Pol S, Wesenfelder L, Dubois F, Roingeard P, Carnot F, Driss F, Brechot C, Goudeau A, Berthelot P
Unité d'Hépatologie, Hôpital Necker, Paris, France.
J Viral Hepat. 1994;1(2):131-7. doi: 10.1111/j.1365-2893.1994.tb00112.x.
It is generally agreed that hepatitis B virus (HBV) replication is reduced by hepatitis delta virus infection (HDV) and augmented by human immunodeficiency virus (HIV) infection. However, the precise nature of the interactions between HBV, HDV and HIV is controversial. The aim of this study was to evaluate the impact of HIV infection on HBV and HDV replication, and on histological scores during delta virus superinfection in HDV-positive, chronic carriers of hepatitis B surface antigen (HBsAg). We studied 38 men and six women, 15 of whom were HIV-positive and all of whom had at least one marker of HDV infection. Serum hepatitis B e antigen (HBeAg), HBV DNA, HDV RNA, anti-delta antigen antibodies (anti-HD) IgM, anti-HD IgG and hepatitis delta antigen (HDAg) were tested for in the serum and liver, respectively; anti-hepatitis C virus (HCV) antibodies were detected using a second-generation recombinant immunoblot assay. Histological specimens were scored blindly according to Knodell's classification for periportal and intralobular necrosis, portal inflammation and fibrosis. HBV DNA was detected more frequently in the HIV-positive patients than in those who were HIV-negative (25 vs 0%; P = 0.01), while markers of HDV replication (serum anti-HD IgM, serum HDV RNA and liver HDAg) were as frequent in the HIV-positive patients (69%, 40% and 50%, respectively) as in those who were HIV-negative (75%, 52% and 30%, respectively; P > 0.05). By contrast, 31% of the HIV-positive patients were serum HDAg-positive compared to only 6% of the HIV-negative patients (P = 0.001). HDV antigenaemia and anti-HD antibodies usually fluctuated in the HIV-positive patients during follow-up. The mean Knodell score was similar in the HIV-positive (11.5 +/- 3.2) and HIV-negative (10.7 +/- 2) subgroups, as was the mean semi-quantitative index of hepatic necrosis, inflammation and fibrosis. Our results provide evidence that in HDV-positive patients: (1) HIV infection counters the inhibitory effect of HDV superinfection on HBV replication; (2) serum anti-HD IgM. HDV RNA and liver HDAg are not more frequent in HIV-positive than in HIV-negative patients, suggesting that HIV infection has no effect on HDV replication (although the significance of the increased frequency of HD antigenaemia remains unclear); (3) the histological severity of liver disease is not influenced by HIV status.
人们普遍认为，丁型肝炎病毒感染（HDV）会降低乙型肝炎病毒（HBV）的复制，而人类免疫缺陷病毒（HIV）感染则会增强HBV的复制。然而，HBV、HDV和HIV之间相互作用的确切性质仍存在争议。本研究的目的是评估HIV感染对HDV阳性的慢性乙型肝炎表面抗原（HBsAg）携带者在丁型病毒重叠感染期间HBV和HDV复制以及组织学评分的影响。我们研究了38名男性和6名女性，其中15人HIV呈阳性，所有人都至少有一项HDV感染标志物。分别检测血清和肝脏中的血清乙型肝炎e抗原（HBeAg）、HBV DNA、HDV RNA、抗丁型抗原抗体（抗-HD）IgM、抗-HD IgG和丁型肝炎抗原（HDAg）；使用第二代重组免疫印迹法检测抗丙型肝炎病毒（HCV）抗体。根据Knodell分类法对门周和小叶内坏死、门脉炎症和纤维化进行组织学标本的盲法评分。HIV阳性患者中HBV DNA的检出率高于HIV阴性患者（25%对0%；P = 0.01），而HDV复制标志物（血清抗-HD IgM、血清HDV RNA和肝脏HDAg）在HIV阳性患者中的出现频率（分别为69%、40%和50%）与HIV阴性患者（分别为75%、52%和30%；P > 0.05）相似。相比之下，31%的HIV阳性患者血清HDAg呈阳性，而HIV阴性患者中这一比例仅为6%（P = 0.001）。在随访期间，HIV阳性患者的HDV血症和抗-HD抗体通常会波动。HIV阳性亚组（11.5 +/- 3.2）和HIV阴性亚组（10.7 +/- 2）的平均Knodell评分相似，肝脏坏死、炎症和纤维化的平均半定量指数也相似。我们的研究结果表明，在HDV阳性患者中：（1）HIV感染抵消了HDV重叠感染对HBV复制的抑制作用；（2）HIV阳性患者血清抗-HD IgM、HDV RNA和肝脏HDAg的出现频率并不高于HIV阴性患者，这表明HIV感染对HDV复制没有影响（尽管HD抗原血症频率增加的意义尚不清楚）；（3）肝脏疾病的组织学严重程度不受HIV状态的影响。
