Desrosiers R C, Daniel M D, Butler C V, Schmidt D K, Letvin N L, Hunt R D, King N W, Barker C S, Hunter E
J Virol. 1985 May;54(2):552-60. doi: 10.1128/JVI.54.2.552-560.1985.
Seventeen isolates of retrovirus D/New England have been obtained from three species of macaques at the New England Regional Primate Research Center. Seven of the isolates were obtained from macaques who subsequently died with the macaque immunodeficiency syndrome; other isolates were obtained from macaques with less severe or other forms of illness. Attempts to isolate type D retrovirus from peripheral lymphocytes of 97 apparently healthy macaques have not been successful. Cloned DNA was prepared from Hirt supernatants of cells infected with one of these isolates (D/New England 398). By restriction endonuclease analysis, cloned pD398 DNA represented full-length viral DNA with one long terminal repeat. A detailed restriction endonuclease map of pD398 was derived and compared with a map of the cloned Mason-Pfizer monkey virus genome. Forty-six percent (13 of 28) of restriction endonuclease sites were found to be conserved when these related viruses were compared. Five of the D/New England isolates, including those from three different macaque species, were examined for strain variability by restriction endonuclease typing. Comparison of over 30 restriction endonuclease sites has not distinguished any of these D/New England isolates. It thus appears that a single strain of type D retrovirus is infecting three different species of macaques in the New England colony. Markedly reduced cross-hybridization was observed between cloned pD398 and Mason-Pfizer monkey virus DNAs at high stringency; this reduced cross-hybridization was localized to the pol-env regions of the genome. Only very weak hybridization of D/New England DNA to cloned squirrel monkey type D retrovirus DNA could be detected even at low-stringency conditions. What role type D retrovirus plays in the immunodeficiency syndrome of macaques remains to be determined.
在新英格兰地区灵长类动物研究中心,已从三种猕猴中分离出17株D型逆转录病毒/新英格兰毒株。其中7株分离自随后死于猕猴免疫缺陷综合征的猕猴;其他分离株则来自病情较轻或患有其他疾病形式的猕猴。从97只明显健康的猕猴外周淋巴细胞中分离D型逆转录病毒的尝试均未成功。从感染其中一种分离株(D/新英格兰398)的细胞的Hirt上清液中制备了克隆DNA。通过限制性内切酶分析,克隆的pD398 DNA代表具有一个长末端重复序列的全长病毒DNA。绘制了pD398的详细限制性内切酶图谱,并与克隆的梅森- Pfizer猴病毒基因组图谱进行了比较。当比较这些相关病毒时,发现46%(28个中的13个)的限制性内切酶位点是保守的。通过限制性内切酶分型检查了5株D/新英格兰分离株,包括来自三种不同猕猴物种的分离株。对30多个限制性内切酶位点的比较并未区分出任何一株D/新英格兰分离株。因此,似乎单一毒株的D型逆转录病毒正在感染新英格兰猴群中的三种不同猕猴物种。在高严谨度下,观察到克隆的pD398与梅森- Pfizer猴病毒DNA之间的交叉杂交明显减少;这种减少的交叉杂交定位于基因组的pol-env区域。即使在低严谨度条件下,也只能检测到D/新英格兰DNA与克隆的松鼠猴D型逆转录病毒DNA的非常微弱的杂交。D型逆转录病毒在猕猴免疫缺陷综合征中起什么作用还有待确定。