More recent swine vesicular disease virus isolates retain binding to coxsackle-adenovirus receptor, but have lost the ability to bind human decay-accelerating factor (CD55)
More recent swine vesicular disease virus isolates retain binding to coxsackle-adenovirus receptor, but have lost the ability to bind human decay-accelerating factor (CD55)
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DOI：
10.1099/vir.0.80669-0
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发表时间：
2005-05-01
影响因子：
3.8
通讯作者：
Spiller, OB
中科院分区：
文献类型：
--
作者：
Jimenez-Clavero, MA;Escribano-Romero, E;Spiller, OB
猪水疱病病毒 (SVDV) 最近由柯萨奇 B 病毒血清型 5 (CVB5) 进化而来，跨越了从人类到猪的物种障碍。在这里，对早期和最近爆发的 SVDV 分离株利用祖病毒受体柯萨奇腺病毒受体 (CAR) 和腐烂加速因子 (DAF; CD55) 的能力进行了比较。通过与抗 DAF 或抗 CAR 抗体预孵育，人 HeLa 细胞上的 CVB5 和 SVDV 分离株 It'66 和 UK'72 的病毒滴度降低；然而，最近的 SVDV 分离株 R1072、R1120 和 SPA'93 并未裂解性感染 HeLa 细胞。对于所有分离株，猪细胞系 IB-RS-2 的 CVB5 和 SVDV 感染均被抗 CAR 抗体完全抑制，并且在细胞与抗猪 DAF 抗体预孵育后没有观察到减少。人 DAF 在猪细胞系 IB-RS-2 中的表达使早期 SVDV 分离株的病毒滴度提高了 25 倍，但对近期 SVDV 分离株的滴度没有影响。通过人 DAF 的表达，放射性标记的 CVB5 与 IB-RS-2 细胞的结合增加了 7 至 8 倍，早期 SVDV 分离株的结合增加了 1.2-1.3 倍，而人 DAF 表达介导的近期 SVDV 分离株的结合没有增加。添加可溶性 hDAF-Fc 抑制了猪细胞的 CVB5 感染，但不抑制 SVDV。所有病毒与可溶性 hCAR-Fc 预孵育可完全阻断 IB-RS-2 猪细胞的感染；对阻断感染所需的可溶性 hCAR-Fc 量的滴定显示，早期分离株 UK'72 最不容易受到抑制，而最新分离株 SPA'93 最容易受到抑制。
Swine vesicular disease virus (SVDV) evolved from coxsackie B virus serotype 5 (CVB5) in the recent past, crossing the species barrier from humans to pigs. Here, SVDV isolates from early and recent outbreaks have been compared for their capacity to utilize the progenitor virus receptors coxsackie-adenovirus receptor (CAR) and decay-accelerating factor (DAF; CD55). Virus titre of CVB5 and SVDV isolates It'66 and UK'72 on human HeLa cells was reduced by pre-incubation with either anti-DAF or anti-CAR antibodies; however, recent SVDV isolates R1072, R1120 and SPA'93 did not infect HeLa cells lytically. CVB5 and SVDV infection of the pig cell line IB-RS-2 was inhibited completely by anti-CAR antibodies for all isolates, and no reduction was observed following pre-incubation of cells with anti-pig DAF antibodies. Expression of human DAF in the pig cell line IB-RS-2 enhanced the virus titre of early SVDV isolates by 25-fold, but had no effect on recent SVDV isolate titre. Binding of radiolabelled CVB5 to IB-RS-2 cells was increased seven- to eightfold by expression of human DAF and binding of early SVDV isolates was increased 1.2-1.3-fold, whereas no increase in binding by recent SVDV isolates was mediated by human DAF expression. Addition of soluble hDAF-Fc inhibited CVB5, but not SVDV, infection of pig cells. Pre-incubation of all viruses with soluble hCAR-Fc blocked infection of IB-RS-2 pig cells completely; titration of the amount of soluble hCAR-Fc required to block infection revealed that early isolate UK'72 was the least susceptible to inhibition, and the most recent isolate, SPA'93, was the most susceptible.