Angel J, Tang B, Feng N, Greenberg H B, Bass D
Department of Medicine, Stanford Digestive Disease Center, Stanford University, California, USA.
J Infect Dis. 1998 Feb;177(2):455-8. doi: 10.1086/517374.
A rotavirus (RV) nonstructural protein, NSP4, has recently been proposed to function as an enterotoxin in the pathogenesis of RV diarrhea. The role of NSP4 in the pathogenesis of RV diarrhea was examined by infecting cystic fibrosis transmembrane conductance regulator (CFTR) knockout mice with virulent murine RV and by comparing deduced amino acid sequences of RV gene 10 encoding NSP4 from three distinct sets of virulent and tissue culture-adapted avirulent variant RVs. Homozygous CFTR (CFTR-/-) mice, which do not respond to any known intestinal secretagogues, experienced diarrhea comparable to that in normal CFTR+/+ littermates after RV challenge. Comparison of amino acid sequences of NSP4 from virulent and attenuated pairs of RVs failed to show consistent or significant changes. Together, these data suggest that enterotoxigenic properties of RV NSP4 are not critical in the pathogenesis of murine RV diarrhea and that attenuation of murine RVs is not usually mediated by mutations in the gene encoding NSP4.
最近有人提出，轮状病毒（RV）的非结构蛋白NSP4在RV腹泻的发病机制中起肠毒素的作用。通过用强毒株鼠RV感染囊性纤维化跨膜传导调节因子（CFTR）基因敲除小鼠，并比较来自三组不同的强毒株和适应组织培养的无毒力变异RV中编码NSP4的RV基因10推导的氨基酸序列，研究了NSP4在RV腹泻发病机制中的作用。纯合CFTR（CFTR-/-）小鼠对任何已知的肠道促分泌剂均无反应，但在受到RV攻击后，其腹泻情况与正常CFTR+/+同窝小鼠相当。对强毒株和减毒株RV的NSP4氨基酸序列进行比较，未发现一致或显著的变化。这些数据共同表明，RV NSP4的产肠毒素特性在鼠RV腹泻的发病机制中并不关键，并且鼠RV的减毒通常不是由编码NSP组4的基因突变介导的。
