Afonso C L, Zsak L, Carrillo C, Borca M V, Rock D L
Plum Island Animal Disease Center, Agricultural Research Service, US Department of Agriculture, Greenport, NY 11944-0848, USA.
J Gen Virol. 1998 Oct;79 ( Pt 10):2543-7. doi: 10.1099/0022-1317-79-10-2543.
Previously, we described a highly conserved nonessential African swine fever virus (ASFV) right variable region gene, NL. Deletion of NL from the European pathogenic isolate E70 resulted in almost complete attenuation of the virus in domestic swine. To study gene function further, NL gene deletion mutants were constructed from two pathogenic African ASFV isolates, Malawi Lil-20/1 (Mal) and Pretoriuskop/96/4 (Pr4). Unexpectedly, both Mal (Mal-deltaNL) and PR4 (Pr4deltaNL) null mutants remained highly virulent when inoculated in swine. Mal-deltaNL exhibited a disease and virulence phenotype indistinguishable from its revertant, Mal-NLR, which caused 100% mortality. Mortality among Pr4deltaNL-infected animals was also high; however, a significant delay in onset of fever and viraemia and in time to death was observed. These data indicate that NL gene function is not required for ASFV virulence and that other yet-to-be identified viral determinants perform significant virulence functions in these African field isolates.
此前，我们描述了一个高度保守的非必需非洲猪瘟病毒（ASFV）右可变区基因NL。从欧洲致病分离株E70中删除NL后，病毒在家猪中的毒力几乎完全减弱。为了进一步研究该基因的功能，我们从两种致病性非洲ASFV分离株马拉维Lil-20/1（Mal）和比勒陀利亚斯科普/96/4（Pr4）构建了NL基因缺失突变体。出乎意料的是，当接种到家猪体内时，Mal（Mal-deltaNL）和PR4（Pr4deltaNL）的无效突变体仍然具有高毒力。Mal-deltaNL表现出与回复株Mal-NLR难以区分的疾病和毒力表型，Mal-NLR导致100%的死亡率。Pr4deltaNL感染动物的死亡率也很高；然而，观察到发热和病毒血症的发作以及死亡时间有显著延迟。这些数据表明，ASFV的毒力不需要NL基因的功能，并且在这些非洲野外分离株中，其他尚未确定的病毒决定因素发挥着重要的毒力功能。
