Category
Poster - Basic
Description
Hepatitis B virus (HBV) infection presents a major global health concern, affecting millions of individuals each year. In-vitro studies have demonstrated the role of serine hydrolase, specifically a/b hydrolase domain-containing 2 (ABHD2) in hepatitis B viral propagation. The downregulation of ABHD2 via antisense oligonucleotides (ASODNs) decreased HBV mRNA and protein levels, implicating the role of ABHD2 in HBV replication and expression. However, the downregulation of ABHD2 was not demonstrated to effectively prevent HBV propagation in further studies. In addition, the mechanism of reducing HBV replication and expression via ABHD2 downregulation is not fully understood. Our research then aims to investigate the mechanism and effects of blocking serine hydrolase via endocannabinoid enzyme inhibitors in hepatocytes that express the HBV virus, specifically HepG2.2.15 cells overexpressing ABHD2. Endocannabinoid enzyme inhibitors, often associated with pain and inflammation, may inhibit serine hydrolase, specifically ABHD2, and ultimately, reduce HBV propagation. Previous studies in HepG2.2.15 cells have described a positive correlation between IL-23 expression and HBV infection and progression into hepatocellular carcinoma (HCC). Similarly, reactive oxygen species (ROS) has been associated with an increase in HBV capsid assembly and HBV DNA in HepG2.2.15 cells. Through quantifying ROS and IL-23, we seek to determine the efficacy of such inhibitors on HBV infection and propagation in-vitro using in HepG2.2.15 cells. This research suggests the possibility of novel drug therapy for regulating HBV propagation through ABHD2 inhibition via endocannabinoid enzyme inhibitors.
Investigation of Novel Endocannabinoid Enzyme Inhibitor ABHD2
Poster - Basic
Hepatitis B virus (HBV) infection presents a major global health concern, affecting millions of individuals each year. In-vitro studies have demonstrated the role of serine hydrolase, specifically a/b hydrolase domain-containing 2 (ABHD2) in hepatitis B viral propagation. The downregulation of ABHD2 via antisense oligonucleotides (ASODNs) decreased HBV mRNA and protein levels, implicating the role of ABHD2 in HBV replication and expression. However, the downregulation of ABHD2 was not demonstrated to effectively prevent HBV propagation in further studies. In addition, the mechanism of reducing HBV replication and expression via ABHD2 downregulation is not fully understood. Our research then aims to investigate the mechanism and effects of blocking serine hydrolase via endocannabinoid enzyme inhibitors in hepatocytes that express the HBV virus, specifically HepG2.2.15 cells overexpressing ABHD2. Endocannabinoid enzyme inhibitors, often associated with pain and inflammation, may inhibit serine hydrolase, specifically ABHD2, and ultimately, reduce HBV propagation. Previous studies in HepG2.2.15 cells have described a positive correlation between IL-23 expression and HBV infection and progression into hepatocellular carcinoma (HCC). Similarly, reactive oxygen species (ROS) has been associated with an increase in HBV capsid assembly and HBV DNA in HepG2.2.15 cells. Through quantifying ROS and IL-23, we seek to determine the efficacy of such inhibitors on HBV infection and propagation in-vitro using in HepG2.2.15 cells. This research suggests the possibility of novel drug therapy for regulating HBV propagation through ABHD2 inhibition via endocannabinoid enzyme inhibitors.
Comments
Undergraduate