Abstract
Sirtuins (SIRTs) are well-known histone deacetylases that are capable of modulating various cellular processes in numerous diseases, including the infection of hepatitis B virus (HBV), which is one of the primary pathogenic drivers of liver cirrhosis and hepatocellular carcinoma. Mounting evidence reveals that HBV can alter the expression levels of all SIRT proteins. In turn, all SIRTs regulate HBV replication via a cascade of molecular mechanisms. Furthermore, several studies suggest that targeting SIRTs using suitable drugs is a potential treatment strategy for HBV infection. Here, we discuss the molecular mechanisms associated with SIRT-mediated upregulation of viral propagation and the recent advances in SIRT-targeted therapy as potential therapeutic modalities against HBV infection.
Highlights
Chronic infection with hepatitis B virus (HBV), which can cause cirrhosis and hepatocellular carcinoma (HCC), remains a serious global public health problem [1, 2]
SIRT6 can interact with HBV core protein (HBc) and suppress viral replication through its deacetylase activity by inhibiting H3K56 acetylation (H3K56ac) and H3K9 acetylation (H3K9ac) on the HBV closed circular DNA (cccDNA) mini-chromosome [21] (Figure 1)
We infer that HBV can alter the expression of SIRTs and that SIRTs are capable of promoting viral replication via multiple pathways
Summary
Fanyun Kong 1†, Qi Li , 1,2† Fulong Zhang 3, Xiaocui Li 1, Hongjuan You 1*, Xiucheng Pan 4, Kuiyang Zheng 1,5 and Renxian Tang 1,5*. Specialty section: This article was submitted to Infectious Diseases–Surveillance, Prevention and Treatment, a section of the journal Frontiers in Medicine. Sirtuins as Potential Therapeutic Targets for Hepatitis B Virus Infection. Sirtuins (SIRTs) are well-known histone deacetylases that are capable of modulating various cellular processes in numerous diseases, including the infection of hepatitis B virus (HBV), which is one of the primary pathogenic drivers of liver cirrhosis and hepatocellular carcinoma. Mounting evidence reveals that HBV can alter the expression levels of all SIRT proteins. All SIRTs regulate HBV replication via a cascade of molecular mechanisms. Several studies suggest that targeting SIRTs using suitable drugs is a potential treatment strategy for HBV infection. We discuss the molecular mechanisms associated with SIRT-mediated upregulation of viral propagation and the recent advances in SIRT-targeted therapy as potential therapeutic modalities against HBV infection
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