![]() ![]() Targeting the host mitochondria is an attractive antiviral target. HCMV large size and slow replication kinetics create a dependency on mitochondria during replication. ![]() Morphological changes mediated through biogenesis and fission/fusion dynamics contribute to strategies to avoid cell death, overcome oxidative stress, and maximize the biosynthetic and bioenergetic outputs of mitochondria.Įmerging data suggests that cytomegalovirus relies on intact, functional host mitochondria for optimal replication. This is achieved through altered metabolism and signaling pathways. The mitochondria are instrumental in meeting the biosynthetic and bioenergetic needs of HCMV replication. In this review, we describe the strategies and targets HCMV uses to control different aspects of mitochondrial function. Human cytomegalovirus (HCMV) has been observed to manipulate numerous mitochondrial functions. Metabolic rewiring of the host cell is required for optimal viral replication. These results suggest that hearing loss caused by MCMV infection may be associated with ROS‑induced inflammation. In addition, MCMV increased the content of reactive oxygen species (ROS). Furthermore, the inflammasome‑associated factors were also increased in cultured spiral ganglion neurons infected with MCMV for 24 h. MCMV sequentially induced inflammasome‑associated factors. Auditory brainstem responses were tested to evaluate hearing at 3 weeks, expression of inflammasome‑-associated factors was assessed by immunofluorescence, western blot analysis, reverse transcription‑quantitative polymerase chain reaction and ELISA. The present study established an experimental model of hearing loss after systemic infection with murine CMV (MCMV) in newborn mice. While the importance of CMV‑induced SNHL has been described, the mechanisms underlying its pathogenesis and the role of inflammatory responses remain elusive. Congenital cytomegalovirus (CMV) infection is the most common infectious cause of sensorineural hearing loss in children. ![]()
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