Caligaris-Cappio F, De Leo A M, Bertero M T
Dipartimento di Scienze Biomediche e Oncologia Umana, Università di Torino, Italy.
Leuk Lymphoma. 1997 Dec;28(1-2):57-63. doi: 10.3109/10428199709058331.
Since hepatitis C virus (HCV) infection is frequently detected in patients with lymphoproliferative or autoimmune disorders and since the virus may infect lymphocytes, the question is raised whether malignant transformation and autoimmune manifestations in the presence of HCV are HCV-related or merely fortuitous. A close association has been firmly established between HCV infection and essential type II mixed cryoglobulinemia (ECM), an indolent lymphoproliferative disorder characterized by cryoprecipitable immune-complexes (IC) that may evolve into classical non Hodgkin's lymphomas (NHL) retaining the ability to produce cryoprecipitable rheumatoid factor (RF). It is reasonable to consider HCV as one cofactor in lymphomagenesis, even if the precise pathogenetic relationship between HCV infection, the chronic presence of cryoprecipitable IC and the development of NHL have not been established yet. Several epidemiological studies have documented the ability of chronic HCV infection to favour the production of autoAb. It is not clear why only some patients with HCV infection develop autoAb, nor why the most frequent autoAb detected in HCV-infected subjects are cryoglobulins. Though a high prevalence of anti-HCV has been found in a variety of systemic and organ-specific autoimmune diseases, it is likely that several of these associations are fortuitous with the notable exception of membranoproliferative glomerulonephritis. As HCV can provoke or exacerbate inflammatory signs and cause the production of RF, it is reasonable to suspect that HCV infection may be able to trigger the development of some connective tissue diseases or to exacerbate their clinical course. Nonetheless, it is clinically prudent to conclude that the pathogenetic relationships of Sjögren syndrome, rheumatoid arthritis and polyarthritis with HCV infection are more likely to be regarded as mediated via the intermediate development of ECM.
由于在淋巴增殖性疾病或自身免疫性疾病患者中经常检测到丙型肝炎病毒（HCV）感染，且该病毒可能感染淋巴细胞，因此就产生了一个问题，即HCV感染时的恶性转化和自身免疫表现是与HCV相关，还是仅仅是偶然发生的。HCV感染与II型原发性混合性冷球蛋白血症（ECM）之间已牢固确立了密切关联，ECM是一种进展缓慢的淋巴增殖性疾病，其特征是可形成冷沉淀的免疫复合物（IC），这些复合物可能演变为经典的非霍奇金淋巴瘤（NHL），并保留产生可形成冷沉淀的类风湿因子（RF）的能力。即使尚未确定HCV感染、可形成冷沉淀的IC的慢性存在与NHL发生之间的确切致病关系，但将HCV视为淋巴瘤发生的一个辅助因素是合理的。多项流行病学研究已证明慢性HCV感染有利于自身抗体的产生。目前尚不清楚为何只有部分HCV感染患者会产生自身抗体，也不清楚为何在HCV感染患者中最常见的自身抗体是冷球蛋白。尽管在各种全身性和器官特异性自身免疫性疾病中均发现抗HCV的高流行率，但除膜增生性肾小球肾炎外，其中一些关联可能是偶然的。由于HCV可引发或加重炎症体征并导致RF产生，因此有理由怀疑HCV感染可能引发某些结缔组织疾病的发生或加剧其临床病程。尽管如此，从临床角度谨慎得出结论，干燥综合征、类风湿关节炎和多关节炎与HCV感染的致病关系更可能被视为是通过ECM的中间发展介导的。
