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Respiratory viral infection can cause severe disease and hospitalization, especially among children, the elderly, and patients with comorbidities. In Brazil, the official surveillance system of severe acute respiratory infection (SARI) investigates influenza A (IAV) and B (IBV) viruses, respiratory syncytial virus (RSV), adenovirus (HAdV), and parainfluenza viruses (hPIV 1-3). In Rio Grande do Sul (RS), Brazil, many fatalities associated with SARI between 2013 and 2017 occurred among patients without underlying diseases and for whom the causative agent had not been identified using official protocols. This cross-sectional study analyzed the presence of coronaviruses (HCoV), bocavirus (HBoV), metapneumovirus (hMPV), and rhinovirus in patients who died of SARI despite not having comorbidities, and that were negative for IAV, IBV, RSV, HAdV, and hPIV. Nasopharyngeal aspirates/swabs from patients were used for nucleic acid extraction. The presence of HCoVs OC43, HKU1, NL63, and 229E; HBoV; hMPV; and rhinovirus was assessed by quantitative reverse transcription-polymerase chain reaction. [https://www.selleckchem.com/products/mira-1.html MIRA-1 compound library inhibitor] Clinical data were also analyzed. Between 2013 and 2017, 16 225 cases of SARI were reported in RS; 9.8% of the patients died; 20% of all fatal cases were patients without comorbidities and for whom no pathogen was detected using standard protocols. Analysis of 271 of these cases identified HCoV in nine cases; HBoV, hMPV, and rhinovirus were detected in 3, 3, and 10 cases, respectively. Of note, patients infected with HCoV were adults. Results reinforce the importance of including coronaviruses in diagnostic panels used by official surveillance systems because besides their pandemic potential, endemic HCoVs are associated to severe disease in healthy adults.<br />The coronavirus disease 2019 (COVID-19) has become a major health threat. To overcome COVID-19, appropriate diagnosis methods are urgently needed. The aim of this study was to clinically evaluate the colloidal gold immunochromatography assay for SARS-Cov-2 IgM/IgG antibody (Ab).<br />Patients confirmed COVID-19 (n = 51) were recruited prospectively from the Musashino Red Cross hospital and Tokyo Medical and Dental University Medical Hospital, between March and May 2020. And the analytical specificity was assessed with serum samples of patients without COVID-19 (n = 100) collected between August to September 2019 before SARS-CoV-2 was first reported in China.<br />Among COVID-19 patients, a total of 87 serum samples were tested for SARS-Cov-2 IgM/IgG Ab assay. IgM was detected 71.0 %, 86.9 %, and 83.3 % at day8-14, 15-28, &gt;29 after symptom onset and IgG was detected in 81.6 %, 87.0 %, and 94.4 %, respectively. The sensitivity of IgM and IgG Ab after day8 assay was significantly higher than before day7, respectively (p=0.0016, 0.0003). There were no positive results in 100 serum samples from patients without COVID-19.<br />The SARS-Cov-2 IgM/IgG Ab assay had 79.7% / 86.1% sensitivity (the 8 days after from onset) and 100% specificity in this population.<br />The SARS-Cov-2 IgM/IgG Ab assay had 79.7% / 86.1% sensitivity (the 8 days after from onset) and 100% specificity in this population.In the last months of 2019, an outbreak of fatal respiratory disease started in Wuhan, China, and quickly spread to other parts of the world. It was named COVID-19, and to date, thousands of cases of infection and death are reported worldwide. This disease is associated with a wide range of symptoms, which makes accurate diagnosis of it difficult. During previous severe acute respiratory syndrome (SARS) pandemic in 2003, researchers found that the patients with fever, cough, or sore throat had a 5% influenza virus-positive rate. This finding made us think that the wide range of symptoms and also relatively high prevalence of death in our patients may be due to the coinfection with other viruses. Thus, we evaluated the coinfection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with other respiratory viruses in dead patients in North Khorasan. We evaluated the presence of influenza A/B virus, human metapneumovirus, bocavirus, adenovirus, respiratory syncytial virus (RSV), and parainfluenza viruses in 105 SARS-CoV-2 positive dead patients, using polymerase chain reaction (PCR) and reverse transcription PCR tests. We found coinfection with influenza virus in 22.3%, RSV, and bocavirus in 9.7%, parainfluenza viruses in 3.9%, human metapneumovirus in 2.9%, and finally adenovirus in 1.9% of SARS-CoV-2 positive dead cases. Our findings highlight a high prevalence of coinfection with influenza A virus and the monopoly of coinfection with Human metapneumovirus in children.Since cytokine release syndrome with elevation of interleukin-6 (IL-6) is considered to be associated with severe cases of coronavirus disease 2019 (COVID-19); IL-6 inhibitors, such as tocilizumab, are expected to be effective for its treatment. This was a retrospective study using a consecutive cohort of 224 patients hospitalized with COVID-19 in March 2020. Patients were divided into those admitted to the intensive care unit (ICU group) and those not (no ICU group), and clinical data including usage of tocilizumab were compared. Correlation between IL-6 value at admission and at peak, and tocilizumab use, as well as clinical outcomes were also investigated. The ICU group had higher rates of pre-existing comorbidities such as hypertension, diabetes, and coronary disease, and higher IL-6 than no ICU group (all P  less then  .05). Age, peak IL-6, and peak d-dimer were significant predictors of in-hospital mortality (1.05 [1.01-1.09], P = .012; 1.001 [1.000-1.002], P = .002; 1.10 [1.03-1.18], P = .008). Receiver operating characteristics curve showed higher predictability of in-hospital mortality with IL-6 at peak than others (area under curve; IL-6 at peak 0.875 [0.87-0.942], IL-6 at admission 0.794 [0.699-0.889], d-dimer at peak 0.787 [0.690-0.883], d-dimer at admission 0.726 [0.625-0.827]). Incidence of fungal infections was significantly higher in patients who were given tocilizumab than those who were not (13.0% vs 1.1%, P  less then  .001). Notably, tocilizumab did not affect in-hospital mortality after adjustment including IL-6 (odds ratio [95% confidential interval] 1.00 [0.27-3.72, P = .998]). Age, peak IL-6, and peak d-dimer levels were significant predictors of in-hospital mortality. Tocilizumab did not decrease in-hospital mortality in our cohort.