ReviewArchives of microbiology2026
Rewiring of host cell signaling in chikungunya virus infection: a mechanism for pathogenesis and therapeutic approaches.
Review in Archives of microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
41493543What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.