Background Family with sequence similarity 26, member F (FAM26F) is an important innate immunity modulator playing a significant role in diverse immune responses, however, the association of FAM26F expression with HBV infection is not yet known. Thus, the current study aims to explore the differential expression of FAM26F in vitro in HepAD38 and HepG2 cell lines upon HBV infection, and in vivo in HBV infected individuals. The effects of antioxidant and calcium inhibitors on the regulation of FAM26F expression were also evaluated. The expression of FAM26F was simultaneously determined with well-established HBV infection markers: IRF3, and IFN-β. Methods The expression of FAM26F and marker genes was analyzed through Real-time qPCR and western blot. Results Our results indicate that the differential expression of FAM26F followed the same trend as that of IRF3 and IFN-β. The in vitro study revealed that, in both HBV infected cell lines, FAM26F expression was significantly down-regulated as compared to uninfected control cells. Treatment of cells with N-acetyl-L-cysteine (NAC), EGTA-AM, BAPTA-AM, and Ru360 significantly upregulated the expression of FAM26F in both the cell lines. Moreover, in in vivo study, FAM26F expression was significantly downregulated in all HBV infected groups as compared to controls (p = 0.0007). The expression was higher in the HBV recovered cases, probably due to the decrease in infection and increase in the immunity of these individuals. Conclusion Our study is the first to show the association of FAM26F with HBV infection. It is proposed that FAM26F expression could be an early predictive marker for HBV infection, and thus is worthy of further investigation.

Background/Aims: Hepatitis B virus induces mitochondrial damage via the production of reactive oxygen species and concomitant with deregulation of calcium homeostasis. The current study evaluates the potential of antioxidant and calcium modulators for inhibition of hepatitis B virus-induced mitochondrial damage using in vitro cell culture models. Materials and Methods: Hepatitis B virus-induced mitochondrial fragmentation was observed by immunofluorescence confocal microscopy in hepatitis B virus-infected cell lines (HepG2 and HepAD38). Differential protein expression of mitochondrial fragmentation markers, dynamin-related protein 1 and phospho-dynamin-related protein 1, were evaluated both pre- and posttreatment with antioxidant N -acetyl- l -cysteine and calcium modulators like 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′ -tetraacetic acid tetrakisacetoxymethyl ester, ethylene-bis (oxyethylenenitrilo) tetraacetic acid glycol ether diamine tetraacetic acid-acetoxymethyl ester, and ruthenium amine complex by western blot analysis. Results: A slight reduction in mitochondrial fragmentation in both cell lines was observed post-antioxidant treatment with a partial prevention observed with calcium modulators. The expression of phospho-dynamin-related protein 1 was significantly upregulated ( P = . 0007, P = .003) in both hepatitis B virus-infected cell lines compared to uninfected cells. In line with these observations, the expression of dynamin-related protein 1 and phospho-dynamin-related protein 1 was found to be significantly downregulated with N -acetyl- l -cysteine treatment in both cell lines ( P = . 003, P = .002), respectively. A nonsignificant trend was observed in the case of calcium modulators treatment. Conclusions: Current study indicates that the mitochondrial fragmentation induced by hepatitis B virus infection can be reduced after antioxidant treatment pointing toward exploring better drug targets for the prevention of hepatitis B virus-induced mitochondrial fragmentation and associated liver damage.