Estimation of immune response (IgG) to SARS-COV2 (COVID-19) after the third COVID-19 wave in Egypt, A cross-sectional Study.

Since the start of the pandemic, the number of cases has been increased rapidly. Due to asymptomatic and mild cases and restricted testing in many geographic locations, the overall number of actual COVID-19 cases is likely significantly higher than the number of verified cases. Several COVID-19-related comorbid diseases impair immune system function, which has an impact on COVID-19 responsiveness. So, we evaluated the immune response to SARS-CoV-2 after the third wave of COVID-19 and assessed the effect of comorbid diseases on this immune response. The current cross-sectional study was conducted in August 2021 after the third wave of COVID-19. The study included 287 participants. All participants were asked about their epidemiological data, comorbid diseases, data suggesting COVID-19 infection, and precautions measures to minimize the exposure to the disease. Of the 278 participants, 50% had a positive IgG response to COVID-19. Regarding comorbid diseases, the IgG antibody titer was significantly lower in patients with chronic kidney diseases (CKD) on dialysis, ischemic heart disease, and chronic obstructive lung diseases than other participants (p= 0.01, p= 0.02, p= 0.005, respectively). Neither precaution measures nor comorbid diseases had a role in risk factors of COVID-19 infections in our participants. In conclusion, high seroprevalence (50%) of SARS-CoV-2 IgG antibody after the third wave of COVID-19 was observed in the current study. Comorbid conditions as hypertension, chronic cardiac diseases, chronic chest problems, and CKD on dialysis could decrease the immune response against COVID-19 infection.

Type VI secretion system (T6SS) in Klebsiella pneumoniae, relation to antibiotic resistance and biofilm formation.

Background and Objectives: The type VI secretion system (T6SS) was identified as a novel virulence factor in many Gram-negative bacteria. This study aimed to investigate the frequency of the T6SS genes in Klebsiella pneumoniae-causing different nosocomial infections, and to study the association between T6SS, antibiotic resistance, and biofilm formation in the isolated bacteria. Materials and Methods: A total of fifty-six non-repetitive K. pneumoniae isolates were collected from different inpatients admitted at Sohag University Hospital from September 2022 to March 2023. Samples were cultured, colonies were identified, and antimicrobial sensitivity was done by VITEK® 2 Compact. Biofilm formation was checked using Congo red agar method. T6SS genes, and capsular serotypes were detected by PCR. Results: Fifty-six K. pneumoniae isolates were obtained in culture. 38 isolates (67.86%) produced biofilm and 44 (78.57%) were positive for T6SS in PCR. There was a significant association between the presence of T6SS and resistance to the following antibiotics: meropenem, ciprofloxacin, and levofloxacin. All biofilm-forming bacteria had T6SS, with significant differences towards T6SS -positive bacteria. There was no significant association between T6SS, and the presence of certain capsular types. Conclusion: The T6SS-positive K. pneumoniae has greater antibiotic resistance, and biofilm-forming ability which is considered a potential pathogenicity of this emerging gene cluster.

Associations between IL-17A G/A-rs2275913 and IL 23R A/G-rs11209026 gene polymorphisms and severe coronavirus disease 2019 (COVID-19).

Severe COVID-19 disease was linked to a severe proinflammatory response and cytokine storm interleukin 17 (IL-17) is one of these cytokines, was associated with severe acute lung injury and multiorgan dysfunction. Single nucleotide polymorphisms (SNPs) in genes coding IL-17 can affect level of IL-17 hence its role in diseases. Also, SNPs in IL-23 R which control IL-23 is the main activator of IL-17 production. This study aimed to determine whether the IL-17A (G/A-rs2275913), IL-23R (A/G rs11209026) SNPs and serum levels of IL-17 were related to the risk of severe COVID-19. This case-control study included 120 confirmed COVID-19 patients, divided into two categories according to the severity of the disease and 74 normal subjects as controls. COVID-19 patients were SARS-CoV-2 positive by a reverse transcription-polymerase chain reaction and subjected to full clinical examinations, routine laboratory tests, and radiographic evaluations. The IL-17 levels were assessed using ELISA method, and genotyping of IL-17A (197 A/G; rs2275913) and IL-23R rs11209026 (A/G) was performed by the TaqMan Genotyping Assay. There were no differences in the distribution of IL-17A or IL-23R genotypes between COVID-19 groups and the control group (p=0.93 and p=0.84, respectively). Severe COVID-19 patients had significantly higher IL-17 serum levels than non-severe COVID-19 (p=0.0001). The GG genotypes of IL-17A were significantly higher in severe COVID-19 patients (p=0.004). Multivariate logistic regression analysis revealed that AG, GG genotypes of IL-17 and IL-17A were independent predictors of COVID-19 disease severity (p < 0.0001, p=0.06 and p=0.04, respectively). ROC curve analysis for IL-17, as predictor of severe COVID-19 disease revealed a sensitivity of 87.9% and specificity of 66.1% at a cutoff point of 114 pg/ml with AUC = 0.799. In conclusion, these findings indicated that IL-17 may be considered a marker of severe COVID-19. IL-17A SNPs may have a role in COVID-19 severity. IL-23R SNPs had no role in COVID-19.