Henderson Gail, Perng Guey-Chuen, Nesburn Anthony B, Wechsler Steven L, Jones Clinton
Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln, Lincoln, Nebraska 68583-0905, USA.
J Neurovirol. 2004 Feb;10(1):64-70. doi: 10.1080/13550280490261716.
When the bovine herpesvirus 1 (BHV-1) latency-related (LR) gene is inserted into the latency-associated transcript (LAT) locus of a herpes simplex virus type 1 (HSV-1) LAT deletion mutant, high levels of spontaneous reactivation from latency and enhanced pathogenesis occur. The LR gene, but not LAT, inhibits caspase 3 cleavage during productive infection. Plasmids containing LAT or the LR gene inhibit caspase 3 activation in transiently transfected cells, suggesting productive infection blocks certain antiapoptotic properties of LAT. These studies demonstrate a correlation between the enhanced pathogenic potential of CJLAT and the LR gene inhibiting caspase 3 cleavage during productive infection.
当将牛疱疹病毒1型(BHV-1)潜伏相关(LR)基因插入单纯疱疹病毒1型(HSV-1)LAT缺失突变体的潜伏相关转录本(LAT)基因座时,会出现高水平的潜伏自发激活和增强的致病性。在增殖性感染期间,LR基因而非LAT抑制半胱天冬酶3的切割。含有LAT或LR基因的质粒在瞬时转染细胞中抑制半胱天冬酶3的激活,这表明增殖性感染阻断了LAT的某些抗凋亡特性。这些研究证明了CJLAT增强的致病潜力与增殖性感染期间LR基因抑制半胱天冬酶3切割之间的相关性。