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Human cytidine deaminase APOBEC3F(A3F)has broad anti-viral activity against hepatitis Bvirus and retroviruses including human immunodeficiency virus type 1.However,its regulation in viralnatural target cells such CD4~+ T lymphocytes,macrophages,and primary liver cells has not been wellstudied.Here we showed that A3F was up-regulated by interferon(IFN)-α in primary hepatocytes andmultiple liver cell lines as well as macrophages.Although the IFN-α signaling pathway was active in Tlymphoid cells and induction of other IFN stimulated genes such as PKR was detected,A3F and APOBEC3G(A3G)were not induced by IFN-α in these cells.Thus,additional factors other than known IFN-stimulatedgenes also regulated IFN-α-induced A3F expression distinctly.A3F and A3G expression levels in primaryhepatocytes,especially after IFN-α stimulation,were comparable to those in CD4~ T lymphocytes in someindividuals.Significant variations of A3F and A3G expression in primary hepatocytes from various subjectswere observed.Individual variations in A3F and/or A3G regulation and expression might influence the clinicaloutcomes of hepatitis B infection.
Human cytidine deaminase APOBEC3F (A3F) has broad anti-viral activity against hepatitis B virus and retroviruses including human immunodeficiency virus type 1.However, its regulation in viral natural target cells such CD4 ~ + T lymphocytes, macrophages, and primary liver cells has not been well established . Here we showed that A3F was up-regulated by interferon (IFN) -α in primary hepatocytes and multiple liver cell lines as well as macrophages. Although the IFN-α signaling pathway was active in Tlymphoid cells and induction of other IFN stimulated genes such as PKR was detected, A3F and APOBEC3G (A3G) were not induced by IFN-α in these cells. Thus, additional factors other than known IFN-stimulated genes also regulated IFN-α-induced A3F expression distinctly. A3F and A3G expression levels in primary hepatocytes, especially after IFN-α stimulation, were comparable to those in CD4 ~ T lymphocytes in some individuals. Verification variations of A3F and A3G expression in primary hepatocytes from various subjectswere observed.Individual variations in A3F and / or A3G regulation and expression might influence the clinical outcomes of hepatitis B infection.