HBV reactivation can occur spontaneously, but it is more frequently triggered by immunosuppressors, immunologic diseases, or transplantation. It can also be caused by coinfection with HCV or HDV, or even by elimination of HCV in patients treated with direct-acting antivirals. In patients receiving antivirals for the treatment of chronic hepatitis, reactivation can also be caused by low levels of the drug (due to lack of therapeutic adherence or interaction with other treatments) or new mutations of the virus.^[1]

Reactivation is characterized by a sudden rise of HBV DNA, which can be followed by an elevation of alanine transaminase (ALT) levels (with or without bilirubin) several weeks after.^[2] It should be treated with a nucleoside/nucleotide analogue (tenofovir or entecavir) as early as possible, regardless of ALT levels. Despite antiviral treatment, up to 25%–50% of patients may still develop severe hepatitis, hepatic failure, or even death.^[3]

HBV 再激活可自发发生，但更常由免疫抑制剂、免疫疾病或移植触发。它也可能是由 HCV 或 HDV​​ 共同感染引起的，甚至是由使用直接抗病毒药物治疗的患者中消除 HCV 引起的。在接受抗病毒药物治疗慢性肝炎的患者中，药物的低水平（由于缺乏治疗依从性或与其他治疗的相互作用）或病毒的新突变也可能导致再激活。^{[ 1 ]}

再激活的特点是 HBV DNA 突然升高，随后几周后丙氨酸转氨酶 (ALT) 水平（有或没有胆红素）升高。^{[ 2 ]}无论 ALT 水平如何，都应尽早使用核苷/核苷酸类似物（替诺福韦或恩替卡韦）进行治疗。尽管进行了抗病毒治疗，高达 25%–50% 的患者仍可能发展为严重肝炎、肝功能衰竭，甚至死亡。^{[ 3 ]}