Miyazawa T, Kawaguchi Y, Kohmoto M, Sakuragi J, Adachi A, Fukasawa M, Mikami T
Department of Veterinary Microbiology, Faculty of Agriculture, University of Tokyo, Japan.
J Gen Virol. 1992 Jun;73 ( Pt 6):1543-6. doi: 10.1099/0022-1317-73-6-1543.
An infectious molecular clone of the TM1 strain of feline immunodeficiency virus (FIV) was transfected into each of one feline (CRFK), two simian (COS and Vero) and two human (SW480 and HeLa) non-lymphoid cell lines, and virus production was assayed on feline T lymphoblastoid MYA-1 cells by monitoring reverse transcriptase activity. Infectious virus was produced in CRFK, Vero and HeLa cells, but not in COS and SW480 cells. When the basal promoter activity of the FIV long terminal repeat (LTR) was examined in these cell lines by using a chloramphenicol acetyltransferase assay, the activity correlated with the virus production in each cell line. Furthermore, when the activity of the FIV LTR was compared with those of three primate lentivirus LTRs, the highest activity in all the cell lines examined was produced by the LTR of simian immunodeficiency virus from African green monkey (SIVAGM), suggesting that it has a wide expression range. In COS and SW480 cells, the activity of the FIV LTR was much lower than that of the SIVAGM LTR. These results indicate that, whereas the primary block to FIV infection of certain cells may occur at the cell surface, the FIV LTR may also participate in controlling virus replication, as an intracellular mechanism.
将猫免疫缺陷病毒（FIV）TM1株的感染性分子克隆转染至一个猫源（CRFK）、两个猿源（COS和Vero）和两个人源（SW480和HeLa）非淋巴细胞系中，通过监测逆转录酶活性，在猫T淋巴母细胞系MYA-1细胞上检测病毒产生情况。在CRFK、Vero和HeLa细胞中产生了感染性病毒，但在COS和SW480细胞中未产生。当通过氯霉素乙酰转移酶测定法检测这些细胞系中FIV长末端重复序列（LTR）的基础启动子活性时，该活性与每个细胞系中的病毒产生情况相关。此外，当将FIV LTR的活性与三种灵长类慢病毒LTR的活性进行比较时，在所有检测的细胞系中，来自非洲绿猴的猿免疫缺陷病毒（SIVAGM）的LTR产生的活性最高，表明其具有广泛的表达范围。在COS和SW480细胞中，FIV LTR的活性远低于SIVAGM LTR。这些结果表明，虽然某些细胞对FIV感染的主要障碍可能发生在细胞表面，但FIV LTR也可能作为一种细胞内机制参与控制病毒复制。
