A DNA transfection system for generation of influenza A virus from eight plasmids.

By E. Hoffmann, G. Neumann, Yoshihiro Kawaoka, G. Hobom, R. Webster. Proceedings of the National Academy of Sciences of the United States of America, 2000

1,648 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Epidemiology, Infectious Diseases

View Paper: https://www.semanticscholar.org/paper/afd44a222c9f2355074b36858a9b60f7d8a0ee7f

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Citations in the corpus

Stability-mediated epistasis constrains the evolution of an influenza protein (2013, methodology): “To confirm this, we used reverse genetics (Hoffmann et al., 2000) to generate GFP-carrying viruses (Bloom et al., 2010) with the polymerase genes from Nanchang/1995 and the remaining genes from the lab-adapted A/WSN/1933 (H1N1) strain (Figure 3—figure supplement 2).”
Rescue of influenza A virus from recombinant DNA. (2007, methodology): “The second strategy was based on the use of bidirectional RNA polymerase I/II plasmids to clone the full-length cDNAs derived from each of the viral genomic segments to drive, after transfection, both the expression of the proteins and the synthesis of each of the negative-sense vRNAs (20, 21 ).”
Functional balance between haemagglutinin and neuraminidase in influenza virus infections (2002, background): “Starting with helper virus dependent systems [for a review see 48], these techniques have later been improved to allow the generation of influenza viruses entirely from cloned DNA [49,50].”
Universal primer set for the full-length amplification of all influenza A viruses (2001, methodology): “After cloning the eight plasmids, we can generate recombinant infectious viruses within one to three days [15].”
Single-Reaction Genomic Amplification Accelerates Sequencing and Vaccine Production for Classical and Swine Origin Human Influenza A Viruses (2009, methodology): “We replaced the mutant NY238-NP clone with another sequence-verified NY238-NP clone that was identified during colony screening and rescued the virus, as described previously (7, 14).”
Mapping person-to-person variation in viral mutations that escape polyclonal serum targeting influenza hemagglutinin (2019, methodology): “(2018) were not sufficient for all the mutational antigenic profiling, so for most of the experiments in the current paper we generated new triplicate stocks of mutant virus libraries using influenza reverse-genetics (Hoffmann et al., 2000).”
Lethal H5N1 influenza viruses escape host anti-viral cytokine responses (2002, methodology): “To investigate the role of the NS gene in the resistance of H5N1/97 viruses to cytokines, we used reverse genetic”
Systematic Identification of H274Y Compensatory Mutations in Influenza A Virus Neuraminidase by High-Throughput Screening (2012, methodology): “The mutant library was transfected into C227 cells (23), which are subclones of 293T cells stably expressing dominant-negative IRF-3 and are able to increase the viral titer by 10%, to generate the viral mutant library using the eight-plasmid reverse-genetics system (24).”
Inferring Stabilizing Mutations from Protein Phylogenies: Application to Influenza Hemagglutinin (2009, methodology): “Influenza reverse genetics The influenza virus was reconstituted from the eight bidirectional reverse genetics plasmids [109] by co-transfecting 250 ng of each plasmid into a co-culture of MDCK and 293T cells in a 6well plate.”
The inherent mutational tolerance and antigenic evolvability of influenza hemagglutinin (2014, methodology): “The genes in each mutant library were cloned at high efficiency into a bidirectional influenza reverse-genetics plasmid (Hoffmann et al., 2000).”
Accurate Measurement of the Effects of All Amino-Acid Mutations on Influenza Hemagglutinin (2016, methodology): “After 24 h, we transfected these co-cultures with bidirectional reverse-genetics plasmids for the seven non-HA segments of the A/WSN/1933 virus (pHW181-PB2, pHW182-PB1, pHW183-PA, pHW185-NP, pHW186-NA, pHW187-M, and pHW188-NS) [13] plus a protein expression plasmid for WSN HA (pHAGE2-CMV-WSNHA, whic”