Preferential association of Hepatitis C virus with apolipoprotein B48-containing lipoproteins
Preferential association of Hepatitis C virus with apolipoprotein B48-containing lipoproteins
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DOI：
10.1099/vir.0.82033-0
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发表时间：
2006-10-01
影响因子：
3.8
通讯作者：
Andre, Patrice
中科院分区：
文献类型：
--
作者：
Diaz, Olivier;Delers, Francois;Andre, Patrice
丙型肝炎病毒(HCV)在细胞培养中的密度与黄病毒科其他成员的密度相当，而在体内发现的感染颗粒部分为低密度组分，与富含三酰甘油(TG)的脂蛋白(TRL)有关。在感染患者的血液中，丙型肝炎病毒以非均质颗粒的形式循环，其中包括脂类病毒颗粒(LLP)，即富含TG的球形颗粒，含有病毒衣壳和RNA。在载脂蛋白组成和餐后动态血脂变化方面，进一步讨论了LVP的双重病毒和脂蛋白性质。LVP和病毒囊膜蛋白上存在TRL，可交换的apoE、-CII和-CIII，但不存在高密度脂蛋白apoA-II。尽管这些禁食患者的血浆中几乎检测不到apoB48，但apoB100和-B48这两种不可交换的apoB亚型在LVP上的表达是相等的。这表明血浆中很大一部分丙型肝炎病毒与含有载脂蛋白B48的LVEF有关。此外，脂肪餐后LVEP在甘油三酯中显著而迅速地增加。由于apoB48仅由肠道合成，这些数据突出了丙型肝炎病毒与乳糜粒(肠道来源的TRL)之间的优先联系。这些数据提出了肠道对病毒载量的贡献的问题，并表明病毒可以利用TRL的组装和分泌来产生自己，并利用TRL的命运将其输送到肝脏。
Hepatitis C virus (HCV) in cell culture has a density comparable to that of other members of the family Flaviviridae, whereas in vivo infectious particles are found partially in low-density fractions, associated with triacylglycerol (TG)-rich lipoproteins (TRLs). In the blood of infected patients, HCV circulates as heterogeneous particles, among which are lipo-viroparticles (LVPs), globular particles rich in TG and containing viral capsid and RNA. The dual viral and lipoprotein nature of LVPs was addressed further with respect to apolipoprotein composition and post-prandial dynamic lipid changes. The TRLs exchangeable apoE, -CII and -CIII, but not the high-density lipoprotein apoA-II, were present on LVPs, as well as the viral envelope proteins. apoB100 and -B48, the two isoforms of the non-exchangeable apoB, were represented equally on LVPs, despite the fact that apoB48 was barely detectable in the plasma of these fasting patients. This indicates that a significant fraction of plasma HCV was associated with apoB48-containing LVF`s. Furthermore, LVPs were enriched dramatically and rapidly in triglycerides after a fat meal. As apoB48 is synthesized exclusively by the intestine, these data highlight the preferential association of HCV with chylomicrons, the intestine-derived TRLs. These data raise the question of the contribution of the intestine to the viral load and suggest that the virus could take advantage of TRL assembly and secretion for its own production and of TRL fate to be delivered to the liver.