Altered TAGLN Expression During HBV Replication Correlates with OPA1 Levels

Abstract

Hepatitis B virus (HBV) exploits host proteins to reshape cellular physiology and metabolism, thereby supporting its replication. Transgelin (TAGLN), an actin-binding protein highly expressed in HBV-associated hepatocellular carcinoma, has a poorly defined role in HBV infection. HBV infection upregulated TAGLN expression both in vitro and in vivo. Silencing TAGLN suppressed HBV replication, increased mitochondrial fission, and elevated intracellular ATP levels. Mitochondrial proteomic analysis identified optic atrophy 1 (OPA1), a mitochondrial dynamin protein, as differentially expressed, with higher levels in HBV-positive HepG2.2.15 cells than in parental HepG2 cells. TAGLN deficiency was associated with reduced OPA1 expression. Similarly, modulation of OPA1 expression was associated with corresponding changes in TAGLN levels and HBV replication. Collectively, these findings indicate an association between TAGLN and OPA1 in the context of HBV replication. However, the precise regulatory hierarchy and molecular basis of this association remain to be determined.