Replication and gene expression of SARS coronavirus and other animal coronaviruses

1)SARS冠状病毒(SARS-CoV)感染的研究：据报道，SARS-CoV通过内体途径进入细胞。我们发现，SARS冠状病毒也直接从细胞表面进入细胞，当细胞附着的病毒用蛋白酶处理时，如诱导的胰酶或弹性蛋白酶。S蛋白的切割以及融合活性。从质膜进入的病毒比通过内体途径的感染效率高100-1000倍。这可能表明SARS-CoV在SARS的主要靶器官肺或肠道中的高复制归因于这些器官中产生的蛋白酶。这种蛋白酶介导的SARS-CoV感染的增强可以解释SARS-CoV感染是如何产生严重的呼吸道疾病的，即使这种病毒被允许在表达其受体ACE2的各种器官中生长。2)小鼠冠状病毒小鼠肝炎病毒(MHV)感染的研究：高度嗜神经的MHV，JIEVIV，通过其受体(CEACAM1)感染的细胞传播到CEACAM1阴性的BHK细胞(称为受体非依赖性感染)。我们发现JHMV病毒粒子可以通过旋转定位直接感染BHK(病毒接种细胞和接种病毒在3000转/分下旋转2小时)，表明JHMV病毒粒子具有独特的感染特性。进一步证明，这一特征依赖于其S蛋白，该蛋白以自然发生的方式被激活进行融合，而不与其特定的受体结合。

1) Research on SARS coronavirus (SARS-CoV) infection :It was reported that SARS-CoV enters into cells via endosomal pathway. We found that SARS-CoV also enters cells directly from cell surface, when cell-attached viruses are treated with proteases, such as trypsin or elastase that induces. S protein cleavage as well as fusion activity. Virus entry from plasma membrane was revealed to result in a 100 to 1000 more efficient infection than the infection via endosomal pathway. This could suggest that high replication of SARS-CoV in the lung or intestine, the major target organs of SARS, is attributed to the proteases produced in those organs. This protease-mediated enhancement of SARS-CoV infection could explain how severe respiratory disease is produced by SARS-CoV infection, even if this virus is allowed to grow in a variety of organs that express its receptor ACE2. Studies are in progress whether such proteases produced in mice induce severe respiratory disease or not.2) Research on murine coronavirus mouse hepatitis virus (MHV) infection :Highly neurotropic MHV, JIEVIV, spreads from cells infected via its receptor (CEACAM1) to CEACAM1-negative BHK cells (called receptor-independent infection). We have shown that JHMV virion can directly infect BHK by spinoculation (virus inoculated cells as well as inoculated viruses were spun at 3000 rpm for 2 h), indicating that JHMV virion has a unique feature for infection. It was further shown that this feature is dependent upon its S protein, which is activated for fusion by a naturally occurring manner, without binding to its specific receptor.