The global public health scenario is worsening gradually as the confirmed cases of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infections are incessantly escalating with every passing day. The pathological condition caused by SARS-CoV-2 is termed as Coronavirus disease 2019 (COVID-19). The understanding of SARS-CoV-2 transmission dynamics, immunopathogenesis, and the need for early-stage diagnosis and the effective therapeutic regime are the few immediate challenges faced by healthcare professionals worldwide. More specifically, the role of SARS-CoV-2 in the host’s immunopathogenesis response is crucial to determine the disease severity and its clinical outcome in COVID-19 patients. In the present review, we provide insights into the SARS-CoV-2 pathology, host immune responses including innate, cellular, and humoral responses, and immunomodulatory functions of SARS-CoV-2 including cytokine storm and immune evasion. We also shed light upon the present clinical and laboratory-based applications enrolled in the SARS-CoV-2 diagnosis. Taking into consideration the pathogenesis and SARS-CoV-2 immune function, in the present review, we finally provide succinct insights into the SARS-CoV-2 transmission dynamics, immunopathogenesis, with the assessment of the current diagnostic and preventive/ therapeutic strategies.
Background Cytochrome P450 system is implicated in vascular pathologies, including stroke. Besides its role as a drug metabolizer, it also plays an important role in the metabolism of several endogenous substances like fatty acids, arachidonic acid, etc., which have pro-inflammatory effects. On the other hand, leptin and adiponectin are two of the most common adipose tissue-derived cytokines (adipokines), which are pro-inflammatory and anti-inflammatory in nature, respectively. Both of them are implicated in the pathogenesis of stroke. Methods We prospectively recruited ischemic stroke patients (within three months of occurrence of an attack of stroke). The occurrence of composite outcome (recurrence of transient ischemic attack/ischemic stroke or death) was evaluated for association with genetic variants of CYP2C19 (allele *2, *17, *3, and *4, i.e., single nucleotide polymorphism (SNP) 1/2/3/4, identified using TaqMan assays and DNA sequencing). Adiponectin and leptin levels were determined using an enzyme-linked immunosorbent assay. Comparisons were made between stroke vs. control patients and between CYP2C19 intermediate metabolizer (IM)/poor metabolizer (PM) vs. extensive metabolizer (EM)/ultra metabolizer (UM) (PM: *2/*2; IM: *1/*2 vs. EM: *1/*1; UM: *1/*17). P < 0.05 was taken as the threshold for statistical significance. Results A total of 204 patients and 101 controls were recruited. With regard to the occurrence of stroke, SNP2 showed a significant positive association. Haplotypes (SNP1/SNP2) AC (OR = 1.75 (1.08-2.83), p = 0.024) and GT (OR = 3.33 (1.53-7.22), p = 0.0026) were strongly associated with the occurrence of ischemic stroke even after adjustment for age and sex (global haplotype association p-value: 0.0062). Haplotype phenotype gender interaction was evident. Among stroke patients, with regard to composite outcome, only SNP1 showed a positive association. The AC haplotype was significantly associated with the occurrence of composite outcome (OR = 2.27 (1.17-4.41), p = 0.016). Among stroke patients, a significant positive association was seen between death and SNP1 (OR = 2.35 (1.13-4.90), p = 0.021) and AC haplotype (OR = 2.73 (1.20-6.22), p = 0.018). However, none of the SNPs or haplotypes showed any association with recurrence. Significant higher leptin and lower adiponectin levels were observed among stroke patients compared to controls. Leptin levels were higher in IM/PM group. IM/PM phenotypes showed a higher incidence of occurrence of composite outcome (hazard ratio = 2.07 (0.96-4.47), p = 0.056). Conclusion CYP2C19 polymorphisms may play a significant role in the pathogenesis of stroke. Leptin could serve as a prominent biomarker of atherosclerosis and inflammation in the early post-stroke period; however, further study is warranted with a larger sample size.
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