Published online Dec 21, 2013. doi: 10.3748/wjg.v19.i47.8902
Revised: October 30, 2013
Accepted: November 18, 2013
Published online: December 21, 2013
Many aspects of cellular physiology display circadian (approximately 24-h) rhythms. Dysfunction of the circadian clock molecular circuitry is associated with human health derangements, including neurodegeneration, increased risk of cancer, cardiovascular diseases and the metabolic syndrome. Viruses triggering hepatitis depend tightly on the host cell synthesis machinery for their own replication, survival and spreading. Recent evidences support a link between the circadian clock circuitry and viruses’ biological cycle within host cells. Currently, in vitro models for chronobiological studies of cells infected with viruses need to be implemented. The establishment of such in vitro models would be helpful to better understand the link between the clock gene machinery and viral replication/viral persistence in order to develop specifically targeted therapeutic regimens. Here we review the recent literature dealing with the interplay between hepatitis B and C viruses and clock genes.
Core tip: New antiviral strategies have been developed, including the interferon/ribavirin-free therapy, to control hepatitis viruses replication. Although, IFN-free regimens have generated excitement among scientists, for the reason that they are better tolerated, they are not still able to completely eradicate the viruses. Here we underline the circadian relationship between host cell and hosted hepatitis viruses, that has to be taken into account in order to optimize the timing of therapeutic regimens, not only to minimize the pharmacological agents’ toxicity but also to improve the efficacy of treatment modalities through optimized timing of therapeutic regimens, targeting in a better way virus replication.