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Be on guard: longer monitoring for very–late onset hepatitis B virus reactivation after chemo-immunotherapy?

It is estimated that more than two billion people worldwide have been exposed to hepatitis B virus (HBV), with more than 260 million people actively infected with HBV, making HBV one of the leading causes of chronic liver disease, cirrhosis and hepatocellular carcinoma [1]. HBV infection is indeed quite difficult to eradicate. It induces robust CD4 and CD8 T-cell responses, followed by HBV-specific T cells that target infected cells and suppress viral replication in addition to the production of neutralizing anti-HBs antibodies by B cells that clear the circulating virus and limit its spread. Unfortunately, these responses are insufficient to eradicate all intrahepatic latent HBV covalently closed circular (ccc)DNA, which constitutes a persisting reservoir of HBV, capable of replicating in the liver if not controlled by a competent host immune system [2,3]. Most infected patients are unaware of their past exposure to HBV, which may have resolved (past HBV infection, diagnosed by HB surface antigen (HBsAg)-negative and HB core antibody (HBcAb)-positive serology] or that they have chronic HBV infection [(CHB) HBsAg positive)]. Reactivation of HBV (HBVr), characterized by a sudden, rapid increase in viral replication (HBV-DNA level) in a patient with CHB or past HBV infection, can occur spontaneously, but it is more commonly triggered by immunosuppressive therapies or biologic modifiers, administered for treatment of cancer, inflammatory diseases or for bone marrow or solid organ transplantations [4]. The variable clinical presentation of HBVr may range from asymptomatic hepatitis to fulminant hepatic failure [5]. Major risk factors for reactivation are: 1. host factors, including male sex, older age, presence of cirrhosis and the nature of the underlying disease necessitating immunosuppression (B-CLL, lymphoma, rheumatoid arthritis, etc.) 2. viral factors, among which are chronic HBV, high baseline HBV-DNA levels, hepatitis B envelope antigen (HBeAg) positivity, co-infection with hepatitis C, hepatitis D and HIV 3. type and degree of immunosuppression [5,6]. The American Gastroenterology Association (AGA) categorized drugs as high, intermediate and low risk, according to their potential to cause HBVr [8]. B-cell-depleting agents, like rituximab, ofatumumab and recently obinutuzumab, are defined as high-risk drugs (causing HBVr in >10% of patients), especially in patients with lymphoma. These agents tend to cause severe HBVr that may lead to liver failure with high mortality rates [4,7] Although in general, the risk for HBVr is much lower in patients with past HBV infection than in patients with CHB [4–6,8], among patients with past HBV, who were treated with rituximab-based immunochemotherapy (without antiviral prophylaxis), HBVr was reported in 16.9–41.5% [4,9,10] reported that many cases of HBVr-related hepatitis flare-ups occur between the end of anti-cancer therapy and the complete recovery of immune functions, suggesting that immune suppression allows extensive viral infection of hepatocytes and thereafter, at a later phase, T cell recovery may lead to extensive hepatocyte damage [10]. The recently published update of the ASCO 2020 provisional Clinical Opinion on HBV infection screening and management of patients receiving anticancer therapy for the treatment of malignant diseases (‘ASCO 2020’) recommends that all patients with cancer, anticipating systemic anticancer therapy should be tested for HBV by 3 tests: HBsAg, HBcAb and antibody to hepatitis B surface antigen (HBsAb) prior to, or at the beginning of systemic anticancer therapy [11]. For patients with past HBV (HBsAg negative, HBcAb positive) receiving anticancer therapies