Association of IL-17F Gene Polymorphism and Its Serum Level with SARS-CoV-2 Infection.

OBJECTIVE: Although multiple studies have addressed the clinical outcomes of coronavirus disease, little data exist regarding the defi- nition of immune and inflammatory profiles associated with this infection. Its clinical manifestations often worsen in association with hypercytokinemia (elevated interleukin 8 and interleukin 17). We conducted this research to elucidate the effect of interleukin 17 levels and interleukin 17F gene polymorphism on the severity and outcomes of coronavirus disease. MATERIAL AND METHODS: Ninety patients with confirmed coronavirus disease and 30 healthy controls were enrolled. Coronavirus disease cases were classified into nonsevere, severe, and critical according to the World Health Organization definition. Approximately 10 mL peripheral blood sample was collected from all patients and controls by venipuncture in-plane and ethylenediaminetetraacetic acid tube. Enzyme-linked immunosorbent assay kits were used for calculating serum interleukin 17 levels, whereas real-time polymerase chain reaction was used for genotyping using the 5'-nuclease allelic discrimination assay for single nucleotide polymorphisms genotyping. RESULTS: As regards interleukin 17 levels, there was a significant elevation of interleukin 17 in coronavirus disease cases compared to control healthy persons (P < .001). Moreover, serum interleukin 17 levels tended to be significantly higher with increased disease sever- ity (P = .004). Patients with critical diseases expressed a significant rise of interleukin 17 compared to severe (P = .03) and nonsevere cases (P = .02). We noted no significant difference between the critical, severe, and nonsevere cases regarding different interleukin 17F genotypes. CONCLUSION: Coronavirus disease is associated with elevated levels of interleukin 17, which tended to be considerably higher with disease severity. However, different interleukin 17F genotypes do not affect either the predisposition or the severity of coronavirus disease.

Molecular Study of Mec-Phenol Soluble Modulin Gene in Methicillin Resistant Staphylococcus Aureus.

BACKGROUND: Staphylococcus aureus (S. aureus) is a main pathogen associated with different types of hospital acquired infections. There are various factors associated with the virulence of S. aureus. Among these factors are biofilm formation, antibiotics resistance, alpha-toxin, and phenol-soluble modulins (PSMs) which are encoded by genes within the core genome. The aims of the present study were to identify the prevalence psm-mec gene in MRSA isolated from different types of hospital acquired infections and to study the association of this gene with biofilm formation capacity in S. aureus. METHODS: The study was a retrospective, cross-sectional study that included 150 isolates of MRSA isolated from different clinical samples. Methicillin resistant S. aureus was identified as resistance to cefoxitin disc by disc diffusion method, biofilm detection by microplate method, and polymerase chain reaction (PCR) was used for detection of PSMα gene. RESULTS: MRSA was identified by phenotypic detection with resistance to cefoxitin disc in 64.7% of the isolated S. aureus. Biofilm formation was detected in 70 isolates (46.7%) with high titer in 61 isolates, intermediate titer in 6 isolates and low titer in 4 isolates. PSMα gene detected in 65 (43.3%) of the isolates, Table 1. There was significant association between the presence of PSMα gene and formation of biofilm (p = 0.0001). All detected PSMα genes were present in 65 (92.8%) of positive S. aureus isolates for biofilm formation. CONCLUSIONS: There was high prevalence of the PSMα gene in MRSA with association with high titer biofilm forming S. aureus. The absence of PSMα gene in MRSA strains may reduce the ability of MRSA to form biofilm.

Telomerase reverse transcriptase (TERT) A1062T mutation as a prognostic factor in Egyptian patients with acute myeloid leukemia (AML).

This study aimed to evaluate the incidence and clinical and prognostic impact of TERT A1062T mutation in AML patients treated at Mansoura Oncology Center. Screening for TERT A1062T mutation in exon 15 of the TERT gene was performed on diagnostic DNA samples from 153 AML patients and 197 healthy subjects as a control group by using sequence-specific primers. TERT A1062T mutation was detected in 18 cases out of 153 patients (11.8 %) and in one out of 197 control group subjects (0.51 %). The achievement of complete remission was significantly higher in AML group with wild type as compared to that in the mutant one (53.3 vs 16.7 %, respectively). In addition, the relapse rate was significantly higher in the mutant patients as compared to those with wild type (62.5 vs 28.2 %, respectively). The AML patients with TERT (A1062T) mutation had shorter overall survival than patients with wild type (P = 0.001). In a multivariable analysis, TERT (A1062T) mutational status is independently worse predictor factor (P = 0.007) when controlling for cytogenetic status (P = <0.001), performance status (P = <0.001) and bone marrow blast cells (P = 0.001). In conclusion, TERT A1062T mutation is an independent negative prognostic factor in AML patients. Therefore, molecular testing for TERT A1062T mutation in patients with AML is recommended in order to delineate their prognostic status.