Gatta A, Giannini C, Lampertico P, Pontisso P, Quarta S, Zignego A L, Atzeni F, Sarzi-Puttini P
Clinical Medicine 5, Department of Clinical and Experimental Medicine, University of Padua, Italy.
Clin Exp Rheumatol. 2008 Jan-Feb;26(1 Suppl 48):S33-8.
Hepatitis B virus (HBV) can be detected in peripheral blood mononuclear cells (PBMCs), mainly B lymphocytes and monocytes. The frequency of PBMC infection is higher in patients with ongoing HBV replication, but can persist for years after the complete resolution of an acute episode of hepatitis B. Infected PBMCs can act as reservoirs for the cell-to-cell transmission of the virus, and vertical transmission studies indicate that the HBV-infected PBMCs of mothers may act as a vector for intrauterine HBV infection. Recent data evaluated whether HBV occult infection could co-operate with HCV infection in the pathogenesis of mixed cryoglobulinemia (MC) and lymphoma and/or whether it may be implicated in the pathogenesis of MC and malignant diseases -B-cell non-Hodgkin's lymphoma (NHL) also independently from HCV. The treatment of chronic HBeAg-negative hepatitis B is intended to ensure the long-term suppression of HBV replication with the aim of halting the progression of liver damage and preventing the development of liver-related complications. This can be done by means of short-term "curative" treatment or long-term "suppressive" therapy. The first approach requires a 48-week course of peginterferon, which controls viral replication (HBV DNA <10.000 copies/ml) in 20-30% of patients; the second requires the long-term (possibly lifetime) administration of nucleoside and/or nucleotide analogues. As none of the currently available drugs alone suppresses viral replication (HBV DNA <200 copies/ml) for five years in all patients, some require a rescue therapy based on the addition of a non-cross-resistant drug, which should be given as early as possible ("on demand" combination therapy). However, the currently available anti-HBV analogues can easily suppress HBV replication for five years in most HBeAg-negative patients. As both strategies have their pros and cons, the best approach needs to be carefully evaluated on an individual basis.
乙型肝炎病毒（HBV）可在外周血单个核细胞（PBMC）中检测到，主要存在于B淋巴细胞和单核细胞中。在持续HBV复制的患者中，PBMC感染频率较高，但在急性乙型肝炎发作完全缓解后仍可持续数年。受感染的PBMC可作为病毒细胞间传播的储存库，垂直传播研究表明，母亲受HBV感染的PBMC可能是宫内HBV感染的载体。最近的数据评估了HBV隐匿感染是否可与丙型肝炎病毒（HCV）感染共同参与混合性冷球蛋白血症（MC）和淋巴瘤的发病机制，以及它是否可能独立于HCV参与MC和恶性疾病——B细胞非霍奇金淋巴瘤（NHL）的发病机制。慢性HBeAg阴性乙型肝炎的治疗旨在确保长期抑制HBV复制，以阻止肝损伤进展并预防肝脏相关并发症的发生。这可以通过短期“治愈性”治疗或长期“抑制性”疗法来实现。第一种方法需要进行48周的聚乙二醇干扰素疗程治疗，可以使20%-30%的患者控制病毒复制（HBV DNA<10,000拷贝/ml）；第二种方法需要长期（可能是终身）服用核苷和/或核苷酸类似物。由于目前可用的药物单独使用均无法在所有患者中持续五年抑制病毒复制（HBV DNA<200拷贝/ml），因此一些患者需要基于添加一种无交叉耐药性药物的挽救治疗，应尽早给予（“按需”联合治疗）。然而，目前可用的抗HBV类似物在大多数HBeAg阴性患者中可轻松抑制HBV复制达五年。由于这两种策略都有其优缺点，因此需要根据个体情况仔细评估最佳治疗方法。
