Russi Sabino, Sansonno Loredana, Sansonno Domenico
Liver Unit, Department of Biomedical Sciences and Human Oncology, University of Bari Medical School, Bari, Italy.
Azienda Ospedaliera "Mellino Mellini", Chiari (BS), Italy.
Curr Drug Targets. 2017;18(7):766-771. doi: 10.2174/1389450117666160201112525.
Hepatitis C virus (HCV) is a major cause of liver-related morbidity and is strongly associated with B-cell lymphoproliferative disorders. Data from epidemiological, biological and clinical investigations support the hypothesis of a pathogenetic role of HCV in at least a subgroup of patients with B-cell non-Hodgkin's lymphoma (B-NHL). Morphologically, HCV-associated B-NHL represents a variety of histological subtypes. The comprehension of the mechanisms of HCV persistence and of its role in the lymphomagenesis will be useful to set new strategies with the aim to prevent and treat HCV-associated B-NHLs. This hypothesis of a virus-induced mechanism of lymphomagenesis arises from the growing evidence that successful antiviral treatment is often linked to regression of some types of HCV-related indolent B-NHLs.
丙型肝炎病毒（HCV）是肝脏相关发病的主要原因，并且与B细胞淋巴增殖性疾病密切相关。流行病学、生物学和临床研究的数据支持HCV在至少一部分B细胞非霍奇金淋巴瘤（B-NHL）患者中具有致病作用这一假说。从形态学上看，HCV相关的B-NHL表现为多种组织学亚型。理解HCV持续存在的机制及其在淋巴瘤发生中的作用，将有助于制定新的策略，以预防和治疗HCV相关的B-NHL。病毒诱导淋巴瘤发生机制这一假说源于越来越多的证据表明，成功的抗病毒治疗通常与某些类型的HCV相关惰性B-NHL的消退有关。
