AI Article Synopsis
- Chikungunya, a viral infection that historically affected mainly East Africa, has become a global health concern due to its rising cases and neurological complications, especially in the Americas since 2014.
- Astrocytes, a type of brain cell, play a key role in the neurological effects of the virus; even after the virus is gone, these cells show signs of activation and change in structure.
- The findings suggest that changes in astrocytes may disrupt communication between glial cells and neurons, potentially leading to long-term neurological issues in those infected with Chikungunya.
Article Abstract
Chikungunya, "that which bends up" in the Makonde dialect, is an emerging global health threat, with increasing incidence of neurological complications. Until 2013, Chikungunya infection had been largely restricted to East Africa and the Indian Ocean, with cases within the USA reported to be from foreign travel. However, in 2014, over 1 million suspected cases were reported in the Americas, and a recently infected human could serve as an unwitting reservoir for the virus resulting in an epidemic in the continental USA. Chikungunya infection is increasingly being associated with neurological sequelae. In this study, we sought to understand the role of astrocytes in the neuropathogenesis of Chikungunya infection. Even after virus has been cleared form the circulation, astrocytes were activated with regard to TLR2 expression. In addition, white matter astrocytes were hypertrophic, with increased arbor volume in gray matter astrocytes. Combined, these would alter the number and distribution of synapses that each astrocyte would be capable of forming. These results provide the first evidence that Chikungunya infection induces morphometric and innate immune activation of astrocytes in vivo. Perturbed glia-neuron signaling could be a major driving factor in the development of Chikungunya-associated neuropathology.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783292 | PMC |
| http://dx.doi.org/10.1007/s13365-015-0378-3 | DOI Listing |
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