Mechanism of SARS coronavirus infection and proliferation

然而，SARS-CoV附着在细胞表面ACE2上，需要澄清对其他细胞表面蛋白的需求。在这项研究中，我们研究了SARS-CoV共受体的性质。利用可溶性SARS-CoV刺突蛋白和化学交联试剂，在刺突- ace2复合体中鉴定出两种l型凝集素DC-SIGN和L-SIGN。在加入Spike之前，ACE2与这些蛋白形成复合物。虽然DC-SIGN和L-SIGN都没有增加SARS-CoV假病毒在细胞表面的吸附，但这些凝集素促进了SARS-CoV在细胞中的结合。胞质内只需要DC-SIGN和L-SIGN区域，而不需要ACE2区域。这些结果提示胞浆内DC-SIGN和L-SIGN在SARS-CoV感染中起作用。

SARS-CoV attaches to the cell surface ACE2, however, requirement of additional cell surface proteins need to be clarified. In this study, we investigated the nature of co-receptors of SARS-CoV. By utilizing soluble SARS-CoV spike protein and a chemical crosslinker reagent, we identified two L-type lectins, DC-SIGN and L-SIGN, in the Spike-ACE2 complex. ACE2 forms complex with these proteins prior to the addition of the Spike. Although neither DC-SIGN nor L-SIGN increased SARS-CoV pseudovirus adsorption to the cell surface, these lectins facilitated incorporation of SARS-CoV in to the cells. Intracytoplasmic region of DC-SIGN and L-SIGN, but not that of ACE2, was required for the incorporation. These results suggest that the intracytoplasmic regions of DC-SIGN and L-SIGN play roles on SARS-CoV infection.