Abstract
The world experienced the outbreak of a new pandemic disease in 2019, known as coronavirus (CoV) disease 2019 (COVID-19), which is caused by the novel severe acute respiratory syndrome-CoV-2 (SARS-CoV-2). The respiratory system is the organ system most commonly affected by COVID-19; however, several other organ systems have been reported to be affected. The SARS-CoV-2 RNA found in infected stub samples can cause lung contagion by binding to the angiotensin-converting enzyme-2 (ACE-2) receptor of the alveolar epithelial cells. The gut microbiota (GM) promote immunity, indicating that the alignment of the microbiota and corresponding metabolic processes in COVID-19 can help to identify novel biomarkers and new therapeutic targets for this disease. The cause of kidney damage in COVID-19 patients is possibly multifactorial, involving a complex mechanism that involves complement dysregulation and thrombotic microangiopathy, as well as the occurrence of a “cytokine storm” syndrome, which are immune responses that are abandoned and dysfunctional with unfavorable prognosis in severe COVID-19 cases. Furthermore, COVID-19 involves a continuous proliferation and activation of macrophages and lymphocytes. SARS-CoV-2 can also bind to the ACE-2 receptor expressed in the cerebral capillary endothelial cells that can invade the blood-brain wall, to penetrate the brain parenchyma. However, in the ongoing pandemic, there has been a surge in studies on a wide range of topics, including causes of respiratory failure, asymptomatic patients, intensive care patients, and survivors. This review briefly describes the damaging effects of COVID-19 on vital human organs and the inhibitory function of the ACE-2 receptor on the GM, which causes gut dysbiosis, and thus, this review discusses topics that have an opportunity for further investigation.
Highlights
Coronavirus (CoV) disease-2019(COVID-19) is a public health concern due to its rapid spread and high mortality rate throughout the world, despite its discovery in late 2019 in Wuhan, the capital of the Hubei province of China[1]
In January 2020, a study reported that RNA detected in COVID-19 patients was similar to the SARS-CoV-2 viral genome responsible for causing bilateral interstitial pneumonia[2]
Mounting evidence suggest that angiotensin-converting enzyme-2 (ACE-2) plays a vital role in the progression of gut dysbiosis in response to renal, metabolic, and cardiovascular distress associated with older age[16,17,18,19]
Summary
Coronavirus (CoV) disease-2019(COVID-19) is a public health concern due to its rapid spread and high mortality rate throughout the world, despite its discovery in late 2019 in Wuhan, the capital of the Hubei province of China[1]. In January 2020, a study reported that RNA detected in COVID-19 patients was similar to the SARS-CoV-2 viral genome responsible for causing bilateral interstitial pneumonia[2] This virus is included in the β-CoV cluster of viruses that causes SARS and Middle East respiratory syndrome (MERS), based on a report by the World Health Organization (WHO)[2,3,4,5]. The symptoms of COVID-19, including shortness of breath, fever, coughing, and pneumonia, typically appear between 2 and 14 days after the viral infection It can harm other organs in the body, such as the intestines, liver, and brain, as well as cause lungrelated problems after hospitalization, which may lead to rapid death compared to those observed in previous cases of SARS- and MERS-CoV infections[6,7,8].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
