Lung Function, Allergic Sensitization and Asthma in School-Aged Children After Viral-Coinfection Bronchiolitis

BACKGROUND. Our main objective was to compare the lung function, the rate of allergic sensitization and the prevalence of asthma at 7-9 years in children hospitalized for bronchiolitis with viral coinfection versus single viral infection.METHODS. Observational study in children with previous bronchiolitis and current age 7-9 years. Clinical data were collected. Fraction of exhaled nitric oxide (FeNO) determination, spirometry and skin prick test for common aeroallergens were performed.RESULTS. A total of 181 children hospitalized for bronchiolitis (40 coinfections and 141 single infections), with median age of 8.3 years (IQR:7.5-9.1) were included. Single-HRV-infections showed lower basal FEV1(%) than coinfections (p=0.04) and lower z-score FEV1 than single-RSV-infections(p=0.04) or coinfections(p=0.02). Also, single-HRV-infections had lower post-bronchodilator FEV1(%) and z-score FEV1 values than coinfections (p=0.03 and p=0.03). Single-HRV-bronchiolitis was an independent risk factor for FEV1<80%(p=0.007). FeNO value >25 ppb was detected in 21(12.5%) cases, without differences between viral groups(p=0.768). The prevalence of allergic sensitization was similar in coinfections (31.4%) versus single infections (38.7%), (p=0.428). The highest frequency of allergic rhinitis was observed in single-HRV patients(p=0.004).The respiratory morbidity at 7-9 years of coinfected patients was similar to the single-HRV ones. In contrast, the likelihood of current asthma was up to 5 times higher in RSV/HRV coinfections than in the single-RSV-infections ones (p=0.012).CONCLUSIONS. The respiratory morbidity at 7-9 years of age after severe bronchiolitis is significantly higher in single-HRV or viral coinfection patients that in single-RSV ones. Single-HRV-bronchiolitis is independently associated with lower lung function at school-age.

Viral Coinfection among COVID-19 Patient Groups: An Update Systematic Review and Meta-Analysis

Background. Coinfections have a potential role in increased morbidity and mortality rates during pandemics. Our investigation is aimed at evaluating the viral coinfection prevalence in COVID-19 patients. Methods. We systematically searched scientific databases, including Medline, Scopus, WOS, and Embase, from December 1, 2019, to December 30, 2020. Preprint servers such as medRxiv were also scanned to find other related preprint papers. All types of studies evaluating the viral coinfection prevalence in COVID-19 patients were considered. We applied the random effects model to pool all of the related studies. Results. Thirty-three studies including 10484 patients were identified. The viral coinfection estimated pooled prevalence was 12.58%; 95% CI: 7.31 to 18.96). Blood viruses (pooled prevalence: 12.48%; 95% CI: 8.57 to 16.93) had the most frequent viral coinfection, and respiratory viruses (pooled prevalence: 4.32%; 95% CI: 2.78 to 6.15) had less frequent viral coinfection. The herpesvirus pooled prevalence was 11.71% (95% CI: 3.02 to 24.80). Also, the maximum and minimum of viral coinfection pooled prevalence were in AMRO and EMRO with 15.63% (95% CI: 3.78 to 33.31) and 7.05% (95% CI: 3.84 to 11.07), respectively. Conclusion. The lowest rate of coinfection belonged to respiratory viruses. Blood-borne viruses had the highest coinfection rate. Our results provide important data about the prevalence of blood-borne viruses among COVID-19 patients which can be critical when it comes to their treatment procedure.

Bacterial and Viral Coinfection in Idiopathic Pulmonary Fibrosis Patients: the Prevalence and Possible Role in Disease Progression

BackgroundIdiopathic pulmonary fibrosis (IPF) is a progressive interstitial pneumonia of unknown etiology with a mean survival rate of less than 3 years. Gap StatementNo previous studies have been performed on the role of co-infection (viral and bacterial infection) in the pathogensis and progression of IPF.AimIn this study, we investigated the role of viral/bacterial infection and coinfection and their possible association with pathogensis and progression of IPF.MethodsWe investigated the prevalence and impact of bacterial and viral coinfection in IPF patients (n = 67) in the context of pulmonary function (FVC, FEV1 and DLCO), disease status and mortality risk. Using principal component analysis (PCA), we also investigated the relationship between and distribution of bacterial and viral co-infection in the IPF cohort.ResultsOf the 67 samples, 17.9% samples were positive for viral infection, 10.4% samples were positive for bacterial infection and 59.7% samples were positive coinfection. We demonstrated that IPF patients who were co-infected had a significantly increased risk of mortality compared (p = 0.031) with IPF patients who were non-infected [Hazard ratio: 8.12; 95% C.I.: 1.3–26.9]. Furthermore, coinfection has also been implicated in disease progression during acute exacerbations in IPF (AE-IPF).ConclusionIn this study, we report for the first time that IPF patients who were coinfected with bacteria and viral infection have significantly decreased FVC and DLCO (% predicted), increased incidence of AE-IPF, increased incidence of death and risk of mortality compared with non-infected IPF patients.

Viral coinfection promotes tuberculosis immunopathogenesis by type I IFN signaling-dependent impediment of Th1 pulmonary influx

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), is often exacerbated upon coinfection, but the underlying immunological mechanisms remain unclear. Here, to elucidate these mechanisms, we used a Mtb and lymphocytic choriomeningitis virus coinfection model. Viral coinfection significantly suppressed Mtb-specific IFN-γ production, with elevated bacterial loads and hyperinflammation in the lungs. Type I IFN signaling blockade rescued the Mtb-specific IFN-γ response and ameliorated lung immunopathology. Single-cell sequencing, tissue immunofluorescence staining, and adoptive transfer experiments revealed that type I IFN signaling produced in response to viral infection inhibited CXCL9/10 production in myeloid cells, resulting in impaired pulmonary migration of Mtb-specific CD4+ T cells from lymph nodes. Thus, virus coinfection-induced type I IFN signaling prior to the pulmonary localization of Mtb-specific Th1 cells exacerbates TB immunopathogenesis by impeding the Mtb-specific Th1 cell influx. Our study highlights another novel negative role of viral coinfection and/or type I IFNs in delaying Mtb-specific Th1 responses in the lung.

Clinical Features and Outcomes of Community-Acquired Pneumonia Caused by Haemophilus Influenza

Background Long regarded as the second most common cause of community-acquired pneumonia (CAP), Haemophilus influenzae has recently been identified with almost equal frequency as pneumococcus in patients hospitalized for CAP. The literature lacks a detailed description of the presentation, clinical features, laboratory and radiologic findings, and outcomes in Haemophilus pneumonia. Methods During 2 prospective studies of patients hospitalized for CAP, we identified 33 patients with Haemophilus pneumonia. In order to provide context, we compared clinical findings in these patients with findings in 36 patients with pneumococcal pneumonia identified during the same period. We included and analyzed separately data from patients with viral coinfection. Patients with coinfection by other bacteria were excluded. Results Haemophilus pneumonia occurred in older adults who had underlying chronic lung disease, cardiac conditions, and alcohol use disorder, the same population at risk for pneumococcal pneumonia. However, in contrast to pneumococcal pneumonia, patients with Haemophilus pneumonia had less severe infection as shown by absence of septic shock on admission, less confusion, fewer cases of leukopenia or extreme leukocytosis, and no deaths at 30 days. Viral coinfection greatly increased the severity of Haemophilus, but not pneumococcal pneumonia. Conclusions We present the first thorough description of Haemophilus pneumonia, show that it is less severe than pneumococcal pneumonia, and document that viral coinfection greatly increases its severity. These distinctions are lost when the label CAP is liberally applied to all patients who come to the hospital from the community for pneumonia.

Characterization of rhinovirus/enterovirus complex infection in children living at high altitudes: A cross sectional study

Background: Respiratory tract infections caused by the rhinovirus/enterovirus (RV/EV) complex have traditionally been considered to be minor, self-limited infections in children, with few complications. There are no previous studies of patients living at high altitudes that characterize severe cases of this infection.Methods: This was a cross-sectional study including patients from 1 month to 18 years old who had been hospitalized for acute respiratory tract infections between October 2015 and December 2019, and had had a viral panel with RT-PCR during their hospitalization.Results: During the study period, 645 RT-PCRs were performed, with the two main etiological agents identified being RV/EV (224) and respiratory syncytial virus (68). The median age of patients with RV/EV complex was 27 months (IQR: 8-70), 55.8% were boys and the average length of hospital stay was 12 days (IQR: 6-24). Severe RV/EV complex infections required more transfers to intensive care (11% vs 47%), showed more viral coinfection (OR: 2.13,95%, 95%CI: 1.42-4.64) and had less bacterial coinfection (OR: 0.55, 95%CI: 0.31-0.98) than RSV infections, with no difference in mortality ( 2.4% vs. 2.1%, P:0.09). Post-transplant patients (OR: 3.35, 95%CI: 1.10-11.34) and those with comorbidities (OR: 3.97, 95%CI: 2.23-7.08) had the highest risk of RV/EV infection. The RV/EV group had a higher risk of presenting acute respiratory distress syndrome (ARDS) (OR: 3.6, 95%CI: 1.07-12:18), especially in premature infants (p: 0.05; exp (B), 2.99; 95%CI= 1.01-8.82), those with heart disease (p: 0.047; exp(B), 2.99; 95%CI = 1.01-8.82) and those with inborn errors of metabolism (p: 0.032; exp (B), 5-01; 95%CI= 1.15-21.81). Conclusions: Respiratory infection due to RV/EV in children who live at high altitudes can frequently be severe, requiring management with intensive care therapy. When compared to RSV, this complex is more frequently associated with viral coinfection and the development of ARDS, especially in risk groups such as those with prematurity, heart disease or inborn errors of metabolism. It is important to see RV / EV as a virus that can have an unsatisfactory course as or more severe than that of other viruses that affect the respiratory tract in children.