验针对辅助受体的治疗，因为HIV在非人源细胞中复制较差，并且还需要克服HIV进入动物细胞的障碍。CCR5也是猿猴免疫缺陷病毒(SIV)的辅助受体，但SIV株系的特性与T-trop相似，而与M-trop相异[18]，因而利用猿猴进行试验不能完全反映HIV-1在体内的情况，所以有人提出利用产生人CD+4 CCR5的转基因小鼠来进行疫苗试验[18]。
HIV gp120与CCR5的相互作用对中和抗体较为敏感，大部分抗体不能阻止gp120与CD4分子的结合，而能阻止与CCR5的结合。因为CCR5是人体中的正常成分，其免疫原性较差，所以也就不能直接用它作为疫苗，但可以用CCR5蛋白来筛选人源抗体库，抗体库具有广泛的多样性，理论上任何抗原都能筛选到相应的抗体。利用β-趋化素在体外可以阻止HIV-1感染，据说在体内用β-趋化素进行治疗时，需将β-趋化素进行修饰，否则会使人体引起炎症反应[19]。
作者单位：中国科学院微生物研究所分子病毒室，北京 100080
参考文献
[1] Gottlieb MS, Schroff R, Schanker HM et al. Pneumocystis carinii pneamonia and mucosal candidias in previously healthy homosexual men. N Engl S Med, 1981, 305:1425～1431
[2] Lifson SO, Reyes GR, McGrath MS et al. AIDS retrovirus induced cytopathology:giant cell formation and involvement of CD4 antigen. Science, 1986,232:1123～1127
[3] Zhang L, Huang Y, He T et al. HIV-I subtype and second-receptor. Nature, 1996,383:768
[4] Weissenhorn W, Dessen A, Harrison SC et al. Atomic strucure of the ectodomain from HIV gp41. Nature, 1997,387:426～430
[5] Cham DC, Fass D, Berger JM et al. Core structure of gp41 from the HIV envelope glycoprotein. Cell, 1997,89:263～273
[6] Wu L, Gerard NP, Wyatt R et al. CD4-induced interaction of primary HIV-I gp-120 glycoproteins with the chemokine receotor R-5. Nature, 1996, 384:179～180
[7] Pleskoff O, Treboute C, Brelot A et al. Identification of a chemoline receptor encoded by human cytomagalovirus as a cofactor for HIV-I entry. Science, 1997, 276:1874～1877
[8] Cheng-Mayer C, Seto D, Tateno M et al. Biologic features of HIV-I that correlate with virulence in the host. Science, 1988,240:80～82
[9] Connor RI, Mohri H, Cao Y et al. Increased viral burden and cytopathicity correlate temporally with CD+4 T lymphocyte decline and clinical progression in human immunodeficiency virus type 1-infected individuals. J Virol, 1993, 67:1772～1777
[10] Feng Y, Broder CC, Kennedy PE et al. HIV-I entry cofactor: functional cDNA cloning of a seven-transmembrane, G protein-coupled receptor. Science, 1996,272:872～877
[11] Fauci AS. Host factors and the pathogenesis of HIV-induced disease. Nature, 1996, 384:529～533
[12] Zhu T, Mo H, Ning W. Genotypic and phenotypic characterization of HIV-I in patients with primary infection. Science, 1993,261:1179～1181
[13] Loetscher P, Seitz M, Baggiolini M et al. Active of NK cell by CCC chmokines, chemotaxis, Ca+2 mobilization, and enzyme release. J Exp Med, 1996,184:569～577
[14] Jackson GG, Perkins JT, Rabenis M et al. Passive immunoneutralization of human immunodeficiency virus in patients with advanced AIDS. Lancet, 1988,2:647～652
[15] Watanable M, Reimann KA, Delong PA et al. Effect of recombinant soluble CD4 in rhesus monkeys infected with simian immunodeficiency virus of macaques. Nature, 1989,337:267～270
[16] Bleul CC, Wu LJ, Hoxie JA et al. The HIV coreceptors CXCR4 and CCR5 are differentially expressed and regulated on human T lymphocytes. Proc Natl Acad Sci USA, 1997,94:1925～1930
[17] Bleul CC, Fuhibrigge RC, Casasnovas JM et al. A highly efficacious lymphocyte chemoattractant, stronal cell-derived factor 1 (SDF-1). J Exp Med, 1996, 184:1101～1110
[18] Marcon L, Choe H, Martin KA. Utilization of C-C chemokine receptor 5 by the envelope lycoproteins of a pathogenic simian immunodeficiency virus, SIVmac 239. J Virol, 1997,71:2522～2527
[19] Mraham S, Paul RC, Laurent P et al. Potent inhibition of HIV-infectivity in macrophages and lymphocytes by a novel CCR5 antagonist. Science, 1997,276:276～279