Over the two years that we have been experiencing the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) pandemic, our challenges have been the race to develop vaccines and the difficulties in fighting against new variants due to the rapid ability of the virus to evolve. In this sense, different organizations have identified and classified the different variants that have been emerging, distinguishing between variants of concern (VOC), variants of interest (VOI), or variants under monitoring (VUM). The following review aims to describe the latest updates focusing on VOC and already de-escalated variants, as well as to describe the impact these have had on the global situation. Understanding the intrinsic properties of SARS-CoV-2 and its interaction with the immune system and vaccination is essential to make out the underlying mechanisms that have led to the appearance of these variants, helping to determine the next steps for better public management of this pandemic.
In December 2019, SARS-CoV-2 was identified in Wuhan, China. Infection by SARS-CoV-2 causes coronavirus disease 2019 (COVID-19), which is characterized by fever, cough, dyspnea, anosmia, and myalgia in many cases. There are discussions about the association of vitamin D levels with COVID-19 severity. However, views are conflicting. The aim of the study was to examine associations of vitamin D metabolism pathway gene polymorphisms with symptomless COVID-19 susceptibility in Kazakhstan. The case-control study examined the association between asymptomatic COVID-19 and vitamin D metabolism pathway gene polymorphisms in 185 participants, who previously reported not having COVID-19, were PCR negative at the moment of data collection, and were not vaccinated. A dominant mutation in rs6127099 (CYP24A1) was found to be protective of asymptomatic COVID-19. Additionally, the G allele of rs731236 TaqI (VDR), dominant mutation in rs10877012 (CYP27B1), recessive rs1544410 BsmI (VDR), and rs7041 (GC) are worth consideration since they were statistically significant in bivariate analysis, although their independent effect was not found in the adjusted multivariate logistic regression model.
There is a complex interaction between glucose and insulin homeostasis pathways, diabetes and autism spectrum disorder (ASD). It is known that neuronal migration pathways may be interrupted by intrauterine hyperinsulinemia and hyperglycemia. Moreover, neonatal hypoglycemia which is related to mitochondrial dysfunction has a potential role that influences ASD pathogenesis [6,7]. We present here a preliminary case-control study on children and adolescents (8 -15 years old) with and without autism spectrum disorder examining the association between genetic polymorphisms impacting glucose and insulin homeostasis and autism spectrum disorder in Kazakhstan. Methods:In this case-control study looking at 211 samples, associations of glucose and insulin homeostasis gene polymorphisms of 10 genes and demographic variables with autism spectrum disorder were examined. Fisher's exact test and multivariate logistic regression models were used to find associations between polymorphisms and other predictors.Results: Preliminary results suggest that there is a complex relation between autism spectrum disorder and genetic variations that are associated with impaired glucose and insulin homeostasis susceptibility. There is a significant association of the T allele of ADIPOQ (rs1501299) (OR=1.75, 95% CI:1.04-2.93, p-value=0.035); the T allele of GCKR (rs1260326) (OR=0.6, 95% CI:0.39-0.93, p-value=0.023); the T allele of SLC30A8 (rs13266634) (OR=1.77, 95% CI:1.12-2.78, p-value=0.014); and the recessive GG genotype of rs10757278 (CDKN2B) (OR=2.58, 95% CI: 1.24-5.36, p-value=0.011) with autism spectrum disorder in the Kazakhstan population. Conclusion:Overall, this preliminary study revealed that there is evidence of significant associations between glucose and insulin homeostasis gene polymorphisms and autism spectrum disorder susceptibility in Kazakhstan and further study in this area to further verify this, is needed.
This article presents novel ideas about classification, genomic structure (inverted regions, mobile genetic elements, plasmids, mobilized and conjugated transposons), pathogenicity factors (adhesins, various enzymes, toxins, in particular, data on enterotoxin fragmentinis BFT - B. fragilis toxin), and the role of their metabolites in the manifestation of pathogenicity. Data on the global prevalence of antibiotic resistance in the clinical B. fragilis strains are presented. Mechanisms of development of the drug resistance are considered and the role of cfiA, tet, nim genes in the development of antibiotic resistance is disclosed. Information on the use of the MALDI-TOF MS (matrix-activated laser desorption-ionization time-of-flight mass spectrometry) method for distinguishing B.fragilis strains into two groups based on the ability to carry carbapenem resistant gene (carrying and not carrying cfiA gene) are presented. Basics of modes of emergence of multi-resistance in clinical strains of B. fragilis are considered. In addition, prospects for genome-wide sequencing in predicting antimicrobial resistance are presented. Currently increasing attention of researchers is payed to increase in resistance of B. fragilis to widely used antimicrobials. This is indeed of a great importance when choosing adequate antimicrobial therapy.
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