Department of Infectious Diseases, Israel Institute for Biological Research, Ness-Ziona, Israel.
Virol J. 2009 Sep 29;6:151. doi: 10.1186/1743-422X-6-151.
Ectromelia virus, a member of the Orthopox genus, is the causative agent of the highly infectious mousepox disease. Previous studies have shown that different poxviruses induce cell-cell fusion which is manifested by the formation of multinucleated-giant cells (polykaryocytes). This phenomenon has been widely studied with vaccinia virus in conditions which require artificial acidification of the medium.
We show that Ectromelia virus induces cell-cell fusion under neutral pH conditions and requires the presence of a sufficient amount of viral particles on the plasma membrane of infected cells. This could be achieved by infection with a replicating virus and its propagation in infected cells (fusion "from within") or by infection with a high amount of virus particles per cell (fusion "from without"). Inhibition of virus maturation or inhibition of virus transport on microtubules towards the plasma membrane resulted in a complete inhibition of syncytia formation. We show that in contrast to vaccinia virus, Ectromelia virus induces cell-cell fusion irrespectively of its hemagglutination properties and cell-surface expression of the orthologs of the fusion inhibitory complex, A56 and K2. Additionally, cell-cell fusion was also detected in mice lungs following lethal respiratory infection.
Ectromelia virus induces spontaneous cell-cell fusion in-vitro and in-vivo although expressing an A56/K2 fusion inhibitory complex. This syncytia formation property cannot be attributed to the 37 amino acid deletion in ECTV A56.
作为正痘病毒属的一员，细小病毒可引起高度传染性的鼠痘疾病。先前的研究表明，不同的痘病毒会诱导细胞-细胞融合，其表现为多核巨细胞（多倍体细胞）的形成。该现象已广泛研究了痘苗病毒在需要人工酸化介质的条件下的情况。
我们表明，在中性 pH 条件下，细小病毒可诱导细胞-细胞融合，并且需要在感染细胞的质膜上存在足够数量的病毒颗粒。这可以通过感染复制病毒及其在感染细胞中的繁殖（“从内部”融合）或通过感染每细胞大量的病毒颗粒（“从外部”融合）来实现。病毒成熟的抑制或病毒向质膜的微管运输的抑制导致合胞体形成的完全抑制。我们表明，与痘苗病毒相反，细小病毒诱导细胞-细胞融合与血凝特性无关，并且与其融合抑制复合物 A56 和 K2 的细胞表面表达无关。此外，在致死性呼吸道感染后，还在小鼠肺部检测到细胞-细胞融合。
尽管表达 A56/K2 融合抑制复合物，但细小病毒在体外和体内诱导自发的细胞-细胞融合。这种合胞体形成特性不能归因于 ECTV A56 的 37 个氨基酸缺失。
