Anti-dengue Potential of Mangiferin: Intricate Network of Dengue to Human Genes.

ABSTRACT

Dengue fever has become one of the deadliest infectious diseases and requires the development of effective antiviral therapies. It is caused by members of the Flaviviridae family, which also cause various infections in humans, including dengue fever, tick-borne encephalitis, West Nile fever, and yellow fever. In addition, since 2019, dengue-endemic regions have been grappling with the public health and socio-economic impact of the ongoing coronavirus disease 19. Co-infections of coronavirus and dengue fever cause serious health complications for people who also have difficulty managing them. To identify the potentials of mangiferin, a molecular docking with various dengue virus proteins was performed. In addition, to understand the gene interactions between human and dengue genes, Cytoscape was used in this research. The Kyoto Encyclopedia of Genes and Genomes software was used to find the paths of Flaviviridae. The Kyoto Encyclopedia of Genes and Genomes and the Reactome Pathway Library were used to understand the biochemical processes involved. The present results show that mangiferin shows efficient docking scores and that it has good binding affinities with all docked proteins. The exact biological functions of type I interferon, such as interferon-α and interferon-ß, were also shown in detail through the enrichment analysis of the signaling pathway. According to the docking results, it was concluded that mangiferin could be an effective drug against the complications of dengue virus 1, dengue virus 3, and non-structural protein 5. In addition, computational biological studies lead to the discovery of a new antiviral bioactive molecule and also to a deeper understanding of viral replication in the human body. Ultimately, the current research will be an important resource for those looking to use mangiferin as an anti-dengue drug. Supplementary Information The online version contains supplementary material available at 10.1007/s43450-022-00258-6.