Changes in distribution and number of mitochondria associated with chikungunya virus infection.

Viruses depend on cell machinery to replicate, which strategically modulates the metabolism and physiology of host cells, changing cell architecture and functions. In this sense, it has been shown that alphavirus induces changes in the membrane, alters glycolysis rates, and even affects autophagy/apoptosis. The genus Alfavirus belongs to the family Togaviridae, including Venezuelan equine encephalitis (VEEV) and Chikungunya virus (CHIKV). The impact of CHIKV on mitochondria structure has not been determined, so this project aimed to evaluate the effects of CHIKV on mitochondria. For this purpose, the immunofluorescence technique evaluated changes in morphology, distribution, and number of mitochondria at 12, 14, 16, and 18 hpi. The data obtained suggest perinuclear clustering, a decrease in the number of mitochondria, and modification of mitochondrial morphology depending on the time of infection. Subsequently, the Macintosh MitoProt program was used to determine whether structural proteins or peptides (capsid, E1, E2, E3, and 6K) had a mitochondrial target, with the capsid protein having the highest score. We hypothesized CHIKV capsid protein is related to altered mitochondrial function, which would contribute to mitochondrial damage. [ABSTRACT FROM AUTHOR]