Cell Research发表两原创论文引起国际媒体关注

我国的学术期刊《细胞研究》(Cell  Research)于1月29日在线发表了中国协和医科大学基础医学院国家分子生物医学重点实验室蒋澄宇研究组的原创性论文SARS  coronavirus  entry  into  host  cells  through  a  novel  clathrin-  and  caveolae-independent  endocytic  pathway  (http://www.nature.com/cr/journal/v18/n2/abs/cr200815a.html,)和美国肯塔基大学医学院Liya  Gu研究组的原创性论文Preferential  loss  of  mismatch  repair  function  in  refractory  and  relapsed  acute  myeloid  leukemia:  potential  contribution  to  AML  progression(http://www.nature.com/cr/journal/v18/n2/abs/cr200814a.html,)。随后迅速引起了国外媒体的关注，路透社和美国《列克星敦先驱者报》当日分别对两篇论文进行了报道(http://www.reuters.com/article/scienceNews/idUST12421920080129?pageNumber=1&virtualBrandChannel=0,，http://www.kentucky.com/148/story/300688.html,)。

一直以来，科学家们对SARS病毒进入和感染宿主细胞的机理存在很多争议，蒋澄宇研究组的最新研究结果发现SARS病毒可以通过细胞膜上的“脂肪筏”入侵宿主细胞，该研究结果将有助于今后进一步研究如何抑止SARS病毒的传播。来自Liya  Gu研究组的研究结果则第一次揭示了急性粒细胞白血病复发同DNA“失配校正”修复功能缺失这样一种致病机理相关，研究还提示有一小部分复发病人是由于癌细胞产生了抗药性而一直存在于体内造成的。

该两项原创性成果均是通过《细胞研究》的稿件“绿色通道”发表的，从文章投稿到接收时间仅为3天。“绿色通道”是《细胞研究》优化优秀稿件紧急处理流程、迅速传播生命科学领域最新原创性基础研究成果的重要举措，以求全方位地为科学家们研究成果的提供更快、更好的服务。此次出版的两篇论文再次得到国外媒体关注，也表明我国自主创办的国际化学术期刊同样能在世界范围内迅速传播重要的科研成果。

生物谷推荐原始出处：

Cell Research (2008) 18:290–301. doi: 10.1038/cr.2008.15; published online 29 January 2008

SARS coronavirus entry into host cells through a novel clathrin- and caveolae-independent endocytic pathway

Hongliang Wang1, Peng Yang1, Kangtai Liu1, Feng Guo1, Yanli Zhang1, Gongyi Zhang2 and Chengyu Jiang1

Correspondence: Chengyu Jiang, Tel: +86-10-65296908; Fax: +86-10-65276551 E-mail: jiang@pumc.edu.cn

Received 27 November 2007; Revised 29 November 2007; Accepted 30 November 2007.

While severe acute respiratory syndrome coronavirus (SARS-CoV) was initially thought to enter cells through direct fusion with the plasma membrane, more recent evidence suggests that virus entry may also involve endocytosis. We have found that SARS-CoV enters cells via pH- and receptor-dependent endocytosis. Treatment of cells with either SARS-CoV spike protein or spike-bearing pseudoviruses resulted in the translocation of angiotensin-converting enzyme 2 (ACE2), the functional receptor of SARS-CoV, from the cell surface to endosomes. In addition, the spike-bearing pseudoviruses and early endosome antigen 1 were found to colocalize in endosomes. Further analyses using specific endocytic pathway inhibitors and dominant-negative Eps15 as well as caveolin-1 colocalization study suggested that virus entry was mediated by a clathrin- and caveolae-independent mechanism. Moreover, cholesterol- and sphingolipid-rich lipid raft microdomains in the plasma membrane, which have been shown to act as platforms for many physiological signaling pathways, were shown to be involved in virus entry. Endocytic entry of SARS-CoV may expand the cellular range of SARS-CoV infection, and our findings here contribute to the understanding of SARS-CoV pathogenesis, providing new information for anti-viral drug research.