Background: Complete SARS-CoV-2 genome sequencing in the early phase of the outbreak in Iran showed two independent viral entries. Subsequently, as part of a genome surveillance project, we aimed to characterize the genetic diversity of SARS-CoV-2 in Iran over one year after emerging. Methods: We provided 319 SARS-CoV-2 whole-genome sequences used to monitor circulating lineages in March 2020-May 2021 time interval. Results: The temporal dynamics of major SARS-CoV-2 clades/lineages circulating in Iran is comparable to the global perspective and represent the 19A clade (B.4) dominating the first disease wave, followed by 20A (B.1.36), 20B (B.1.1.413), 20I (B.1.1.7), leading the second, third and fourth waves, respectively. We observed a mixture of circulating B.1.36, B.1.1.413, B.1.1.7 lineages in winter 2021, paralleled in a fading manner for B.1.36/B.1.1.413 and a growing rise for B.1.1.7, prompting the fourth outbreak. Entry of the Delta variant, leading to the fifth disease wave in summer 2021, was detected in April 2021. This study highlights three lineages as hallmarks of the SARS-CoV-2 outbreak in Iran; B4, dominating early periods of the epidemic, B.1.1.413 (B.1.1 with the combination of [D138Y-S477N-D614G] spike mutations) as a characterizing lineage in Iran, and the co-occurrence of [I100T-L699I] spike mutations in half of B.1.1.7 sequences mediating the fourth peak. It also designates the renowned combination of G and GR clades’ mutations as the top recurrent mutations. Conclusion: In brief, we provided a real-time and comprehensive picture of the SARS-CoV-2 genetic diversity in Iran and shed light on the SARS-CoV-2 transmission and circulation on the regional scale.
Introduction Vaccination plays a fundamental role in mastering the COVID‐19 pandemic and protecting vulnerable groups. Persons with autoimmune inflammatory rheumatic diseases (AIIRD) requiring immunosuppressive therapies are prioritized for vaccination. However, data concerning immunogenicity and safety of the BBIBP‐CorV vaccine in immunosuppressed patients are not found. This study presents data on the efficacy and safety of the BBIBP‐CorV vaccine in immunosuppressed patients compared to healthy controls. Methods Study population consisted of 100 healthy controls and 100 patients with AIIRD. Vaccination was performed according to national guidelines with the BBIBP‐CorV vaccine. SARS‐CoV‐2 neutralizing antibody titers were quantified by enzyme‐linked immunosorbent assay before initial vaccination and 1–3 months after secondary vaccination. Adverse events were assessed before study initiation and 7 days after the second dose. Disease activity was studied before entering the study and 3–8 weeks after the second dose. Results Vaccination‐induced positive immunogenic response rates and SARS‐CoV‐2 neutralizing antibody titers were significantly lower in the AIIRD patients than healthy subjects (p < .05). There are significant differences in neutralizing antibody titers among patients suffering from rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis, and ankylosing spondylitis (p < .01–.05). The rates of seropositive vaccine responses were similarly distributed across all diseases. Healthy and AIIRD individuals had a similar profile in adverse events. No significant difference was observed in SARS‐CoV‐2 antibody titers between subjects suffering from side effects and those who did not have. SARS‐CoV‐2 neutralizing antibody levels were significantly higher in subjects with a history of COVID‐19 infection than seronegative individuals (p < .01–0.05). Seropositive subjects had a significant increase in the percentage of vaccine‐related adverse events compared to seronegative persons (p < .05). Despite a minor change in the disease activity of patients with RA and SLE, disease activity indices were overall stable in the AIIRD patients. Conclusion These findings revealed that the BBIBP‐CorV vaccine is effective in the development of neutralizing antibodies in immunosuppressed patients without considerable reactogenicity or induction of disease flares.
BACKGROUND: Considerable evidence supports that SLE could be related to apoptotic cells and EBV infection. OBJECTIVE: The aim of this study was to identify the transcriptional signature of EBV infection in SLE patients for survey of the molecular apoptosis signaling pathways. METHODS: The PBMCs gene expression profiles of healthy control and SLE patients were obtained from GEO. Functional annotation and signaling pathway enrichment were carried out using DAVID, KEGG. To validate bioinformatics analysis the changes in genes expression of some of obtained genes, Real time PCR was performed on PBMCs from 28 SLE patients and 18 controls. RESULTS: We found that mean viral load was 6013 ± 390.1 copy/μg DNA from PBMCs in all patients. QRT-PCR results showed that the expression of the DUSP1 and LAMP3 genes which had most changes in the logFC among 4 candidate genes, increased significantly in comparison with control. The consistent expression of LMP2 as viral latency gene involve in apoptosis signaling pathways was detected in SLE patients with EBV viral load and some controls. CONCLUSIONS: The study indicated that some cellular genes may have an important role in pathogenesis of SLE through apoptosis signaling pathways. Beside, EBV infection as an environmental risk factor for SLE may affect the dysfunction of apoptosis.
Background: About 70% of individuals worldwide suffer from herpes simplex virus 1 (HSV-1). Several studies have reported that selenium and supernatant of probiotic bacteria are antiviral; nevertheless, their effect alone or synergistically on HSV-1 is unknown. Objectives: The present study aimed to evaluate the antiviral effects of Bacillus clausii supernatant, selenium (Se), and their combination on HSV-1. Methods: After determining cytotoxicity by the MTT assay, selenium and B. clausii supernatants were added to HeLa cells 24 hours before (pre-infection treatment) and after (post-infection treatment) HSV-1 inoculation. After 47 hours of incubation at 37°C, the viral titer and expression levels of the unique long 47 (UL47) gene were determined by the 50% tissue culture infectious dose (TCID50) and real-time polymerase chain reaction methods, respectively. Results: The bacterial supernatant in dilutions of 1:4 and 1:8, selenium in concentrations of 0.5 and 1 μM, and a combination of them had a cytotoxicity level lower than 80% in HeLa cells. The HSV-1 titers in pre-infection and post-infection assays with a dilution of 1:4 supernatant decreased by about 2.16 and 1 log10 TCID50/mL, respectively. Moreover, 1 μM Se could reduce the virus titer by 2.33 log10 TCID50/mL. The virus titer showed a greater decrease when Se and the bacterial supernatants were combined than when only one of the two was used. The highest selectivity index (SI) was obtained when selenium and bacterial supernatant were combined (SI = 29.2). The combined use of 1 μM Se and a 1:4 dilution of B. clausii supernatant caused the greatest drop in virus titer (3.3 log10 TCID50/mL) in comparison to other treatment conditions. The UL47 gene expression was reduced by Se at concentrations of 0.5 and 1 μM by about 1.6- and 2-fold, respectively. The UL47 expression showed a higher decline when selenium and bacterial supernatant were combined than when only one of the two was employed, which is similar to viral titer data. Conclusions: Selenium and the supernatant of B. clausii have potent antiviral activity against HSV-1. The combination of selenium and the bacterial supernatant has a synergistic effect in reducing HSV-1 replication. However, further research is required to fully understand how they inhibit viruses.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.