Virus load and virus shedding of SARS-CoV-2 and their impact on patient outcomes.

BACKGROUND: Understanding a virus shedding patterns in body fluids/secretions is important to determine the samples to be used for diagnosis and to formulate infection control measures. AIM: To investigate the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) shedding patterns and its risk factors. METHODS: All laboratory-confirmed coronavirus disease 2019 patients with complete medical records admitted to the Shenzhen Third People's Hospital from January 28, 2020 to March 8, 2020 were included. Among 145 patients (54.5% males; median age, 46.1 years), three (2.1%) died. The bronco-alveolar lavage fluid (BALF) had the highest virus load compared with the other samples. The viral load peaked at admission (3.3 × 108 copies) and sharply decreased 10 d after admission. RESULTS: The viral load was associated with prolonged intensive care unit (ICU) duration. Patients in the ICU had significantly longer shedding time compared to those in the wards (P < 0.0001). Age > 60 years [hazard ratio (HR) = 0.6; 95% confidence interval (CI): 0.4-0.9] was an independent risk factor for SARS-CoV-2 shedding, while chloroquine (HR = 22.8; 95%CI: 2.3-224.6) was a protective factor. CONCLUSION: BALF had the highest SARS-CoV-2 load. Elderly patients had higher virus loads, which was associated with a prolonged ICU stay. Chloroquine was associated with shorter shedding duration and increased the chance of viral negativity.

Hydrogen gas protects against serum and glucose deprivation­induced myocardial injury in H9c2 cells through activation of the NF­E2­related factor 2/heme oxygenase 1 signaling pathway.

Ischemia or hypoxia­induced myocardial injury is closely associated with oxidative stress. Scavenging free radicals and/or enhancing endogenous antioxidative defense systems may be beneficial for the impediment of myocardial ischemic injury. Hydrogen (H2) gas, as a water­ and lipid­soluble small molecule, is not only able to selectively eliminate hydroxyl (·OH) free radicals, but also to enhance endogenous antioxidative defense systems in rat lungs and arabidopsis plants. However, thus far, it has remained elusive whether H2 gas protects cardiomyocytes through enhancement of endogenous antioxidative defense systems. In the present study, the cardioprotective effect of H2 gas against ischemic or hypoxic injury was investigated, along with the underlying molecular mechanisms. H9c2 cardiomyoblasts (H9c2 cells) were treated in vitro with a chemical hypoxia inducer, cobalt chloride (CoCl2), to imitate hypoxia, or by serum and glucose deprivation (SGD) to imitate ischemia. Cell viability and intracellular ·OH free radicals were assessed. The role of an endogenous antioxidative defense system, the NF­E2­related factor 2 (Nrf2)/heme oxygenase 1 (HO­1) signaling pathway, was evaluated. The findings revealed that treatment with CoCl2 or SGD markedly reduced cell viability in H9c2 cells. H2 gas­rich medium protected against cell injury induced by SGD, but not that induced by CoCl2. When the cells were exposed to SGD, levels of intracellular ·OH free radicals were markedly increased; this was mitigated by H2 gas­rich medium. Exposure of the cells to SGD also resulted in significant increases in HO­1 expression and nuclear Nrf2 levels, and the HO­1 inhibitor ZnPP IX and the Nrf2 inhibitor brusatol aggravated SGD­induced cellular injury. H2 gas­rich medium enhanced SGD­induced upregulation of HO­1 and Nrf2, and the HO­1 or Nrf2 inhibition partially suppressed H2 gas­induced cardioprotection. Furthermore, following genetic silencing of Nrf2 by RNA interference, the effects of H2 gas on the induction of HO­1 and cardioprotection were markedly reduced. In conclusion, H2 gas protected cardiomyocytes from ischemia­induced myocardial injury through elimination of ·OH free radicals and also through activation of the Nrf2/HO­1 signaling pathway.