BACKGROUND: As the world settles down from the COVID-19 pandemic, many countries are faced with an unexpected outbreak of monkeypox infection. Monkeypox is a zoonotic disease caused by monkeypox virus (MPXV), which is an enveloped, double stranded DNA virus belonging to the Poxviridae family. Presently, we construct and analyze the phylo-geo-network and the corresponding haplogroups. Presently, we performed the haplogroup analysis with their defining mutations and phylogenetic lineage study along with geographical distributions with the aim to understand the evolutionary path of the MPXV across the world. RESULTS: Information about 719 full length genomes of MPXV were collected from GISAID repository and the sequences extracted from NCBI. The alignment of 719 MPXV genomes and their subsequent analysis revealed a total of 1530 segregating sites of which 330 were parsimony informative (PI) sites. The variations had a positive value of Tajima's D statistic indicating some mutations being prevalent and hence balancing selection. A total of 39 haplogroups were observed in the phylo-geo-network and their defining mutations along with the evolutionary path has been discussed. The phylo-geo-network revealed the nodal haplogroup is represented by GISAID ID 13889450, haplogroup A1, an isolate from Germany, having a total of 296 identical sequences in the study incident across 22 countries. The localized evolution is highlighted by country specific sequences and haplogroups. USA had a total of 58 genomes and 13 haplogroups as compared to Peru (89 genomes, 7 haplogroups) and Germany (26 genomes, 6 haplogroups). CONCLUSIONS: The evolution of MPXV can be happening in a localized manner and hence accumulation of variations in the MPXV genomes needs to be monitored in order to be prepared for any possible threats.
For the past decades, inflammatory signals have been considered a possible key for pharmacological interventions. There are several compounds and/or molecules that have been known as most promising medication against inflammation and its mediated chronic disorders. Inflammasomes could be recognized as a trigger by detrimental stimuli as pathogenic attack and endogenous signals mediated injury inside the cells. In addition, there has been an inflammatory key mechanism involved in cancers including glioblastoma multiforme (GBM). GBM has been considered the foremost aggressive primary brain tumors in adult stage. There is a scattered beam of light on both cellular and molecular links in inflammation and GBM. However, the immune response of GBM has been characterized extensively by macrophages and lymphocytes related to tumors, and some recent investigations have pinpointed the focus of inflammasomes on the progression of GBM. Nevertheless, risk factors linked with GBM are still debatable. In our study, the most considerable compounds and their bonded and/or targeted proteins have depicted the most promising highlights under in silico condition. Our in silico investigations have revealed a powerful pharmacological agents/compound against inflammasome-mediated GBM.
