Research progress on the mechanism of multiple organ dysfunction in patients with COVID-19.

The pathogen of COVID-19 is 2019-nCoV, which belongs to the beta coronavirus. Angiotensin-converting enzyme 2 (ACE2) is the receptor of 2019-nCoV as the same of SARS-CoV. Most of the severe patients were the elderly with underlying diseases, which may be related to the decrease in the number of naive T cells. In addition to pulmonary symptoms, COVID-19 can also cause multiple organ dysfunction and even multiple organ failure (liver, nervous system, heart, kidney, etc.). Pathogenic mechanisms such as direct virus invasion, cytokine storm, endothelial cells damage, and down-regulation of ACE2 may play important roles in the severity of the disease.Copyright © 2021 Chinese Medical Association

Research progress on the mechanism of multiple organ dysfunction in patients with COVID-19.

The pathogen of COVID-19 is 2019-nCoV, which belongs to the beta coronavirus. Angiotensin-converting enzyme 2 (ACE2) is the receptor of 2019-nCoV as the same of SARS-CoV. Most of the severe patients were the elderly with underlying diseases, which may be related to the decrease in the number of naive T cells. In addition to pulmonary symptoms, COVID-19 can also cause multiple organ dysfunction and even multiple organ failure (liver, nervous system, heart, kidney, etc.). Pathogenic mechanisms such as direct virus invasion, cytokine storm, endothelial cells damage, and down-regulation of ACE2 may play important roles in the severity of the disease.Copyright © 2021 Chinese Medical Association

Research progress on the mechanism of multiple organ dysfunction in patients with COVID-19.

The pathogen of COVID-19 is 2019-nCoV, which belongs to the beta coronavirus. Angiotensin-converting enzyme 2 (ACE2) is the receptor of 2019-nCoV as the same of SARS-CoV. Most of the severe patients were the elderly with underlying diseases, which may be related to the decrease in the number of naive T cells. In addition to pulmonary symptoms, COVID-19 can also cause multiple organ dysfunction and even multiple organ failure (liver, nervous system, heart, kidney, etc.). Pathogenic mechanisms such as direct virus invasion, cytokine storm, endothelial cells damage, and down-regulation of ACE2 may play important roles in the severity of the disease.Copyright © 2021 Chinese Medical Association

COVID-19 pandemic: A multidisciplinary perspective on the pathogenesis of a novel coronavirus from infection, immunity and pathological responses.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus2 (SARS-CoV-2), has spread to more than 200 countries and regions, having a huge impact on human health, hygiene, and economic activities. The epidemiological and clinical phenotypes of COVID-19 have increased since the onset of the epidemic era, and studies into its pathogenic mechanisms have played an essential role in clinical treatment, drug development, and prognosis prevention. This paper reviews the research progress on the pathogenesis of the novel coronavirus (SARS-CoV-2), focusing on the pathogenic characteristics, loci of action, and pathogenic mechanisms leading to immune response malfunction of SARS-CoV-2, as well as summarizing the pathological damage and pathological manifestations it causes. This will update researchers on the latest SARS-CoV-2 research and provide directions for future therapeutic drug development.

Correlation Between Coronavirus Disease 2019 and Olfactory Dysfunction.

A great number of patients with Coronavirus Disease 2019 (COVID-19) experience olfactory dysfunction, typically of a short duration and with a high incidence rate, during the early stages of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This kind of olfactory dysfunction appears more likely in young people and women. This study presents a review of the clinical features and pathogenic mechanism of the olfactory dysfunction related to SARS-CoV-2 infection, aiming to provide a clinical reference for the diagnosis, differential diagnosis, treatment, and prevention of olfactory dysfunction in COVID-19 patients.

SARS-CoV-2: Origin, Evolution, and Targeting Inhibition.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused an outbreak in Wuhan city, China and quickly spread worldwide. Currently, there are no specific drugs or antibodies that claim to cure severe acute respiratory diseases. For SARS-CoV-2, the spike (S) protein recognizes and binds to the angiotensin converting enzyme 2 (ACE2) receptor, allowing viral RNA to enter the host cell. The main protease (Mpro) is involved in the proteolytic process for mature non-structural proteins, and RNA-dependent RNA polymerase (RdRp) is responsible for the viral genome replication and transcription processes. Owing to the pivotal physiological roles in viral invasion and replication, S protein, Mpro, RdRp are regarded as the main therapeutic targets for coronavirus disease 2019 (COVID-19). In this review, we carried out an evolutionary analysis of SARS-CoV-2 in comparison with other mammal-infecting coronaviruses that have sprung up in the past few decades and described the pathogenic mechanism of SARS-CoV-2. We displayed the structural details of S protein, Mpro, and RdRp, as well as their complex structures with different chemical inhibitors or antibodies. Structural comparisons showed that some neutralizing antibodies and small molecule inhibitors could inhibit S protein, Mpro, or RdRp. Moreover, we analyzed the structural differences between SARS-CoV-2 ancestral S protein and D614G mutant, which led to a second wave of infection during the recent pandemic. In this context, we outline the methods that might potentially help cure COVID-19 and provide a summary of effective chemical molecules and neutralizing antibodies.

Oral Symptoms Associated with COVID-19 and Their Pathogenic Mechanisms: A Literature Review.

Since the worldwide spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, management of coronavirus disease 2019 (COVID-19) has been challenging for healthcare providers. The oral cavity is referred to as a target of SARS-CoV-2. The aim of this study was to review oral symptoms specific to COVID-19 patients from the point of view of symptom prevalence and pathogenesis and to speculate the pathogenic mechanisms underlying them. Scientific articles were retrieved by searching PubMed/MEDLINE, Google Scholar, medRxiv, and bioRxiv from 3 February 2020 to 31 December 2020, and they were reviewed by title, abstract, and text for relevance. The literature search indicated that COVID-19 patients frequently present with gustatory dysfunction, xerostomia, and oral mucosal lesions, while their prevalence is likely to vary by country, age, gender, and disease severity. Gustatory dysfunction and xerostomia appear at an early stage of SARS-CoV-2 infection and last relatively long. One of possible pathogenic mechanisms of both symptoms is attributed to the expression of viral cellular entry-relevant receptors in taste cells and salivary glands. Dental professionals who can first become aware of oral symptoms associated with COVID-19 will play a more active role in and make a greater contribution to diagnosis and prevention of COVID-19.

Pericytes Within A Pulmonary Neurovascular Unit in Coronavirus Disease 2019 Elicited Pathological Changes.

A pericyte-centered theory suggesting that embolisms occurring within the microvasculature of a neurovascular unit that can result in either parenchymal hemorrhage or intravascular congestion is presented here. Dysfunctional microvascular pericytes are characterized by their location in the neurovascular unit, either on the arteriole or venule side. Pathophysiological and pathological changes caused by coronavirus disease 2019 (COVID-19) include pulmonary hypertension, edema, focal hemorrhage, microvascular congestion, and thrombosis. In this paper, the application of the pericytes-centered hypothesis to COVID-19 has been presented by proposing the concept of a pulmonary neurovascular unit (pNVU). The application of this concept implies that human lungs contain approximately 300 million pNVUs. This concept of existing local regulation of microvascular blood flow is supported by the observation of pathophysiology in pulmonary embolism and in acute high-altitude illness. The autonomic control seen in these three disease states matches blood flow with oxygen supply in each pNVU to maintain physiological blood oxygen saturation level. This paper illustrates how the malfunction of microvascular pericytes may cause focal hemorrhage, edema or microvascular congestion and thrombosis. A bypass existing in each pNVU would autonomically deviate blood flow from a COVID-19-affected pNVU to other healthy pNVUs. This action would prevent systemically applied medicines from reaching the therapeutic threshold in COVID-19-affected pNVUs. While testing this hypothesis with experimental evidence is urgently needed, supporting therapy aimed at improving microcirculation or rebuilding the physiological function of microvascular pericytes is recommended as a potentially effective treatment of COVID 19.

Research Progress of Genetic Structure, Pathogenic Mechanism, Clinical Characteristics, and Potential Treatments of Coronavirus Disease 2019.

Coronavirus disease 2019 (COVID-19) is a global pandemic infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), and currently affects more than 8 million people worldwide. SARS-CoV-2 mainly invades the cells by binding to the angiotensin converting enzyme 2 (ACE2) receptor, leading to the injury of respiratory system, cardiovascular system, digestive system, and urinary system, and even secondary to acute respiratory distress syndrome (ARDS) and systemic inflammatory response, resulting in multiple organ failure. In this review, mainly focusing on biogenesis and pathogenic mechanisms, we describe the recent progress in our understanding of SARS-CoV-2 and then summarize and discuss its crucial clinical characteristics and potential mechanism in different systems. Additionally, we discuss the potential treatments for COVID-19, aiming at a better understanding of the pathogenesis of SARS-CoV-2 and providing new ideas for the personalized treatment of COVID-19.

Systematic Comparison of Two Animal-to-Human Transmitted Human Coronaviruses: SARS-CoV-2 and SARS-CoV.

After the outbreak of the severe acute respiratory syndrome (SARS) in the world in 2003, human coronaviruses (HCoVs) have been reported as pathogens that cause severe symptoms in respiratory tract infections. Recently, a new emerged HCoV isolated from the respiratory epithelium of unexplained pneumonia patients in the Wuhan seafood market caused a major disease outbreak and has been named the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This virus causes acute lung symptoms, leading to a condition that has been named as "coronavirus disease 2019" (COVID-19). The emergence of SARS-CoV-2 and of SARS-CoV caused widespread fear and concern and has threatened global health security. There are some similarities and differences in the epidemiology and clinical features between these two viruses and diseases that are caused by these viruses. The goal of this work is to systematically review and compare between SARS-CoV and SARS-CoV-2 in the context of their virus incubation, originations, diagnosis and treatment methods, genomic and proteomic sequences, and pathogenic mechanisms.