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Development of an Infectious Clone System to Study the Life Cycle of Hazara Virus

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Development of an Infectious Clone System to Study the Life Cycle of Hazara Virus Development of an Infectious Clone System to Study the Life Cycle of Hazara Virus Jack Fuller Submitted in accordance with the requirements for the degree of Doctor of Philosophy The University of Leeds Faculty of Biological Sciences July 2020 i The candidate confirms that the work submitted is his own and that appropriate credit has been given where reference has been made to the work of others. This copy has been supplied on the understanding that it is copyright material and that no quotation from the thesis may be published without proper acknowledgement. © 2020 The University of Leeds and Jack Fuller ii Acknowledgements I would like to thank my supervisors, John, Jamel and Roger for their endless support and fresh ideas throughout my PhD. A special thanks go to John for always providing enthusiasm and encouragement, especially during the tougher times of the project! I would also like to thank everyone in 8.61, not only for making my time at Leeds enjoyable, but for helping me develop as a scientist through useful critique and discussion. A special thanks goes to Francis Hopkins, for welcoming me into the Barr group and providing a constant supply of humour and to Ellie Todd, for listening to my endless whines and gripes, and for providing welcome distractions in the form of her PowerPoint artwork. Outside of the lab, my mum deserves a special mention for always being the voice of reason and support at the end of the phone, but also for pushing me to succeed throughout my entire education. I have no doubts I would not be in the position I am now without her! Finally, a huge thanks to my partner Hannah, who has been there to support me through all the highs and lows of my PhD, and has sacrificed many weekend trips to allow me to finish experiments and to tend to my viruses! iii Abstract Crimean-Congo hemorrhagic fever orthonairovirus (CCHFV) is a negative sense single stranded RNA virus, capable of causing fatal hemorrhagic fever in humans. Currently, an infectious clone system exists for CCHFV, however, owing to the high containment level required for experimentation with this virus, its potential is limited. Here, a highly efficient infectious clone system was developed for recovery of Hazara virus (HAZV), the first such orthonairovirus system able to be used in biosafety level 2 facilities, providing a valuable tool for increasing our understanding of these viruses. Mechanisms of viral subversion of cellular trafficking pathways involved in viral entry, gene expression, assembly and egress are poorly understood for HAZV and CCHFV. The infectious clone system was adapted to express eGFP, enabling screening of an siRNA library targeting genes involved in cellular trafficking networks via live-cell fluorescent imaging, the first such screen for a nairovirus. Screening revealed an important role for subunits of the coat protein 1 vesicle coatomer (COPI), normally involved in regulation of Golgi / ER cargo trafficking. The effect was observed at multiple stages of the HAZV life cycle; an early stage prior to and including gene expression, and also a later stage during assembly and egress of infectious virus, with COPI-knockdown reducing titres by approximately 100-fold. In addition to gain of function mutations, such as the reporter virus discussed above, the infectious clone system represents a powerful tool for exploring the role of individual nucleotides, amino acids and entire open reading frames within the viral genome. Both CCHFV and HAZV contain a well-documented, highly conserved caspase cleavage motif on the apex of the arm domain on the nucleoprotein (N). Whilst previous literature has demonstrated this motif to be cleaved as purified protein, limited data exists as to its role in the context of viral replication in a cellular system. To this end, the infectious clone system described above was used to create a panel of mutants targeting this conserved caspase cleavage motifs within HAZV N. HAZV bearing an uncleavable DQVE sequence rescued efficiently with growth rates equivalent to those of wild-type virus in both mammalian and tick cells, showing this site was dispensable for virus iv multiplication. In contrast, substitution of the DQVD motif with the similarly uncleavable AQVA sequence could not be rescued despite repeated efforts. Together, these results highlight the importance of this caspase cleavage site in the HAZV life cycle but reveal the DQVD sequence performs a critical, as yet unknown, role aside from caspase cleavage. v Table of contents Acknowledgements ......................................................................................... iii Abstract ............................................................................................................ iv Table of figures ................................................................................................ ix Table of tables .................................................................................................. xi Abbreviations .................................................................................................. xii 1 Introduction ................................................................................................ 1 1.1 General introduction ................................................................................... 1 1.1.1 Discovery of CCHFV and HAZV .............................................................................. 1 1.1.2 CCHFV and HAZV classification ............................................................................. 2 1.1.3 Transmission, vectors and hosts ............................................................................. 5 1.1.4 Epidemiology and global distribution of CCHFV ..................................................... 7 1.1.5 Diagnosis of CCHF .................................................................................................. 9 1.1.6 Clinical manifestations and treatment options ......................................................... 9 1.2 The virus .................................................................................................... 12 1.2.1 Virus structure ....................................................................................................... 12 1.2.2 Viral genome structure .......................................................................................... 13 1.3 The replication cycle of CCHFV and HAZV .............................................. 14 1.3.1 Binding and entry .................................................................................................. 14 1.3.2 Replication ............................................................................................................. 16 1.3.3 Assembly and egress ............................................................................................ 18 1.4 Virally encoded proteins ........................................................................... 19 1.4.1 S segment ............................................................................................................. 19 1.4.2 M segment ............................................................................................................. 24 1.4.3 L Segment ............................................................................................................. 26 1.5 Nairoviral reverse genetics systems ........................................................ 27 1.5.1 Minigenome system .............................................................................................. 28 1.5.2 VLP system ........................................................................................................... 31 1.5.3 Infectious clone...................................................................................................... 32 1.6 Apoptotic response to HAZV / CCHFV infection ..................................... 35 1.7 Project aims ............................................................................................... 36 2 Materials and methods ............................................................................ 38 2.1 Materials..................................................................................................... 38 2.1.1 Vectors .................................................................................................................. 38 2.1.2 Bacterial cell lines .................................................................................................. 38 2.1.3 Mammalian cell lines ............................................................................................. 38 vi 2.1.4 Tick cell lines ......................................................................................................... 39 2.1.5 Hazara virus strain ................................................................................................ 39 2.2 General methods ....................................................................................... 39 2.2.1 Manipulation of recombinant DNA......................................................................... 39 2.2.2 Cell culture methods .............................................................................................. 42 2.2.3 Transfections ......................................................................................................... 44 2.2.4 Analysis of protein expression ............................................................................... 46 2.2.5 Virological techniques ..........................................................................................
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