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1.
Front Public Health ; 10: 1050034, 2022.
Article in English | MEDLINE | ID: covidwho-2163194

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen that causes coronavirus disease 2019 (COVID-19), infects humans through a strong interaction between the viral spike protein (S-protein) and angiotensin converting enzyme 2 (ACE2) receptors on the cell surface. The infection of host lung cells by SARS-CoV-2 leads to clinical symptoms in patients. However, ACE2 expression is not restricted to the lungs; altered receptors have been found in the nasal and oral mucosa, vessel, brain, pancreas, gastrointestinal tract, kidney, and heart. The future of COVID-19 is uncertain, however, new viral variants are likely to emerge. The SARS-CoV-2 Omicron variant has a total of 50 gene mutations compared with the original virus; 15 of which occur in the receptor binding domain (RBD). The RBD of the viral S-protein binds to the human ACE2 receptor for viral entry. Mutations of the ACE2-RBD interface enhance tight binding by increasing hydrogen bond interactions and expanding the accessible surface area. Extracorporeal membrane oxygenation, hyperbaric oxygen, and aggressive dialysis for the treatment of COVID-19 have shown various degrees of clinical success. The use of decoy receptors based on the ACE2 receptor as a broadly potent neutralizer of SARS-CoV-2 variants has potential as a therapeutic mechanism. Drugs such as 3E8 could block binding of the S1-subunit to ACE2 and restrict the infection of ACE2-expressing cells by a variety of coronaviruses. Here, we discuss the development of ACE2-targeted strategies for the treatment and prevention of COVID-19.


Subject(s)
COVID-19 , SARS-CoV-2 , Humans , Angiotensin-Converting Enzyme 2/chemistry , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/therapy , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/chemistry , Spike Glycoprotein, Coronavirus/metabolism , Peptidyl-Dipeptidase A/chemistry , Peptidyl-Dipeptidase A/genetics , Peptidyl-Dipeptidase A/metabolism
2.
researchsquare; 2022.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2274352.v1

ABSTRACT

Background Since March 2022, the SARS-CoV-2 Omicron variant, mainly the BA.2 sub-lineage, has swept throughout Shanghai, China and caused a wide range of infections. Patients with chronic kidney disease (CKD) are particularly vulnerable to the subvariant and have unique clinical manifestations and outcomes, which have not been studied yet.Methods We retrospective collected data from 2140 hospitalized patients with SARS-CoV-2 Omicron infection from March 29, 2022, to May 17, 2022. Demographic characteristics, clinical symptoms, ancillary examination results, and treatments were described respectively. Presence of COVID-19 pneumonia, disease severity (according to WHO), composite outcome (critical COVID-19 and death), and negative conversion time were defined as primary outcomes. Multivariate analyses were used to evaluate risk factors affecting the primary outcomes.Results The main clinical types of CKD group were severe and critical. Negative conversion time varies according to the stage of CKD patients. The CKD group was more likely to have pneumonia, respiratory and circulatory support, severe disease and death, as compared to the non-CKD group. CKD and the number of comorbidities were found to be risk factors for pneumonia, critical COVID-19and composite outcome among Omicron patients.Conclusion We provided the first snapshot of clinical characteristics and outcomes of CKD patients in the Omicron wave, highlighting the vulnerability of CKD population and providing clues for future studies in special or immunocompromised populations.


Subject(s)
Pneumonia , Death , COVID-19 , Renal Insufficiency, Chronic
3.
Front Cardiovasc Med ; 9: 890967, 2022.
Article in English | MEDLINE | ID: covidwho-1902939

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a highly contagious disease. Most infected patients manifest mild flu-like symptoms, but in some cases, the patients rapidly develop severe lung infections and pneumonia. It is estimated that about 15-20% of patients with COVID-19 develop hypoxemia and require some form of oxygen therapy and ventilation support. Further, exacerbation of the disease usually requires an emergency tracheal intubation, where the patients are more prone to coughing and aerosol diffusion, placing the anesthesiologist at an extremely high risk of infection. In this review, after a brief introduction to the epidemiology and pathogenesis of the COVID-19, we describe various recommendations that the anesthesiologists should employ to avoid the chances of infection during the management of severely ill patients. We describe key steps such as not removing the patient's mask prematurely and using sedatives, analgesics, and muscle relaxants for rapid and orderly intubation. The use of spinal cord and regional nerve block anesthesia should also be promoted to avoid general anesthesia. Since the patients with COVID-19 may also have disorders related to other parts of the body (other than lungs), short-acting drugs are recommended to actively maintain the perfusion pressure of the peripheral and important organs without metabolism of the drugs by the liver and kidney. Multimodal analgesia is advocated, and non-steroidal anti-inflammatory analgesic drugs can be used appropriately. In this review, we also discuss key studies and experiences of anesthesiologists from China, highlights research findings, and inform on the proper management of patients with perspective on anesthesiologists.

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