Murthy H M, Judge K, DeLucas L, Padmanabhan R
Center for Macromolecular Crystallography, University of Alabama at Birmingham, 1918 University Boulevard, 79 THT MCLM 244, Birmingham, AL, 35294-0005, USA.
J Mol Biol. 2000 Aug 25;301(4):759-67. doi: 10.1006/jmbi.2000.3924.
Dengue viruses are members of the Flaviviridae and cause dengue fever and the more severe dengue hemorrhagic fever. Although nearly 40 % of the world's population is at risk of dengue infection, there is currently no effective vaccine or chemotherapy for the disease. Processing of the dengue polyprotein into structural and non-structural proteins in a host, which is essential for assembly of infective virions, is carried out by the combined action of host proteases and the trypsin-like, two-component viral NS2B/NS3 serine protease. Although NS2B strongly stimulates the catalytic NS3 protease domain, the latter is fully active against small substrates and possesses detectable activity against larger substrates, making both forms of the enzyme possible targets for drug design. In the crystal structure of a complex of the protease with a Bowman-Birk inhibitor reported here, an Arg residue at the P1 position of the inhibitor is bound in a manner distinctly different from that in other serine proteases of comparable specificity. However, because the regulatory component, NS2B, is not present in the complex, the physiological implications of this observations are currently unclear. The redundant nature of interaction of P1 Arg and Lys residues with Asp129, Tyr150 and Ser163 of the enzyme provides an explanation for the observed behavior of several site-specific mutants of Asp129 in the protease. The strong level of conservation of residues in the protease that interact with the P1 Arg, along with conservation of Arg at P1 of most cleavage sites in other flaviviruses, suggests that observations from this structure are likely to be applicable to many flaviviruses. The structure provides a starting point for design of site-specific mutations to probe the mechanism of catalysis by the catalytic domain, its activation by the regulatory domain and for design of specific inhibitors of enzymatic activity.
登革病毒属于黄病毒科,可引起登革热以及更为严重的登革出血热。尽管全球近40%的人口有感染登革热的风险,但目前尚无针对该疾病的有效疫苗或化疗方法。在宿主中将登革病毒多聚蛋白加工成结构蛋白和非结构蛋白,这对于感染性病毒粒子的组装至关重要,这一过程是由宿主蛋白酶以及胰蛋白酶样的双组分病毒NS2B/NS3丝氨酸蛋白酶共同作用完成的。虽然NS2B强烈刺激催化性NS3蛋白酶结构域,但后者对小底物具有完全活性,对大底物也具有可检测到的活性,这使得该酶的两种形式都可能成为药物设计的靶点。在此报道的蛋白酶与鲍曼-伯克抑制剂复合物的晶体结构中,抑制剂P1位置的一个精氨酸残基的结合方式与其他具有类似特异性的丝氨酸蛋白酶明显不同。然而,由于复合物中不存在调节成分NS2B,目前尚不清楚这一观察结果的生理学意义。P1精氨酸和赖氨酸残基与酶的Asp129、Tyr150和Ser163之间相互作用的冗余性质,为蛋白酶中Asp129的几个位点特异性突变的观察行为提供了解释。与P1精氨酸相互作用的蛋白酶中残基的高度保守水平,以及其他黄病毒大多数切割位点P1处精氨酸的保守性,表明从该结构获得的观察结果可能适用于许多黄病毒。该结构为设计位点特异性突变以探究催化结构域的催化机制、其被调节结构域激活的机制以及设计酶活性的特异性抑制剂提供了一个起点。