In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[Q]: A reverse genetics system for the avian coronavirus infectious bronchitis virus (IBV) has been described in which a full-length cDNA, corresponding to the IBV (Beaudette-CK) genome, was inserted into the vaccinia virus genome following in vitro assembly of three contiguous cDNAs [Casais, R., Thiel, V., Siddell, S.G., Cavanagh, D., Britton, P., 2001. Reverse genetics system for the avian coronavirus infectious bronchitis virus. J. Virol. 75, 12359-12369]. The method has subsequently been used to generate a recombinant IBV expressing a chimaeric S gene [Casais, R., Dove, B., Cavanagh, D., Britton, P., 2003. Recombinant avian infectious bronchitis virus expressing a heterologous spike gene demonstrates that the spike protein is a determinant of cell tropism. J. Virol. 77, 9084-9089]. Use of vaccinia virus as a vector for the full-length cDNA of the IBV genome has the advantage that modifications can be made to the IBV cDNA using homologous recombination, a method frequently used to insert and delete sequences from the vaccinia virus genome. We describe the use of homologous recombination as a method for modifying the Beaudette full-length cDNA, within the vaccinia virus genome, without the requirement for in vitro assembly of the IBV cDNA. To demonstrate the feasibility of the method we exchanged the ectodomain of the Beaudette spike gene for the corresponding region from IBV M41 and generated two recombinant infectious bronchitis viruses (rIBVs) expressing the chimaeric S protein, validating the method as an alternative way for generating rIBVs.
[A]: Generation of a recombinant avian coronavirus infectious bronchitis virus using transient dominant selection

[Q]: A major obstacle to anticipating the cross-species transmission of zoonotic diseases and developing novel strategies for their control is the scarcity of data informing how these pathogens circulate within natural reservoir populations. Vampire bats are the primary reservoir of rabies in Latin America, where the disease remains among the most important viral zoonoses affecting humans and livestock. Unpredictable spatiotemporal dynamics of rabies within bat populations have precluded anticipation of outbreaks and undermined widespread bat culling programs. By analysing 1146 vampire bat-transmitted rabies (VBR) outbreaks in livestock across 12 years in Peru, we demonstrate that viral expansions into historically uninfected zones have doubled the recent burden of VBR. Viral expansions are geographically widespread, but severely constrained by high elevation peaks in the Andes mountains. Within Andean valleys, invasions form wavefronts that are advancing towards large, unvaccinated livestock populations that are heavily bitten by bats, which together will fuel high transmission and mortality. Using spatial models, we forecast the pathways of ongoing VBR epizootics across heterogeneous landscapes. These results directly inform vaccination strategies to mitigate impending viral emergence, reveal VBR as an emerging rather than an enzootic disease and create opportunities to test novel interventions to manage viruses in bat reservoirs.
[A]: Spatial expansions and travelling waves of rabies in vampire bats

[Q]: word count: 359 20 Text word count: 4423 21 22 All rights reserved. No reuse allowed without permission. ABSTRACT 23 The 3-to-5 exoribonuclease in coronavirus (CoV) nonstructural protein 14 (nsp14-ExoN) 24 mediates RNA proofreading during genome replication. ExoN catalytic residues are arranged in 25 three motifs: I (DE), II (E), III (D). Alanine substitution of the motif I residues (AA-E-D, four 26 nucleotide substitutions) in murine hepatitis virus (MHV) and SARS-CoV yields viable mutants 27 with impaired replication and fitness, increased mutation rates, and attenuated virulence in vivo. 28 Despite these impairments, MHV-and SARS-CoV ExoN motif I AA mutants (ExoN-AA) have 29 not reverted at motif I in diverse in vitro and in vivo environments, suggesting that profound 30 fitness barriers prevent motif I reversion. To test this hypothesis, we engineered MHV-ExoN-AA 31 with 1, 2 or 3 nucleotide mutations along genetic pathways to AA-to-DE reversion. We show 32 that engineered intermediate revertants were viable but had no increased replication or 33 competitive fitness compared to MHV-ExoN-AA. In contrast, a low passage (P10) MHV-ExoN-34 AA showed increased replication and competitive fitness without reversion of ExoN-AA. 35 Finally, engineered reversion of ExoN-AA to ExoN-DE in the presence of ExoN-AA passage-36 adaptive mutations resulted in significant fitness loss. These results demonstrate that while 37 reversion is possible, at least one alternative adaptive pathway is more rapidly advantageous than 38 intermediate revertants and may alter the genetic background to render reversion detrimental to 39 fitness. Our results provide an evolutionary rationale for lack of ExoN-AA reversion, illuminate 40 potential multi-protein replicase interactions and coevolution, and support future studies aimed at 41 stabilizing attenuated CoV ExoN-AA mutants. 42 43 All rights reserved. No reuse allowed without permission. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/618249 doi: bioRxiv preprint Coronaviruses encode an exoribonuclease (ExoN) that is important for viral replication, fitness, 45 and virulence, yet coronaviruses with a defective ExoN (ExoN-AA) have not reverted under 46 diverse experimental conditions. In this study, we identify multiple impediments to MHV-ExoN-47 AA reversion. We show that ExoN-AA reversion is possible but evolutionarily unfavorable. 48 Instead, compensatory mutations outside of ExoN-AA motif I are more accessible and beneficial 49 than partial reversion. We also show that coevolution between replicase proteins over long-term 50 passage partially compensates for ExoN-AA motif I but renders the virus inhospitable to a 51 reverted ExoN. Our results reveal the evolutionary basis for the genetic stability of ExoN-52 inactivating mutations, illuminate complex functional and evolutionary relationships between 53 coronavirus replicase proteins, and identify potential mechanisms for stabilization of ExoN-AA 54 coronavirus mutants. 55 All rights reserved. No reuse allowed without permission.
[A]:
Fitness barriers limit reversion of a proofreading-deficient coronavirus 1 2