Rewiring of host cell signaling in chikungunya virus infection: a mechanism for pathogenesis and therapeutic approaches.

Chikungunya virus (CHIKV) is one of the well-known arboviruses, transmitted via Aedes mosquitoes and infects humans through vector bites. The virus is endemic in certain countries; however, there is evidence suggesting that CHIKV may become widespread in non-endemic countries and may cause a significant burden on global health status in the future. In this context, exploring the characteristics of CHIKV enhances our understanding of it. This literature review examines alterations in host cell signaling induced by CHIKV, including those related to the phosphatidylinositol 3-kinase (PI3K)/Akt, mitogen-activated protein kinase (MAPK), janus kinase/signal transducers and activators of transcription (JAK/STAT), Wnt, transforming growth factor-β (TGF-β), and P53 pathways. We also review the effect of CHIKV on mitochondria and related processes, such as apoptosis, ferroptosis, and autophagy. The altered signals are involved in viral infection and manifestation. In that case, they may be suitable therapeutic targets for treating and preventing CHIKV. Multiple studies reveal that CHIKV infection alters the PI3K/AKT and MAPK pathways, indicating their essential involvement in host signaling. Hence, these pathways (and also other mentioned ones) may be proper candidates for treatment or prevention of the virus. Further studies are required to explore more details about CHIKV-induced intracellular signaling alternation and its subsequent effects. These findings provide a deeper understanding of the fundamental molecular mechanisms underlying CHIKV infection, paving the way for the development of antiviral strategies.