COVID-19 is a novel coronavirus with an outbreak of unusual viral pneumonia in Wuhan, China, and then pandemic. Based on its phylogenetic relationships and genomic structures the COVID-19 belongs to genera Betacoronavirus. Human Betacoronaviruses (SARS-CoV-2, SARS-CoV, and MERS-CoV) have many similarities, but also have differences in their genomic and phenotypic structure that can influence their pathogenesis. COVID-19 is containing singlestranded (positive-sense) RNA associated with a nucleoprotein within a capsid comprised of matrix protein. A typical CoV contains at least six ORFs in its genome. All the structural and accessory proteins are translated from the sgRNAs of CoVs. Four main structural proteins are encoded by ORFs 10, 11 on the one-third of the genome near the 3 0 -terminus. The genetic and phenotypic structure of COVID-19 in pathogenesis is important. This article highlights the most important of these features compared to other Betacoronaviruses.
Background Autophagy is one of the important mechanisms in cell maintenance, which is considered associated with different pathological conditions such as viral infections. In this current study, the expression level and polymorphisms in some of the most important genes in the autophagy flux in COVID‐19 patients were evaluated. Materials and methods This cross‐sectional study was conducted among 50 confirmed COVID‐19 patients and 20 healthy controls. The COVID‐19 patients were divided into a severe group and a mild group according to their clinical features. The expression levels of ATG5, ATG16L1, LC3, and BECN1 were evaluated by the 2 ‐∆∆CT method and beta‐actin as the internal control. The polymorphisms of the ATG5 (rs506027, rs510432) and ATG16L1 (rs2241880 or T300A) were evaluated by the Sanger sequencing following the conventional PCR. Results The mean age of the included patients was 58.3±17.9 and 22 (44%) were female. The expression levels of the LC3 were downregulated while BECN1 and ATG16L1 genes represent an up‐regulation in COVID‐19 patients. The polymorphism analysis revealed the ATG16L1 rs2241880 and AGT5 rs506027 polymorphism frequencies are statistically significantly different between COVID‐19 and Healthy controls. Conclusion The autophagy alteration represents an association with COVID‐19 pathogenesis and severity. The current study is consistent with the alteration of autophagy elements in COVID‐19 patients by mRNA expression level evaluation. Furthermore, ATG16L1 rs2241880 and AGT5 rs506027 polymorphisms seem to be important in COVID‐19 and are highly suggested for further investigations.
Kaposi's sarcoma‐associated herpesvirus (KSHV), also known as human herpes virus 8 (HHV‐8), causes primary effusion lymphoma, multicentric Castleman's disease, and Kaposi's sarcoma. Few antiviral drugs are available to efficiently control KSHV infection, and therefore, the development of novel, effective anti‐KSHV treatments is needed. The aim of this study was to determine the antiviral activity of ethanolic and aqueous extracts, essential oils, and certain flavonoids (hesperidin, eupafolin, and vicenin) derived from Thymus capitatus (commonly known as thyme). We assessed the toxicity of these different extracts and components in RPE‐1 cell cultures using the MTS test and evaluated their antiviral effect using the TCID50 method. The mechanism of action was determined through time‐of‐addition tests as well as viral entry, attachment, and virucidal assays. Additionally, western blot analysis was also used to assess their modes of action. Total treatment assay showed that the aqueous extract of T. capitatus has the highest inhibitory effect against KSHVLYT with an EC50 value of 0.2388 µg·mL−1. Both hesperidin and eupafolin showed the ability to inactivate viral infection in a dose–response manner (EC50 values of 0.2399 and 1.396 µm, respectively). Moreover, they were able to inactivate KSHVLyt postinfection by reducing viral protein expression. In summary, the effective antiviral property of the aqueous extract is likely a result of the inhibition of viral growth within the host cells by both hesperidin and eupafolin.
Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) has high mortality due to the widespread infection and the strong immune system reaction. Interleukins (ILs) are among the main immune factors contributing to the deterioration of the immune response and the formation of cytokine storms in coronavirus disease 2019 (COVID-19) infections. Introduction: This review article investigated the relationship between virus structure, risk factors, and patient plasma interleukin levels in infections caused by the coronavirus family. Method: The keywords "interleukin," "coronavirus structure," "plasma," and "risk factors" were the main words searched to find a relationship among different interleukins, coronavirus structures, and risk factors in ISI, PUBMED, SCOPUS, and Google Scholar databases. Results: Patients with high-risk conditions with independent panels of immune system markers are more susceptible to death caused by SARS-CoV2. IL-4, IL-10, and IL-15 are probably secreted at different levels in patients with coronavirus infections despite the similarity of inflammatory markers during coronavirus infections. SARS-CoV2 and SARS-CoV increase the secretion of IL-4 in the Middle East respiratory syndrome coronavirus (MERS-CoV) infection, while it remains unchanged in MERS-CoV infection. MERS-CoV infection demonstrates increased IL-10 levels. However, IL-10 levels increase during SARS-CoV infection, and different levels are recorded in SARS-CoV2. MERS-CoV increases IL-15 secretion while its levels remain unchanged in SARS-CoV2. Conclusion: In conclusion, the different structures of SARS-CoV2, such as length of spike or nonstructural proteins (NSPs), and susceptibility of patients based on their risk factors may lead to differences in immune marker secretion and pathogenicity. Therefore, identifying and controlling interleukin levels can play a significant role in controlling the symptoms and the development of individual-specific treatments.
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