Pathogenic Th1 responses in CHIKV-induced inflammation and their modulation upon Plasmodium parasites co-infection.
Anthony Torres-RuestaTeck-Hui TeoYi-Hao ChanLaurent RéniaLisa F P NgPublished in: Immunological reviews (2019)
The induction of polyarthritis and polyarthralgia is a hallmark of arthritogenic alphavirus infections, with an exceptionally higher morbidity observed with chikungunya virus (CHIKV). While the mechanisms underlying these incapacitating acute symptoms remain partially understood, the progression to chronic conditions in some cases remains unanswered. The highly pro-inflammatory nature of alphavirus disease has suggested the involvement of virus-specific, joint-infiltrating Th1 cells as one of the main pathogenic mediators of CHIKV-induced joint pathologies. This review summarizes the role of cell-mediated immune responses in CHIKV pathogenesis, with a specific focus on pro-inflammatory Th1 responses in the development of CHIKV joint inflammation. Furthermore, due to the explosive nature of arthritogenic alphavirus outbreaks and their recent expansion across the world, co-infections with other highly prevalent pathogens such as malaria are likely to occur but the pathological outcomes of such interactions in humans are unknown. This review will also discuss the potential impact of malaria co-infections on CHIKV pathogenesis and their relevance in alphavirus control programs in endemic areas.
Keyphrases
- plasmodium falciparum
- oxidative stress
- drug induced
- diabetic rats
- high glucose
- induced apoptosis
- zika virus
- public health
- liver failure
- single cell
- endothelial cells
- type diabetes
- toll like receptor
- dendritic cells
- depressive symptoms
- cell proliferation
- bone marrow
- cell therapy
- physical activity
- cell death
- mesenchymal stem cells
- metabolic syndrome
- respiratory failure
- climate change
- risk assessment