknown. Using a mouse model of a seasonally circulating parainfluenza virus, we found that acute infection of tolerant lung allografts results in temporary reductions of both bronchus-associated lymphoid tissue size and abundance of graft-resident Foxp3 cells, but doesn't trigger rejection.

Murine parainfluenza virus persists in lung innate immune cells sustaining chronic lung pathology.

Common respiratory viruses, including the human parainfluenza viruses, threaten human health seasonally and associate with the development of chronic lung diseases. Evidence suggests that these viruses can persist, but the sources of viral products in vivo and their impact on chronic respiratory diseases remain unknown. Using the murine parainfluenza virus Sendai, we demonstrate that viral protein and RNA persist in lung macrophages, type 2 innate lymphoid cells (ILC2s) and dendritic cells long after the infectious virus is cleared.

Murine Parainfluenza Virus Persists in Lung Innate Immune Cells Sustaining Chronic Lung Pathology.

Respiratory viruses including the human parainfluenza viruses (hPIVs) are a constant burden to human health, with morbidity and mortality frequently increased after the acute phase of the infection. Although is proven that respiratory viruses can persist , the mechanisms of virus or viral products persistence, their sources, and their impact on chronic respiratory diseases are unknown. Here, we used Sendai virus (SeV) to model hPIV infection in mice and test whether virus persistence associates with the development of chronic lung disease.

Fibroblast growth factor-9 expression in airway epithelial cells amplifies the type I interferon response and alters influenza A virus pathogenesis.

Influenza A virus (IAV) preferentially infects conducting airway and alveolar epithelial cells in the lung. The outcome of these infections is impacted by the host response, including the production of various cytokines, chemokines, and growth factors. Fibroblast growth factor-9 (FGF9) is required for lung development, can display antiviral activity in vitro, and is upregulated in asymptomatic patients during early IAV infection.

SARS-CoV-2-triggered neutrophil extracellular traps mediate COVID-19 pathology.

Severe COVID-19 patients develop acute respiratory distress syndrome that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that neutrophil extracellular traps (NETs) have been described as important mediators of tissue damage in inflammatory diseases, we investigated whether NETs would be involved in COVID-19 pathophysiology. A cohort of 32 hospitalized patients with a confirmed diagnosis of COVID-19 and healthy controls were enrolled.

Circulation profile of respiratory viruses in symptomatic and asymptomatic children from Midwest Brazil.

Acute respiratory infection (ARI) is a major cause of morbidity and mortality worldwide. Most of these infections are caused by viruses. Infections pose as important triggers of acute episodes of chronic respiratory diseases (CRD).

Detection of Influenza A(H3N2) Virus RNA in Donated Blood.

Influenza A virus infection has rarely been documented to cause viremia. In 28 blood donations in Brazil that were deferred because of postdonation information, we identified influenza A(H3N2) virus RNA in 1 donation using metagenomic analysis. Our finding implies theoretical risk for viremia and transfusion transmission.

IL-33 and ST2 as predictors of disease severity in children with viral acute lower respiratory infection.

Background: Mechanisms influencing severity of acute lower respiratory infection (ALRI) in children are not established. We aimed to assess the role of inflammatory markers and respiratory viruses in ALRI severity.

Methods: Concentrations of interleukin(IL)-33, soluble suppression of tumorigenicity (sST)2, IL-1ß, tumor necrosis factor α, IL-4, IL-6 and IL- 8 and types of respiratory viruses were evaluated in children at the first and fifth days after hospital admission.

Asthma exacerbations in a subtropical area and the role of respiratory viruses: a cross-sectional study.

Background: Multiple factors are involved in asthma exacerbations, including environmental exposure and viral infections. We aimed to assess the association between severe asthma exacerbations, acute respiratory viral infections and other potential risk factors.

Methods: Asthmatic children aged 4-14 years were enrolled for a period of 12 months and divided into two groups: those with exacerbated asthma (group 1) and non-exacerbated asthma (group 2).