Corrigendum to "Clinical Characteristics of Asymptomatic Patients with SARS-CoV-2 in Zhejiang: An Imperceptible Source of Infection".

[This corrects the article DOI: 10.1155/2020/2045341.].

Clinical Characteristics of Asymptomatic Patients with SARS-CoV-2 in Zhejiang: An Imperceptible Source of Infection.

Objective: Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus SARS-CoV-2, was first identified in December 2019 in Wuhan, China, and has since spread globally, resulting in an ongoing pandemic. However, the study of asymptomatic patients is still rare, and the understanding of its potential transmission risk is still insufficient. In this study, epidemiological investigations were conducted in the Zhejiang province to understand the epidemiology and clinical characteristics of asymptomatic patients with COVID-19. Methods: This retrospective study was carried out on 22 asymptomatic patients and 234 symptomatic patients with COVID-19 who were hospitalized in Zhejiang Duodi Hospital from January 21 to March 16, 2020. The characteristics of epidemiology, demography, clinical manifestations, and laboratory data of mild patients were compared and analyzed. Results: The median age was 28 years in asymptomatic patients and 48 years in symptomatic patients. The proportion who were female was 77.3% in asymptomatic patients and 36.3% in symptomatic patients (p < 0.001). The proportion of patients with coexisting diseases was 4.5% in asymptomatic patients and 38.0% in symptomatic patients (p=0.002). The proportion of patients with increased CRP was 13.6% in the asymptomatic group and 61.1% in the symptomatic group (p < 0.001). The proportion of patients received antiviral therapy was 45.5% in the asymptomatic group and 97.9% in the symptomatic group (p < 0.001). The proportion of patients received oxygen therapy was 22.7% in the asymptomatic group and 99.1% in symptomatic patients (p < 0.001). By March 16, 2020, all patients were discharged from the hospital, and no symptoms had appeared in the asymptomatic patients during hospitalization. The median course of infection to discharge was 21.5 days in asymptomatic patients and 22 days in symptomatic patients. Conclusions: Asymptomatic patients are also infectious; relying only on clinical symptoms, blood cell tests, and radiology examination will lead to misdiagnosis of most patients, leading to the spread of the virus. Investigation of medical history is the best strategy for screening asymptomatic patients, especially young people, women, and people without coexisting disease, who are more likely to be asymptomatic when infected. Although the prognosis is good, isolation is critical for asymptomatic patients, and it is important not to end isolation early before a nucleic acid test turns negative.

Response of patients with chest tightness variant asthma with routine asthma treatment regimen: A 1-year multicenter, prospective, real-world study.

BACKGROUND: Asthmatic patients with chest tightness as their only presenting symptom (chest tightness variant asthma [CTVA]) have clinical characteristics of eosinophilic airway inflammation similar to those of classic asthma (CA); however, whether CTVA has similar response to antiasthma treatment as compared with CA remains unclear. OBJECTIVE: The response of 76 CTVA patients to standard asthma treatments with inhaled corticosteroids with long-acting beta-agonists was explored in a 52-week multicenter, prospective, real-world study. RESULTS: After 52 weeks of treatment with therapy regimens used for CA, the mean 5-point Asthma Control Questionnaire (ACQ-5) score decreased markedly from 1.38(first administration) to 0.71 (52 weeks, mean decrease: 0.674, 95%CI: 0.447-0.900, P<.001).The mean asthma quality-of-life questionnaire (AQLQ) score increased from 5.77 (first administration) to 6.20 (52 weeks, mean increase: 0.441, 95% CI 0.258-0.625, P<.001). Furthermore, at week 52, FVC, FEV1 %, the diurnal variation in PEFand the PD20-FEV1 were significantly improved. Subgroup analysis revealed that the patients at first administration in the responsive group had higher ACQ-5 scores than those in the nonresponsive group (P < .05). CONCLUSION: In conclusion, patients with CTVA had a good therapeutic response to the guideline-recommended routine treatment (containing inhaled corticosteroids). The association between the treatment response and the severity of CTVA suggested that CTVA patients with higher ACQ-5 scores had better therapeutic effects.

Author Correction: Eosinophil differentiation in the bone marrow is promoted by protein tyrosine phosphatase SHP2.

Since the publication of the article, the authors became aware that Figs. 1c, 5k and 6m contained errors in representative image and PAS score in control groups. The corrected Figs. 1c, 5k, and 6m are given below, and the figure legends are the same as original.

Deletion of Shp2 in bronchial epithelial cells impairs IL-25 production in vitro, but has minor influence on asthmatic inflammation in vivo.

Shp2 played an important role in cigarette-smoke-mediated inflammation, surfactant homeostasis and asthmatic airway remodeling. However, whether shp2 plays a key role in epithelium-associated allergic reaction is still unknown. In this study, LPS and OVA were observed to induce the production of IL-25 in bronchial epithelial cells in vitro via the activation of MAPK p38 and JNK. Furthermore, blockage of Shp2 by its specific inhibitor PHPS1 or by siRNA-mediated depletion was found to reduce the production of IL-25 in epithelial cells as well as the up-regulated LPS-triggered activation of JNK but not p38. To confirm the role of intra-bronchial epithelial Shp2 in OVA-induced allergic reaction, we generated CC10-rtTA/(tetO)7-Cre/Shp2f/f mice, where Shp2 was conditionally knocked out in bronchial epithelial cells. Surprisingly, specific deletion of Shp2 in bronchial epithelial cells showed a mild but insignificant effect on the expressions of epithelium-derived cytokines as well as TH2 and TH17 polarization following allergen-induced murine airway inflammation. Collectively, our data suggested that deletion of Shp2 impaired IL-25 production in bronchial epithelial cells in vitro, but might yet have minor influence on OVA-induced allergic reaction in vivo.

Nuclear erythroid 2 p45-related factor-2 Nrf2 ameliorates cigarette smoking-induced mucus overproduction in airway epithelium and mouse lungs.

BACKGROUND AND OBJECTIVE: Nuclear erythroid 2 p45-related factor-2 (Nrf2) is known to play important roles in airway disorders, whereas little has been investigated about its direct role in airway mucus hypersecretion. The aim of this study is to determine whether this factor could protect pulmonary epithelium and mouse airway from cigarette-induced mucus overproduction. METHODS: Using genetic approaches, the role of Nrf2 on cigarette smoking extracts (CSE) induced MUC5AC expression was investigated in lung A549 cells. Nrf2 deficiency mice were smoked for various periods, and the airway inflammation and mucus production was characterized. RESULTS: Acute smoking exposure induced expression of MUC5AC and Nrf2 in both A549 cells and mouse lungs. Genetic ablation of Nrf2 augmented, whereas overexpression of this molecule ameliorated CSE-induced expression of MUC5AC. Nrf2 knockout mice, after exposure to cigarette smoking, displayed enhanced airway inflammation and mucus production. CONCLUSION: Nrf2 negatively regulated smoking-induced mucus production in vitro and in vivo, suggesting therapeutic potentials of this factor in airway diseases with hypersecreted mucus.

Inhibition of allergen-induced airway remodeling by neonatal bacillus Calmette-Guerin vaccination is associated with interferon-gamma-producing T cells but not regulatory T cells in mice.

BACKGROUND: Epidemiological assessments of patients and studies using animal models show that exposure to Mycobacterium bovis bacillus Calmette-Guerin (BCG) vaccine in early life prevents asthma development. However, little is known about the potential of neonatal BCG vaccination in preventing the development of airway remodeling of asthma. OBJECTIVE: To investigate the effects of multiple BCG vaccinations of neonates on the airway remodeling in mice and the accompanied pulmonary T cell responses. METHODS: BALB/c neonates were vaccinated with BCG 3 times. At 5 and 7 weeks of age, the mice were sensitized and then challenged with aerosolized ovalbumin (OVA) 3 times per week for 8 successive weeks. The extent of airway remodeling and induced pulmonary T cell responses were characterized. RESULTS: Multiple BCG vaccinations of neonates reduced OVA-induced remodeling events, including levels of peribronchial α-smooth muscle actin, peribronchial fibrosis, and airway epithelial mucin accumulation. The BCG vaccinations also decreased peribronchial cells expression of transforming growth factor beta 1 (TGF-ß1). In contrast, BCG vaccinations increased the frequency of interferon-gamma (IFN-γ)-producing T cells in the lung and IFN-γ level in BALF, with no effects on pulmonary regulatory T cells and IL-17-producing T cells. CONCLUSIONS: Our data suggest that multiple BCG vaccinations of neonates reduced metrics characteristic of allergen-induced airway remodeling. More importantly, this decrease was not associated with an increased number of pulmonary regulatory T cells but instead correlated with an increase of IFN-γ-producing T cells.