Summary To date, seven human coronaviruses (HCoVs) have been detected: HCoV‐NL63, HCoV‐229E, HCoV‐HKU1, HCoV‐OC43, severe acute respiratory syndrome coronavirus (SARS‐CoV), Middle East respiratory syndrome coronavirus (MERS‐CoV) and SARS‐CoV‐2. Four of these viruses, including HCoV‐NL63, ‐229E, ‐HKU1 and ‐OC43, usually cause mild‐to‐moderate respiratory diseases with a seasonal pattern. Since 2000, three new HCoVs have emerged with a significant mortality rate. Although SARS‐CoV and MERS‐CoV caused an epidemic in some countries, SARS‐CoV‐2 escalated into a pandemic. All HCoVs can cause severe complications in the elderly and immunocompromised individuals. The bat origin of HCoVs, the presence of intermediate hosts and the nature of their viral replication suggest that other new coronaviruses may emerge in the future. Despite the fact that all HCoVs share similarities in viral replication, they differ in their accessory proteins, incubation period and pathogenicity. This study aims to review these differences between the seven HCoVs.

Recently, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of coronavirus disease 2019 (COVID-19), has led to a worldwide pandemic with millions of infected patients. Alteration in humans’ microbiota was also reported in COVID-19 patients. The alteration in human microbiota may contribute to bacterial or viral infections and affect the immune system. Moreover, human’s microbiota can be altered due to SARS-CoV-2 infection, and these microbiota changes can indicate the progression of COVID-19. While current studies focus on the gut microbiota, it seems necessary to pay attention to the lung microbiota in COVID-19. This study is aimed at reviewing respiratory microbiota dysbiosis among COVID-19 patients to encourage further studies on the field for assessment of SARS-CoV-2 and respiratory microbiota interaction.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), has led to huge concern worldwide. Some SARS-CoV-2 infected patients may experience post–COVID-19 complications such as multisystem inflammatory syndrome, defined by symptoms including fever and elevated inflammatory markers (such as elevation of C reactive protein (CRP), erythrocyte sedimentation rate, fibrinogen, procalcitonin test, D-dimer, ferritin, lactate dehydrogenase or IL-6, presence of neutrophilia, lymphopenia, decreased albumin, and multiple organ dysfunction). Post–COVID-19 complications may also manifest as autoimmune diseases such as Guillain-Barré syndrome and systemic lupus erythematosus. Signaling disorders, increased inflammatory cytokines secretion, corticosteroid use to treat COVID-19 patients, or impaired immune responses are suggested causes of autoimmune diseases in these patients. In this review, we discuss the molecular and pathophysiological mechanisms and therapeutic opportunities for multisystem inflammatory syndrome and autoimmune diseases following SARS-CoV-2 infection with the aim to provide a clear view for health care providers and researchers.

Background To provide information about pathogens’ coinfection prevalence with SARS‐CoV‐2 could be a real help to save patients’ lives. This study aims to evaluate the pathogens’ coinfection prevalence among COVID‐19 patients. Method In order to find all of the relevant articles, we used systematic search approach. Research‐based databases including PubMed, Web of Science, Embase, and Scopus, without language restrictions, were searched to identify the relevant bacterial, fungal, and viral coinfections among COVID‐19 cases from December 1, 2019, to August 23, 2021. In order to dig deeper, other scientific repositories such as Medrxiv were probed. Results A total of 13,023 studies were found through systematic search. After thorough analysis, only 64 studies with 61,547 patients were included in the study. The most common causative agents of coinfection among COVID‐19 patients were bacteria (pooled prevalence: 20.97%; 95% CI: 15.95–26.46; I2: 99.9%) and less frequent were virus coinfections (pooled prevalence: 12.58%; 95% CI: 7.31–18.96; I2: 98.7%). The pooled prevalence of fungal coinfections was also 12.60% (95% CI: 7.84–17.36; I2: 98.3%). Meta‐regression analysis showed that the age sample size and WHO geographic region did not influenced heterogeneity. Conclusion We identified a high prevalence of pathogenic microorganism coinfection among COVID‐19 patients. Because of this rate of coinfection empirical use of antibacterial, antifungal, and antiviral treatment are advisable specifically at the early stage of COVID‐19 infection. We also suggest running simultaneously diagnostic tests to identify other microbiological agents’ coinfection with SARS‐CoV‐2.

Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) emerged in December 2019 in Wuhan province, China. SARS-CoV-2 causes coronavirus disease 2019 . Angiotensin-converting enzyme 2 (ACE2) has an essential role as a receptor in the entry of the SARS-CoV-2 into the host cells. It has been declared, ACE2 expresses in the lungs, heart, kidneys, placenta, and liver. This study reviews the liver's markers' characteristics in patients with COVID-19 to achieve novel insights in improving clinical treatment. Liver disease and chronic kidney disease patients are susceptible to COVID-19. There is limited information about the effects of SARS-COV-2 on patients with preexisting liver associated disorders, including chronic hepatitis B virus or hepatitis C virus, primary biliary cirrhosis, nonalcoholic fatty liver disease, and more are yet to be understood. By considering conducted studies in this manner since ACE2 receptors, which are the primary receptors for SRAS-CoV-2, exist on the liver and lungs, heart, kidneys, and placenta, SRAS-CoV-2 can infect liver cells too. Consequently, this infection will have resulted in liver function tests' escalated levels and total bilirubin as biochemical biomarkers. Further investigations need to be done to point out the hepatic manifestations of COVID-19's infected patients with chronic liver disease and improve clinical management and more stringent preventive measures for this type of infected patients.