Long noncoding RNA GAS5 does not regulate HBV replication

Hepatitis B virus (HBV) infection remains a severe health burden worldwide. Emerging long noncoding RNAs (lncRNAs) are hijacked to enhance virus replication or employed by the host to stimulate immune responses to clear the virus. LncRNA growth arrest‐specific transcript 5 (GAS5) can regulate RNA virus by suppressing the replication of both hepatitis C virus and human immunodeficiency virus. In this study, we explored the changes of HBV replication by overexpressing or knocking down GAS5 in HepAD38 cell and HepG2 cell transfected with pHBV1.2. We found HBV can induce the expression of GAS5. However, GAS5 had no effect on extracellular HBsAg and HBeAg, nor intracellular HBV RNA and HBV DNA. In addition, GAS5 possessed similar expression levels between stable HBV‐producing cell lines and hepatoma cell lines. Furthermore, GAS5 showed no difference between healthy subjects and patients with chronic HBV in multiple GEO microarray data sets by GEO2R analysis. Taken together these results, GAS5 does not modulate the replication of HBV but it inhibits cell proliferation in HepAD38. This provides insights into the possible roles of GAS5 in HBV infection. Highlight HBV induced the expression of GAS5. GAS5 did not regulate HBV replication but inhibited cell proliferation. GAS5 showed no difference between healthy individuals and patients with chronic HBV infection.