Hew Kelly, Dahlroth Sue-Li, Veerappan Saranya, Pan Lucy Xin, Cornvik Tobias, Nordlund Pär
Division of Structural Biology and Biochemistry, Nanyang Technological University, School of Biological Sciences, Singapore, Singapore.
Division of Biophysics, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
PLoS One. 2015 Dec 2;10(12):e0143947. doi: 10.1371/journal.pone.0143947. eCollection 2015.
Varicella zoster virus (VZV) is a highly infectious human herpesvirus that is the causative agent for chicken pox and shingles. VZV encodes a functional thymidylate synthase (TS), which is the sole enzyme that produces dTMP from dUMP de novo. To study substrate binding, the complex structure of TSVZV with dUMP was determined to a resolution of 2.9 Å. In the absence of a folate co-substrate, dUMP binds in the conserved TS active site and is coordinated similarly as in the human encoded TS (TSHS) in an open conformation. The interactions between TSVZV with dUMP and a cofactor analog, raltitrexed, were also studied using differential scanning fluorimetry (DSF), suggesting that TSVZV binds dUMP and raltitrexed in a sequential binding mode like other TS. The DSF also revealed interactions between TSVZV and in vitro phosphorylated brivudine (BVDUP), a highly potent anti-herpesvirus drug against VZV infections. The binding of BVDUP to TSVZV was further confirmed by the complex structure of TSVZV and BVDUP solved at a resolution of 2.9 Å. BVDUP binds similarly as dUMP in the TSHS but it induces a closed conformation of the active site. The structure supports that the 5-bromovinyl substituent on BVDUP is likely to inhibit TSVZV by preventing the transfer of a methylene group from its cofactor and the subsequent formation of dTMP. The interactions between TSVZV and BVDUP are consistent with that TSVZV is indeed a target of brivudine in vivo. The work also provided the structural basis for rational design of more specific TSVZV inhibitors.
水痘带状疱疹病毒(VZV)是一种具有高度传染性的人类疱疹病毒,是水痘和带状疱疹的病原体。VZV编码一种功能性胸苷酸合成酶(TS),它是唯一能从dUMP从头合成dTMP的酶。为了研究底物结合情况,确定了TSVZV与dUMP的复合物结构,分辨率为2.9 Å。在没有叶酸辅底物的情况下,dUMP结合在保守的TS活性位点,并且在开放构象中与人类编码的TS(TSHS)中的结合方式类似。还使用差示扫描荧光法(DSF)研究了TSVZV与dUMP和一种辅因子类似物雷替曲塞之间的相互作用,表明TSVZV像其他TS一样以顺序结合模式结合dUMP和雷替曲塞。DSF还揭示了TSVZV与体外磷酸化的布立伏定(BVDUP)之间的相互作用,BVDUP是一种针对VZV感染的高效抗疱疹病毒药物。TSVZV与BVDUP的复合物结构以2.9 Å的分辨率解析,进一步证实了BVDUP与TSVZV的结合。BVDUP在TSHS中与dUMP的结合方式类似,但它会诱导活性位点的封闭构象。该结构表明,BVDUP上的5-溴乙烯基取代基可能通过阻止其辅因子的亚甲基转移以及随后的dTMP形成来抑制TSVZV。TSVZV与BVDUP之间的相互作用与TSVZV在体内确实是布立伏定的靶点这一观点一致。这项工作还为更特异性的TSVZV抑制剂的合理设计提供了结构基础。