Witwer Kenneth W, Buchanan Erin L, Myers Stephanie L, McAlexander Melissa A
Department of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, 733 North Broadway, BRB Suite 831, Baltimore, MD, 21025, USA.
J Neuroinflammation. 2015 Sep 4;12:159. doi: 10.1186/s12974-015-0380-y.
Pilakka-Kanthikeel et al. recently reported higher levels of the retroviral restriction factor sterile alpha motif and histidine/aspartic acid domain-containing protein 1 (SAMHD1) in astrocytes than in microglia, suggesting that SAMHD1 levels might explain in part the relatively refractory nature of astrocytes to retroviral replication. These findings are consistent with our studies of simian and human immunodeficiency virus infection of astrocytes and macrophages. Similarly, a role for two host microRNAs in post-transcriptional regulation of SAMHD1 agrees with our in vitro results and those of others. However, data from an animal model of HIV neurologic disorders may not be consistent with robust miRNA-mediated regulation of SAMHD1 in vivo.
皮拉卡-坎蒂凯尔等人最近报告称，星形胶质细胞中逆转录病毒限制因子无菌α基序和含组氨酸/天冬氨酸结构域蛋白1（SAMHD1）的水平高于小胶质细胞，这表明SAMHD1水平可能部分解释了星形胶质细胞对逆转录病毒复制相对难治的特性。这些发现与我们对星形胶质细胞和巨噬细胞感染猿猴免疫缺陷病毒和人类免疫缺陷病毒的研究一致。同样，两种宿主微小RNA在SAMHD1转录后调控中的作用与我们和其他人的体外研究结果相符。然而，来自HIV神经疾病动物模型的数据可能与体内微小RNA对SAMHD1的强大调控作用不一致。
