2M, UCD-CASL (Complex and Adaptive Systems Laboratory), University College Dublin, Belfield, Dublin 4, Ireland.
J Virol. 2010 Apr;84(7):3644-53. doi: 10.1128/JVI.01959-09. Epub 2010 Jan 13.
Previous relatively small studies have associated particular amino acid replacements and deletions in the HIV-1 nef gene with differences in the rate of HIV disease progression. We tested more rigorously whether particular nef amino acid differences and deletions are associated with HIV disease progression. Amino acid replacements and deletions in patients' consensus sequences were investigated for 153 progressor (P), 615 long-term nonprogressor (LTNP), and 2,311 unknown progressor sequences from 582 subtype B HIV-infected patients. LTNPs had more defective nefs (interrupted by frameshifts or stop codons), but on a per-patient basis there was no excess of LTNP patients with one or more defective nef sequences compared to the Ps (P = 0.47). The high frequency of amino acid replacement at residues S(8), V(10), I(11), A(15), V(85), V(133), N(157), S(163), V(168), D(174), R(178), E(182), and R(188) in LTNPs was also seen in permuted datasets, implying that these are simply rapidly evolving residues. Permutation testing revealed that residues showing the greatest excess over expectation (A(15), V(85), N(157), S(163), V(168), D(174), R(178), and R(188)) were not significant (P = 0.77). Exploratory analysis suggested a hypothetical excess of frameshifting in the regions (9)SVIG and (118)QGYF among LTNPs. The regions V(10) and (152)KVEEA of nef were commonly deleted in LTNPs. However, permutation testing indicated that none of the regions displayed significantly excessive deletion in LTNPs. In conclusion, meta-analysis of HIV-1 nef sequences provides no clear evidence of whether defective nef sequences or particular regions of the protein play a significant role in disease progression.
先前的一些相对较小的研究已经将 HIV-1 nef 基因中的特定氨基酸替换和缺失与 HIV 疾病进展速度的差异联系起来。我们更严格地测试了特定 nef 氨基酸差异和缺失是否与 HIV 疾病进展有关。在来自 582 名 B 型 HIV 感染者的 153 名进展者(P)、615 名长期非进展者(LTNP)和 2311 名未知进展者的共识序列中,研究了氨基酸替换和缺失。与 P 相比,LTNP 具有更多的缺陷 nef(由移码或终止密码子引起的中断),但在每位患者的基础上,LTNP 患者中具有一个或多个缺陷 nef 序列的比例并不比 P 多(P=0.47)。在 LTNPs 中,S(8)、V(10)、I(11)、A(15)、V(85)、V(133)、N(157)、S(163)、V(168)、D(174)、R(178)、E(182)和 R(188)残基的氨基酸替换频率很高,在置换数据集也有发现,这表明这些残基只是快速进化的残基。置换检验显示,表现出与预期值最大偏差的残基(A(15)、V(85)、N(157)、S(163)、V(168)、D(174)、R(178)和 R(188))没有显著差异(P=0.77)。探索性分析表明,在 LTNPs 中存在(9)SVIG 和(118)QGYF 区域的假设性移码过度。nef 中的 V(10)和(152)KVEEA 区域在 LTNPs 中通常缺失。然而,置换检验表明,nef 中没有任何区域在 LTNPs 中显示出明显的过度缺失。总之,对 HIV-1 nef 序列的荟萃分析没有提供明确的证据表明缺陷 nef 序列或蛋白质的特定区域在疾病进展中是否发挥重要作用。