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Graphical abstract, Chemokines are crucial inflammatory mediators needed during an immune response to clear pathogens. However, their excessive release is the main cause of hyperinflammation. In the recent COVID-19 outbreak, chemokines may be the direct cause of acute respiratory disease syndrome, a major complication leading to death in about 40% of severe cases. Several clinical investigations revealed that chemokines are directly involved in the different stages of SARS-CoV-2 infection. Here, we review the role of chemokines and their receptors in COVID-19 pathogenesis to better understand the disease immunopathology which may aid in developing possible therapeutic targets for the infection.

Acute respiratory tract infections (ARTIs) are among the leading causes of morbidity and mortality in children. The viral etiology of ARTIs was investigated over 3 years (October 2012–September 2015) in 2575 children in Parma, Italy, using indirect immunofluorescent staining of respiratory samples for viral antigens, cell culture, and molecular assays. Respiratory viruses were detected in 1299 cases (50.44%); 1037 (79.83%) were single infections and 262 (20.17%) mixed infections. The highest infection incidence was in children aged >6 months to ≤3 years (57.36%). Human respiratory syncytial virus (27.12%) and human adenovirus (23.58%) were the most common viruses identified. The virus detection rate decreased significantly between the first and third epidemic season (53.9% vs. 43.05%, P, Highlights • Respiratory viruses were assessed in children from October 2012 to September 2015. • Viruses were detected using antigen and molecular assays, and cell culture. • Respiratory syncytial virus and adenovirus were the most common viruses detected. • Influenza virus and respiratory syncytial virus detection showed seasonal variation. • Respiratory virus detection was highest in children aged >6 months to ≤3 years.

Background The impact of viral infections on acute exacerbations in idiopathic pulmonary fibrosis (IPF) and/or non-IPF interstitial lung disease (ILDs) has been scarcely described. Objectives To elucidate the frequency of virus infections in patients with IPF or non-IPF ILDs including idiopathic interstitial pneumonia (IIP) or connective tissue disease (CTD)-associated pneumonia, and its influence on their short-term mortality. Methods We prospectively enrolled adult patients with acute exacerbation of IPF and non-IPF ILDs who were admitted to the hospital during the last 3 years, and examined the respiratory samples obtained from nasopharyngeal, sputum, and bronchoalveolar lavage fluid. Results A total of 78 patients were identified, consisting of 27 patients with acute exacerbation of IPF and 51 patients with non-IPF ILDs (IIP: n = 27, CTD-associated IP: n = 24). Of all patients, 15 (19.2%) had viruses detected in their respiratory samples including the human herpesvirus 7 (HHV7; n = 4) and cytomegalovirus (CMV) plus HHV7 (n = 3). The proportion of virus infections in the IPF and non-IPF ILDs groups was comparable. The Kaplan-Meier survival curves over 60 days revealed a lower survival probability in the virus positive group (n = 15, 60%) than in the virus negative group (n = 60, 83.3%, p

Highlights ► NK cells and CD8+ T-cells expand relatively late following pneumovirus infection. ► Memory CD8+ T-cells support type 1 skewing of pneumovirus-specific responses. ► Memory CD8+ T-cells prevent pneumovirus-induced immunopathology. ► CD8+ T-cell targeted immunization protects against pneumovirus-induced disease., Pneumoviruses such as pneumonia virus of mice (PVM), bovine respiratory syncytial virus (bRSV) or human (h)RSV are closely related pneumoviruses that cause severe respiratory disease in their respective hosts. It is well-known that T-cell responses are essential in pneumovirus clearance, but pneumovirus-specific T-cell responses also are important mediators of severe immunopathology. In this study we determined whether memory- or pre-existing, transferred virus-specific CD8+ T-cells provide protection against PVM-induced disease. We show that during infection with a sublethal dose of PVM, both natural killer (NK) cells and CD8+ T-cells expand relatively late. Induction of CD8+ T-cell memory against a single CD8+ T-cell epitope, by dendritic cell (DC)-peptide immunization, leads to partial protection against PVM challenge and prevents Th2 differentiation of PVM-induced CD4 T-cells. In addition, adoptively transferred PVM-specific CD8+ T-cells, covering the entire PVM-specific CD8+ T-cell repertoire, provide partial protection from PVM-induced disease. From these data we infer that antigen-specific memory CD8+ T-cells offer significant protection to PVM-induced disease. Thus, CD8+ T-cells, despite being a major cause of PVM-associated pathology during primary infection, may offer promising targets of a protective pneumovirus vaccine.