Kewalramani V N, Park C S, Gallombardo P A, Emerman M
Fred Hutchinson Cancer Research Center, Division of Molecular Medicine, Seattle, Washington 98104, USA.
Virology. 1996 Apr 15;218(2):326-34. doi: 10.1006/viro.1996.0201.
Using recombinant proteins as standards, we calculated the amount of Vpr and Vpx present in HIV-2ROD particles. We find 2000-3000 copies of Vpx per particle but only 40-50 copies of Vpr. We investigated the reasons for this discrepancy between Vpx and Vpr and found that viral factors, including HIV-2 Vpx, do not restrict its incorporation. Instead, the accumulation of HIV-2ROD Vpr during infection is restricted by a short protein half-life which acts to limit its virion incorporation. The half-life of HIV-2 Vpr was calculated to be about 90 min, while HIV-2 Vpx and HIV-1 Vpr had half-lifes of 36 and 20 hr, respectively. Moreover, while both HIV-1 Vpr and HIV-2 Vpr cause cells to accumulate in G2 of the cell cycle, the effect of HIV-2 Vpr is attenuated relative to HIV-1 Vpr. Thus, protein stability correlates with both the function of Vpr and its virion incorporation.
以重组蛋白作为标准，我们计算了HIV-2 ROD颗粒中Vpr和Vpx的含量。我们发现每个颗粒中有2000 - 3000个Vpx拷贝，但Vpr只有40 - 50个拷贝。我们研究了Vpx和Vpr之间这种差异的原因，发现包括HIV-2 Vpx在内的病毒因子并不限制其掺入。相反，HIV-2 ROD Vpr在感染过程中的积累受到短蛋白半衰期的限制，该半衰期限制了其病毒体掺入。HIV-2 Vpr的半衰期计算约为90分钟，而HIV-2 Vpx和HIV-1 Vpr的半衰期分别为36小时和20小时。此外，虽然HIV-1 Vpr和HIV-2 Vpr都导致细胞在细胞周期的G2期积累，但相对于HIV-1 Vpr，HIV-2 Vpr的作用减弱。因此，蛋白质稳定性与Vpr的功能及其病毒体掺入均相关。
