Pager Cara Theresia, Dutch Rebecca Ellis
Department of Molecular and Cellular Biochemistry, University of Kentucky, College of Medicine, Lexington, 40536-0509, USA.
J Virol. 2005 Oct;79(20):12714-20. doi: 10.1128/JVI.79.20.12714-12720.2005.
Proteolytic processing of paramyxovirus fusion (F) proteins is essential for the generation of a mature and fusogenic form of the F protein. Although many paramyxovirus F proteins are proteolytically processed by the cellular protease furin at a multibasic cleavage motif, cleavage of the newly emerged Hendra virus F protein occurs by a previously unidentified cellular protease following a single lysine at residue 109. We demonstrate here that the cellular protease cathepsin L is involved in converting the Hendra virus precursor F protein (F(0)) to the active F(1) + F(2) disulfide-linked heterodimer. To initially identify the class of protease involved in Hendra virus F protein cleavage, Vero cells transfected with pCAGGS-Hendra F or pCAGGS-SV5 F (known to be proteolytically processed by furin) were metabolically labeled and chased in the absence or presence of serine, cysteine, aspartyl, and metalloprotease inhibitors. Nonspecific and specific protease inhibitors known to decrease cathepsin activity inhibited proteolytic processing of Hendra virus F but had no effect on simian virus 5 F processing. We next designed shRNA oligonucleotides to cathepsin L which dramatically reduced cathepsin L protein expression and enzyme activity. Cathepsin L shRNA-expressing Vero cells transfected with pCAGGS-Hendra F demonstrated a nondetectable amount of cleavage of the Hendra virus F protein and significantly decreased membrane fusion activity. Additionally, we found that purified human cathepsin L processed immunopurified Hendra virus F(0) into F(1) and F(2) fragments. These studies introduce a novel mechanism for primary proteolytic processing of viral glycoproteins and also suggest a previously unreported biological role for cathepsin L.
副粘病毒融合(F)蛋白的蛋白水解加工对于产生成熟且具有融合活性的F蛋白至关重要。尽管许多副粘病毒F蛋白在多碱性切割基序处被细胞蛋白酶弗林蛋白酶进行蛋白水解加工,但新出现的亨德拉病毒F蛋白的切割是由一种先前未鉴定的细胞蛋白酶在第109位残基的单个赖氨酸之后进行的。我们在此证明细胞蛋白酶组织蛋白酶L参与将亨德拉病毒前体F蛋白(F(0))转化为活性F(1)+F(2)二硫键连接的异二聚体。为了初步鉴定参与亨德拉病毒F蛋白切割的蛋白酶类别,用pCAGGS-亨德拉F或pCAGGS-SV5 F(已知被弗林蛋白酶进行蛋白水解加工)转染的Vero细胞在有无丝氨酸、半胱氨酸、天冬氨酸和金属蛋白酶抑制剂的情况下进行代谢标记和追踪。已知可降低组织蛋白酶活性的非特异性和特异性蛋白酶抑制剂抑制了亨德拉病毒F的蛋白水解加工,但对猿猴病毒5 F的加工没有影响。接下来,我们设计了针对组织蛋白酶L的短发夹RNA寡核苷酸,其显著降低了组织蛋白酶L蛋白表达和酶活性。用pCAGGS-亨德拉F转染的表达组织蛋白酶L短发夹RNA的Vero细胞显示出无法检测到的亨德拉病毒F蛋白切割量,并且膜融合活性显著降低。此外,我们发现纯化的人组织蛋白酶L将免疫纯化的亨德拉病毒F(0)加工成F(1)和F(2)片段。这些研究引入了一种病毒糖蛋白初级蛋白水解加工的新机制,也提示了组织蛋白酶L以前未报道的生物学作用。