The Mitochondrial Function of Patient's Chronic Hepatitis C Over Respiratory States Ranging

Abstract

Background: Most of these studies were directed at liver mitochondria and hepatitis C virus (HCV) establishes a chronic infection in the face of an active immune response and the host oxidative defense. However, little is known about how the virus can survive in a highly oxidative environment given that oxidative stress is such a prominent clinical feature associated with hepatitis C infection. The aim of using adenosine triphosphate (ADP) recycling technology is to assess erythrocyte mitochondrial function of patient’s chronic hepatitis C over respiratory states ranging NAD/NADH₂.

Methods: The 62 HCV⁺ patients and 24 healthy controls were enrolled in the present cross-sectional study. The patients were selected on the basis of their stable clinical condition over the past 3 months. Mitochondrial integrity was assessed by cytochrome C release using a commercial kit indicating a mean of 96% intact mitochondria. Intrinsic NADH fluorescence was monitored in isolated mitochondria as a marker of the mitochondrial NADH redox state.

Results: Mitochondrial fission is the key determinant of mitochondrial quality control, and HCV modulates these key processes in the adaptation to cellular physiological perturbations associated with infection to promote viral persistence. Mitochondrial fission is not invariably associated with cell death but can also protect cells from death induced by oxidative stress and Ca²⁺-dependent apoptotic stimuli.

Conclusions: The mechanism by which reactive oxygen species (ROS) suppresses HCV replication is still not completely clear but it is likely to involve calcium and the dissociation of HCV replication complex from the membranes. Detailed understanding of the mechanism by which ROS suppresses HCV replication and how acetaldehyde, NADH and ROS affect HCV will require additional studies.




Clin Infect Immun. 2018;3(2):60-64
doi: https://doi.org/10.14740/cii82e