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.
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.
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.
The severe acute respiratory syndrome (SARS-CoV-2), a newly emerging of coronavirus, continues to infect humans in the absence of a viable treatment. Neutralizing antibodies that disrupt the interaction of RBD and ACE2 has been under the spotlight as a way of developing the COVID-19 treatment. Some animals, such as llamas, manufacture heavy-chain antibodies that have a single variable domain (VHH) instead of two variable domains (VH/VL) as opposed to typical antibodies. Nanobodies are antigen-specific, single-domain, changeable segments of camelid heavy chain-only antibodies that are recombinantly produced. These types of antibodies exhibit a wide range of strong physical and chemical properties, like high solubility, and stability. The VHH's high-affinity attachment to the receptor-binding domain (RBD) allowed the neutralization of SARS-CoV-2. To tackle COVID-19, some nanobodies are being developed against SARS-CoV-2, some of which have been recently included in clinical trials. Nanobody therapy may be useful in managing the COVID-19 pandemic as a potent and low-cost treatment. This paper describes the application of nanobodies as a new class of recombinant antibodies in COVID-19 treatment.
Hepatitis A virus (HAV) is one of the well-known viruses that cause hepatitis all around the globe. Although this illness has decreased in developed countries due to extensive immunization, numerous developing and under-developed countries are struggling with this virus. HAV infection can be spread by oral-fecal contact, and there are frequent epidemics through nutrition. Improvements in socioeconomic and sanitary circumstances have caused a shift in the disease’s prevalence worldwide. Younger children are usually asymptomatic, but as they become older, the infection symptoms begin to appear. Symptoms range from slight inflammation and jaundice to acute liver failure in older individuals. While an acute infection may be self-limiting, unrecognized persistent infections, and the misapplication of therapeutic methods based on clinical guidelines are linked to a higher incidence of cirrhosis, hepatocellular carcinoma, and mortality. Fortunately, most patients recover within two months of infection, though 10–15% of patients will relapse within the first six months. A virus seldom leads to persistent infection or liver damage. The mainstay of therapy is based on supportive care. All children from 12–23 months, as well as some susceptible populations, should receive routine vaccinations, according to the Centers for Disease Control and Prevention and the American Academy of Pediatrics. Laboratory diagnosis of HAV is based on antigen detection, checking liver enzyme levels, and antibody screening. Furthermore, polymerase chain reaction (PCR) technology has identified HAV in suspected nutrition sources; therefore, this technique is used for preventative measures and food-related laws.
After the announcement of a new coronavirus in China in December 2019, which was then called SARS-CoV-2, this virus changed to a global concern and it was then declared as a pandemic by WHO. Human leukocyte antigen (HLA) alleles, which are one of the most polymorphic genes, play a pivotal role in both resistance and vulnerability of the body against viruses and other infections as well as chronic diseases. The association between HLA alleles and preexisting medical conditions such as cardiovascular diseases and diabetes mellitus is reported in various studies. In this review, we focused on the bioinformatic HLA studies to summarize the HLA alleles which responded to SARS-CoV-2 peptides and have been used to design vaccines. We also reviewed HLA alleles that are associated with comorbidities and might be related to the high mortality rate among COVID-19 patients. Since both genes and patients’ medical conditions play a key role in both severity of the disease and the mortality rate in COVID-19 patients, a better understanding of the connection between HLA alleles and SARS-CoV-2 can provide a wider perspective on the behavior of the virus. Such understanding can help scientists, especially in terms of protecting healthcare workers and designing effective vaccines.
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