Hall G A, Bridger J C, Brooker B E, Parsons K R, Ormerod E
Vet Pathol. 1984 Mar;21(2):208-15. doi: 10.1177/030098588402100213.
Fourteen gnotobiotic calves were killed 0.5 to ten days after infection with Newbury agent SRV-1 and the changes in small intestinal structure and function were assessed, qualitatively and quantitatively, by light microscopy, scanning and transmission electron microscopy, enzymology and xylose absorption. The first enterocytes detected as infected by immunoperoxidase were those on the sides of villi at the base. Subsequently exfoliation of degenerate enterocytes resulted in stunted villi; mucosal beta-galactosidase activity fell and there was xylose malabsorption. Small intestinal damage, first detected at 12 hours after infection but almost repaired by ten days, was restricted to the anterior half of the small intestine. In the distal small intestine, where no virus-induced damage occurred, villi lengthened--possibly due to increased mitosis of crypt cells stimulated by enteroglucagon release.
十四头无菌犊牛在感染纽伯里因子SRV - 1后0.5至十天被处死，通过光学显微镜、扫描和透射电子显微镜、酶学及木糖吸收试验，对小肠结构和功能的变化进行了定性和定量评估。通过免疫过氧化物酶检测到的首批被感染的肠上皮细胞是位于绒毛基部侧面的细胞。随后，变性肠上皮细胞的脱落导致绒毛发育不良；黏膜β - 半乳糖苷酶活性下降，出现木糖吸收不良。小肠损伤在感染后12小时首次被检测到，但在十天时几乎已修复，损伤局限于小肠的前半部分。在远端小肠，未发生病毒诱导的损伤，绒毛变长——这可能是由于肠高血糖素释放刺激隐窝细胞有丝分裂增加所致。
