Johansson Cecilia, Jonsson Mari, Marttila Marko, Persson David, Fan Xiao-Long, Skog Johan, Frängsmyr Lars, Wadell Göran, Arnberg Niklas
Department of Virology, Umeå University, Umeå, Sweden.
J Virol. 2007 Jan;81(2):954-63. doi: 10.1128/JVI.01995-06. Epub 2006 Nov 1.
Most adenoviruses bind to the coxsackie- and adenovirus receptor (CAR). Surprisingly, CAR is not expressed apically on polarized cells and is thus not easily available to viruses. Consequently, alternative mechanisms for entry of coxsackievirus and adenovirus into cells have been suggested. We have found that tear fluid promotes adenovirus infection, and we have identified human lactoferrin (HLf) as the tear fluid component responsible for this effect. HLf alone was found to promote binding of adenovirus to epithelial cells in a dose-dependent manner and also infection of epithelial cells by adenovirus. HLf was also found to promote gene delivery from an adenovirus-based vector. The mechanism takes place at the binding stage and functions independently of CAR. Thus, we have identified a novel binding mechanism whereby adenovirus hijacks HLf, a component of the innate immune system, and uses it as a bridge for attachment to host cells.
大多数腺病毒与柯萨奇病毒和腺病毒受体（CAR）结合。令人惊讶的是，CAR在极化细胞的顶端并不表达，因此病毒不易接触到它。因此，有人提出了柯萨奇病毒和腺病毒进入细胞的替代机制。我们发现泪液可促进腺病毒感染，并且我们已确定人乳铁蛋白（HLf）是造成这种效应的泪液成分。单独的HLf被发现以剂量依赖的方式促进腺病毒与上皮细胞的结合，以及腺病毒对上皮细胞的感染。还发现HLf可促进基于腺病毒的载体的基因传递。该机制发生在结合阶段，且独立于CAR起作用。因此，我们确定了一种新的结合机制，即腺病毒劫持先天免疫系统的成分HLf，并将其用作附着于宿主细胞的桥梁。
