Burke B, Bridger J C, Desselberger U
Clinical Microbiology and Public Health Laboratory, Addenbrooke's Hospital, Cambridge, United Kingdom.
Virology. 1994 Aug 1;202(2):754-9. doi: 10.1006/viro.1994.1397.
We previously described a marked increase in the pathogenicity of a cell culture grown porcine rotavirus, PRV 4F, during serial passage in gnotobiotic piglets (Bridger et al., 1992). Here we report close temporal correlation between this change in pathogenicity and an amino acid change within a highly conserved hydrophobic domain of VP4 at position 469. Cell culture grown PRV 4F is unique in having a hydrophilic residue, glutamine, at amino acid 469; all previously sequenced VP4s have hydrophobic leucine or phenylalanine residues at the corresponding position. The detection of a point mutation causing a deduced amino acid change from glutamine to leucine at amino acid 469 of PRV 4F VP4 in virus obtained from one piglet at the second serial passage correlated exactly with the emergence of viral pathogenicity. However, given the multifactorial nature of virus pathogenicity, genetic studies are required to ascertain the degree to which this mutation is responsible for the observed change in pathogenicity.
我们之前曾描述过，在无菌仔猪中连续传代培养的猪轮状病毒PRV 4F的致病性显著增加（Bridger等人，1992年）。在此，我们报告了这种致病性变化与VP4高度保守疏水结构域中第469位氨基酸变化之间的紧密时间相关性。在细胞培养中生长的PRV 4F的独特之处在于，其第469位氨基酸为亲水性残基谷氨酰胺；所有先前测序的VP4在相应位置均具有疏水性亮氨酸或苯丙氨酸残基。在第二次连续传代时从一头仔猪获得的病毒中，检测到PRV 4F VP4的第469位氨基酸发生了一个点突变，导致推导的氨基酸从谷氨酰胺变为亮氨酸，这与病毒致病性的出现恰好相关。然而，鉴于病毒致病性的多因素性质，需要进行遗传学研究以确定该突变对所观察到的致病性变化的责任程度。
