Thoughts on diagnosis and treatment plan of patients infected with severe acute respiratory syndrome coronavirus 2 omicron variant in large shelter hospitals in Shanghai

The epidemic caused by the infection of severe acute respiratory syndrome coronavirus 2 omicron variant broke out in Shanghai in Mar. 2022. Omicron variant has characteristics such as strong concealment and rapid transmission, resulting in significant differences between the current round of epidemic and that in Wuhan. The number of infected patients (mainly asymptomatic infected patients) increased rapidly in a short term. Based on dynamic zero policy, shelter hospitals were set up in time in Shanghai to treat the patients. It is suggested that medical resources and patient characteristics should be taken into account in the independent cabin of a shelter hospital with more than 10 000 beds, and the clinical medical practice should be divided to 5 modes (universal education and management, community outpatient clinic, ward duty, emergency rescue, and temporary observation and transport) to optimize the allocation of medical resources, so as to further enhance the treatment capacity and efficiency of shelter hospitals.

GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia.

Severe cases of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are associated with elevated blood glucose levels and metabolic complications. However, the molecular mechanisms for how SARS-CoV-2 infection alters glycometabolic control are incompletely understood. Here, we connect the circulating protein GP73 with enhanced hepatic gluconeogenesis during SARS-CoV-2 infection. We first demonstrate that GP73 secretion is induced in multiple tissues upon fasting and that GP73 stimulates hepatic gluconeogenesis through the cAMP/PKA signaling pathway. We further show that GP73 secretion is increased in cultured cells infected with SARS-CoV-2, after overexpression of SARS-CoV-2 nucleocapsid and spike proteins and in lungs and livers of mice infected with a mouse-adapted SARS-CoV-2 strain. GP73 blockade with an antibody inhibits excessive glucogenesis stimulated by SARS-CoV-2 in vitro and lowers elevated fasting blood glucose levels in infected mice. In patients with COVID-19, plasma GP73 levels are elevated and positively correlate with blood glucose levels. Our data suggest that GP73 is a glucogenic hormone that likely contributes to SARS-CoV-2-induced abnormalities in systemic glucose metabolism.