Identification of Postentry Restrictions to Mason-Pfizer Monkey Virus Infection in New World Monkey Cells
Identification of Postentry Restrictions to Mason-Pfizer Monkey Virus Infection in New World Monkey Cells
复制标题
DOI：
10.1128/jvi.00269-08
复制
发表时间：
2008-11-15
影响因子：
5.4
通讯作者：
Hunter, Eric
中科院分区：
文献类型：
--
作者：
Diehl, William E.;Stansell, Elizabeth;Hunter, Eric
TRIM 5 α已被证明是γ逆转录病毒和慢病毒宿主范围的主要试验后决定因素，最近还被证明是γ逆转录病毒和慢病毒宿主范围的主要试验后决定因素。然而，TRIM 5 α对其他逆转录病毒的限制潜力在很大程度上尚未开发。我们试图确定梅森-辉瑞猴病毒（M-PMV）（一种从恒河猴中分离的原型β逆转录病毒）是否对TRIM 5 alpha的限制敏感。筛选来自旧世界和新世界灵长类物种的细胞系，以确定它们对水泡性口炎病毒G蛋白假型M-PMV感染的易感性。发现从旧世界灵长类动物建立的所有测试的细胞系对M-PMV感染敏感。然而，从三种新世界猴种建立的成纤维细胞特异性地抵抗这种病毒的感染。在允许的细胞系中外源表达来自绢毛猴或松鼠猴的TRIM 5 α导致对M-PMV感染的阻断。蜘蛛猴来源的耐药细胞系中的限制被确定发生在试验后阶段。然而，蜘蛛猴TRIM 5 α在允许细胞中的表达未能限制M-PMV感染，并且干扰蜘蛛猴成纤维细胞中的内源性TRIM 5 α未能缓解对感染性的阻断。我们的研究结果表明，TRIM 5 α特异性延伸到β逆转录病毒，并表明新世界的猴子已经进化出额外的机制，以限制至少一种灵长类β逆转录病毒的感染。
TRIM5 alpha has been shown to be a major postentry determinant of the host range for gammaretroviruses and lentiviruses and, more recently, spumaviruses. However, the restrictive potential of TRIM5 alpha against other retroviruses has been largely unexplored. We sought to determine whether or not Mason-Pfizer monkey virus (M-PMV), a prototype betaretrovirus isolated from rhesus macaques, was sensitive to restriction by TRIM5 alpha. Cell lines from both Old World and New World primate species were screened for their susceptibility to infection by vesicular stomatitis virus G protein pseudotyped M-PMV. All of the cell lines tested that were established from Old World primates were found to be susceptible to M-PMV infection. However, fibroblasts established from three New World monkey species specifically resisted infection by this virus. Exogenously expressing TRIM5 alpha from either tamarin or squirrel monkeys in permissive cell lines resulted in a block to M-PMV infection. Restriction in the resistant cell line of spider monkey origin was determined to occur at a postentry stage. However, spider monkey TRIM5 alpha expression in permissive cells failed to restrict M-PMV infection, and interference with endogenous TRIM5 alpha in the spider monkey fibroblasts failed to relieve the block to infectivity. Our results demonstrate that TRIM5 alpha specificity extends to betaretroviruses and suggest that New World monkeys have evolved additional mechanisms to restrict the infection of at least one primate betaretrovirus.