Abstract

Background:Re-emerging viral attacks are catastrophic for health and economy. It is crucial to grasp the viral life cycle, replication and mutation policies and attack strategies. It is also absolute to fathom the cost-efficient antiviral remedies earliest possible.Methods:We propose to use a lab-grown organ (re-cellularized scaffold of sheep kidney) for viral culture and understand its interaction with extra-cellular matrices of the host tissue.Results:Our findings showed that the chikungunya virus (CHIKV) could be better replicated in tissue-engineered bio models than cell culture. A decrease in ds-DNA levels emphasized that CHIKV propagates within the re-cellularized and cell culture models. There was an increase in the viral titres (pfu/ml) in re-cellularized scaffolds and control groups. The lipid peroxidation levels were increased as the infection was progressed in cell culture as well as re-cellularized and control groups. The onset and progress of the CHIKV attacks (cellular infection) lead to transmembrane domain fatty acid peroxidation and DNA breakdown, landing in cellular apoptosis. Simultaneously cell viability was inversely proportional to non-viability, and it decreased as the infection progressed in all infected groups. Histological findings and extracellular matrix evaluation showed the impairment in medullary, cortex regions due to propagation of CHIKV and plaques generations.Conclusion:This method will be a breakthrough for future virus culture, drug interaction and to study its effect on extracellular matrix alterations. This study will also allow us to investigate the correct role of any vaccine or antiviral drugs and their effects on re-engineered organ matrices before moving towards the animal models.Graphical abstract

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