Vaccinia virus envelope D8L protein binds to cell surface chondroitin sulfate and mediates the adsorption of intracellular mature virions to cells
Vaccinia virus envelope D8L protein binds to cell surface chondroitin sulfate and mediates the adsorption of intracellular mature virions to cells
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DOI：
10.1128/jvi.73.10.8750-8761.1999
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发表时间：
1999-10-01
影响因子：
5.4
通讯作者：
Chang, W
中科院分区：
文献类型：
--
作者：
Hsiao, JC;Chung, CS;Chang, W
我们先前表明，在病毒感染过程中，牛痘病毒的细胞内成熟病毒粒子（IMV）的包膜A27 L蛋白与细胞表面硫酸乙酰肝素结合。在本研究中，我们确定了另一种病毒包膜蛋白，D8 L，结合细胞上的硫酸软骨素。可溶性D8 L蛋白干扰野生型牛痘病毒粒子吸附到细胞，表明在病毒进入中的作用。为了探索细胞表面糖胺聚糖和牛痘病毒的相互作用，我们从对照病毒WR 32 -7/Ind 14 K（A27 L（+）D8 L（+））产生突变体病毒，其在A27 L或D8 L基因的表达中有缺陷（A27 L（+）D8 L（-）或A27 L（-）D8 L（+））或两者都有缺陷（A27 L（-）D8 L（-））。A27 L（+）D8 L（+）和A27 L（-）D8 L（+）突变体在BSC 40细胞中生长良好，与先前的观察结果一致。然而，A27 L（+）D8 L（-）和A27 L（-）D8 L（-）病毒在BSC 40细胞中的IMV滴度降低，仅达到对照病毒水平的10%。这些数据表明D8 L蛋白在细胞培养物中的WR 32 -7/Ind 14 K病毒生长中起重要作用。而A27 L蛋白不能与D8 L蛋白互补。A27 L（+）D8 L（-）和G27 L（-）D8 L（-）突变体病毒的低滴度不是由于IMV的形态发生缺陷，并且突变体病毒粒子表现出与对照病毒粒子相似的砖形。此外，A27 L（+）D8 L（-）和A27 L（-）D8 L（-）突变病毒粒子的感染性是A27 L（+）D8 L（+）对照病毒的感染性的6 - 10%。病毒体结合试验显示A27 L（+）D8 L（-）和A27 L（-）D8 L（-）突变体病毒体与BSC 40细胞的结合较差，表明病毒D8 L蛋白与细胞表面硫酸软骨素的结合对于牛痘病毒进入可能是重要的。
We previously showed that an envelope A27L protein of intracellular mature virions (IMV) of vaccinia virus binds to cell surface heparan sulfate during virus infection. In the present study we identified another viral envelope protein, D8L, that binds to chondroitin sulfate on cells. Soluble D8L protein interferes with the adsorption of wild-type vaccinia virions to cells, indicating a role in virus entry. To explore the interaction of cell surface glycosaminoglycans and vaccinia virus, we generated mutant viruses from a control virus, WR32-7/Ind14K (A27L(+) D8L(+)) to be defective in expression of either the A27L or the D8L gene (A27L(+) D8L(-) or A27L(-) D8L(+)) or both (A27L(-) D8L(-)). The A27L(+) D8L(+) and A27L(-) D8L(+) mutants grew well in BSC40 cells, consistent with previous observations. However, the IMV titers of A27L(+) D8L(-) and A27L(-) D8L(-) viruses in BSC40 cells were reduced, reaching only 10% of the level for the control virus. The data suggested an important role for D8L protein in WR32-7/Ind14K virus growth in cell cultures. A27L protein, on the other hand, could not complement the functions of D8L protein. The low titers of the A27L(+) D8L(-) and G27L(-) D8L(-) mutant viruses were not due to defects in the morphogenesis of IMV, and the mutant virions demonstrated a brick shape similar to that of the control virions. Furthermore, the infectivities of the A27L(+) D8L(-) and A27L(-) D8L(-) mutant virions were 6 to 10% of that of the A27L(+) D8L(+) control virus. Virion binding assays revealed that A27L(+) D8L(-) and A27L(-) D8L(-) mutant virions bound less well to BSC40 cells, indicating that binding of viral D8L protein to cell surface chondroitin sulfate could be important for vaccinia virus entry.