replication of the viral genome that occurs once the virus enters the host cell, is an energy-consuming process. In the cells affected by Hep C virus (HCV) cytoplasmic ATP levels are significantly decreased due to an active energy consumption by the virus. However, elevated levels of cytoplasmic ATP can also be noted, which can be explained by either involvement of ATP-generating machinery, or transportation of ATP though membrane-to-membrane communication between mitochondria and replication compartments. Lipophagy for energy production that is being induced by the presence of HCV in the host cell remains unclear. Virus utilizes membranes of autophagic vacuoles for replication of its RNA. When autophagy pathway is impaired, this leads to attenuated virion production. Studies indicate an up-regulation of lipogenic enzymes and proteins related to ?-oxidation, and DCI is believed to be a crucial component for productive HCV infection through regulation of mitochondrial fatty acids (FA) oxidation. Other studies find a down-regulation of genes responsible for degradation and oxidation of FAs, and an up-regulation of genes controlling metabolism and transport of FAs.
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