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The COVID-19 pandemic, caused by the SARS-CoV-2 coronavirus, has triggered a worldwide health emergency. Here, we show that ferritin-like Dps from hyperthermophilic Sulfolobus islandicus, covalently coupled with SARS-CoV-2 antigens via the SpyCatcher system, forms stable multivalent dodecameric vaccine nanoparticles that remain intact even after lyophilisation. Immunisation experiments in mice demonstrated that the SARS-CoV-2 receptor binding domain (RBD) coupled to Dps (RBD-S-Dps) elicited a higher antibody titre and an enhanced neutralising antibody response compared to monomeric RBD. A single immunisation with RBD-S-Dps completely protected hACE2-expressing mice from serious illness and led to viral clearance from the lungs upon SARS-CoV-2 infection. Our data highlight that multimerised SARS-CoV-2 subunit vaccines are a highly efficacious modality, particularly when combined with an ultra-stable scaffold.
Ralf Salzer; Jordan J. Clark; Marina Vaysburd; Veronica T. Chang; Anna Albecka; Leo Kiss; Parul Sharma; Andres Gonzalez Llamazares; Anja Kipar; Julian A. Hiscox; Andrew Owen; A. Radu Aricescu; James P. Stewart; Leo C. James; Jan Löwe. Single‐dose immunisation with a multimerised SARS‐CoV‐2 receptor binding domain (RBD) induces an enhanced and protective response in mice. FEBS Letters 2021, 1 .
AMA StyleRalf Salzer, Jordan J. Clark, Marina Vaysburd, Veronica T. Chang, Anna Albecka, Leo Kiss, Parul Sharma, Andres Gonzalez Llamazares, Anja Kipar, Julian A. Hiscox, Andrew Owen, A. Radu Aricescu, James P. Stewart, Leo C. James, Jan Löwe. Single‐dose immunisation with a multimerised SARS‐CoV‐2 receptor binding domain (RBD) induces an enhanced and protective response in mice. FEBS Letters. 2021; ():1.
Chicago/Turabian StyleRalf Salzer; Jordan J. Clark; Marina Vaysburd; Veronica T. Chang; Anna Albecka; Leo Kiss; Parul Sharma; Andres Gonzalez Llamazares; Anja Kipar; Julian A. Hiscox; Andrew Owen; A. Radu Aricescu; James P. Stewart; Leo C. James; Jan Löwe. 2021. "Single‐dose immunisation with a multimerised SARS‐CoV‐2 receptor binding domain (RBD) induces an enhanced and protective response in mice." FEBS Letters , no. : 1.
The COVID-19 pandemic, caused by the SARS-CoV-2 coronavirus, has triggered a worldwide health emergency. So far, several different types of vaccines have shown strong efficacy. However, both the emergence of new SARS-CoV-2 variants and the need to vaccinate a large fraction of the world’s population necessitate the development of alternative vaccines, especially those that are simple and easy to store, transport and administer. Here, we showed that ferritin-like Dps protein from hyperthermophilic Sulfolobus islandicus can be covalently coupled with different SARS-CoV-2 antigens via the SpyCatcher system, to form extremely stable and defined multivalent dodecameric vaccine nanoparticles that remain intact even after lyophilisation. Immunisation experiments in mice demonstrated that the SARS-CoV-2 receptor binding domain (RBD) coupled to Dps (RBD-S-Dps) shows particular promise as it elicited a higher antibody titre and an enhanced neutralising antibody response compared to the monomeric RBD. Furthermore, we showed that a single immunisation with the multivalent RBD-S-Dps completely protected hACE2-expressing mice from serious illness and led to efficient viral clearance from the lungs upon SARS-CoV-2 infection. Our data highlight that multimerised SARS-CoV-2 subunit vaccines are a highly efficacious modality, particularly when combined with an ultra-stable scaffold.
Ralf Salzer; Jordan J. Clark; Marina Vaysburd; Veronica T. Chang; Anna Albecka; Leo Kiss; Parul Sharma; Andres Gonzalez Llamazares; Anja Kipar; Julian A. Hiscox; Andrew Owen; A. Radu Aricescu; James P. Stewart; Leo C. James; Jan Löwe. Single-dose immunisation with a multimerised SARS-CoV-2 receptor binding domain (RBD) induces an enhanced and protective response in mice. 2021, 1 .
AMA StyleRalf Salzer, Jordan J. Clark, Marina Vaysburd, Veronica T. Chang, Anna Albecka, Leo Kiss, Parul Sharma, Andres Gonzalez Llamazares, Anja Kipar, Julian A. Hiscox, Andrew Owen, A. Radu Aricescu, James P. Stewart, Leo C. James, Jan Löwe. Single-dose immunisation with a multimerised SARS-CoV-2 receptor binding domain (RBD) induces an enhanced and protective response in mice. . 2021; ():1.
Chicago/Turabian StyleRalf Salzer; Jordan J. Clark; Marina Vaysburd; Veronica T. Chang; Anna Albecka; Leo Kiss; Parul Sharma; Andres Gonzalez Llamazares; Anja Kipar; Julian A. Hiscox; Andrew Owen; A. Radu Aricescu; James P. Stewart; Leo C. James; Jan Löwe. 2021. "Single-dose immunisation with a multimerised SARS-CoV-2 receptor binding domain (RBD) induces an enhanced and protective response in mice." , no. : 1.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus disease 2019 (COVID-19). Sequencing the viral genome as the outbreak progresses is important, particularly in the identification of emerging isolates with different pathogenic potential and to identify whether nucleotide changes in the genome will impair clinical diagnostic tools such as real-time PCR assays. Although single nucleotide polymorphisms and point mutations occur during the replication of coronaviruses, one of the biggest drivers in genetic change is recombination. This can manifest itself in insertions and/or deletions in the viral genome. Therefore, sequencing strategies that underpin molecular epidemiology and inform virus biology in patients should take these factors into account. A long amplicon/read length-based RT-PCR sequencing approach focused on the Oxford Nanopore MinION/GridION platforms was developed to identify and sequence the SARS-CoV-2 genome in samples from patients with or suspected of COVID-19. The protocol, termed Rapid Sequencing Long Amplicons (RSLAs) used random primers to generate cDNA from RNA purified from a sample from a patient, followed by single or multiplex PCRs to generate longer amplicons of the viral genome. The base protocol was used to identify SARS-CoV-2 in a variety of clinical samples and proved sensitive in identifying viral RNA in samples from patients that had been declared negative using other nucleic acid-based assays (false negative). Sequencing the amplicons revealed that a number of patients had a proportion of viral genomes with deletions.
Shona C. Moore; Rebekah Penrice-Randall; Muhannad Alruwaili; Nadine Randle; Stuart Armstrong; Catherine Hartley; Sam Haldenby; Xiaofeng Dong; Abdulrahman Alrezaihi; Mai Almsaud; Eleanor Bentley; Jordan Clark; Isabel García-Dorival; Paul Gilmore; Ximeng Han; Benjamin Jones; Lisa Luu; Parul Sharma; Ghada Shawli; Yani Sun; Qin Zhao; Steven T. Pullan; Daniel P. Carter; Kevin Bewley; Jake Dunning; En-Min Zhou; Tom Solomon; Michael Beadsworth; James Cruise; Derrick W. Crook; David A. Matthews; Andrew D. Davidson; Zana Mahmood; Waleed Aljabr; Julian Druce; Richard Vipond; Lisa Ng; Laurent Renia; Peter J. M. Openshaw; J. Kenneth Baillie; Miles W. Carroll; James Stewart; Alistair Darby; Malcolm Semple; Lance Turtle; Julian A. Hiscox. Amplicon-Based Detection and Sequencing of SARS-CoV-2 in Nasopharyngeal Swabs from Patients With COVID-19 and Identification of Deletions in the Viral Genome That Encode Proteins Involved in Interferon Antagonism. Viruses 2020, 12, 1164 .
AMA StyleShona C. Moore, Rebekah Penrice-Randall, Muhannad Alruwaili, Nadine Randle, Stuart Armstrong, Catherine Hartley, Sam Haldenby, Xiaofeng Dong, Abdulrahman Alrezaihi, Mai Almsaud, Eleanor Bentley, Jordan Clark, Isabel García-Dorival, Paul Gilmore, Ximeng Han, Benjamin Jones, Lisa Luu, Parul Sharma, Ghada Shawli, Yani Sun, Qin Zhao, Steven T. Pullan, Daniel P. Carter, Kevin Bewley, Jake Dunning, En-Min Zhou, Tom Solomon, Michael Beadsworth, James Cruise, Derrick W. Crook, David A. Matthews, Andrew D. Davidson, Zana Mahmood, Waleed Aljabr, Julian Druce, Richard Vipond, Lisa Ng, Laurent Renia, Peter J. M. Openshaw, J. Kenneth Baillie, Miles W. Carroll, James Stewart, Alistair Darby, Malcolm Semple, Lance Turtle, Julian A. Hiscox. Amplicon-Based Detection and Sequencing of SARS-CoV-2 in Nasopharyngeal Swabs from Patients With COVID-19 and Identification of Deletions in the Viral Genome That Encode Proteins Involved in Interferon Antagonism. Viruses. 2020; 12 (10):1164.
Chicago/Turabian StyleShona C. Moore; Rebekah Penrice-Randall; Muhannad Alruwaili; Nadine Randle; Stuart Armstrong; Catherine Hartley; Sam Haldenby; Xiaofeng Dong; Abdulrahman Alrezaihi; Mai Almsaud; Eleanor Bentley; Jordan Clark; Isabel García-Dorival; Paul Gilmore; Ximeng Han; Benjamin Jones; Lisa Luu; Parul Sharma; Ghada Shawli; Yani Sun; Qin Zhao; Steven T. Pullan; Daniel P. Carter; Kevin Bewley; Jake Dunning; En-Min Zhou; Tom Solomon; Michael Beadsworth; James Cruise; Derrick W. Crook; David A. Matthews; Andrew D. Davidson; Zana Mahmood; Waleed Aljabr; Julian Druce; Richard Vipond; Lisa Ng; Laurent Renia; Peter J. M. Openshaw; J. Kenneth Baillie; Miles W. Carroll; James Stewart; Alistair Darby; Malcolm Semple; Lance Turtle; Julian A. Hiscox. 2020. "Amplicon-Based Detection and Sequencing of SARS-CoV-2 in Nasopharyngeal Swabs from Patients With COVID-19 and Identification of Deletions in the Viral Genome That Encode Proteins Involved in Interferon Antagonism." Viruses 12, no. 10: 1164.
Yellow fever virus (YFV), a member of the Flaviviridae family, is an arthropod-borne virus that can cause severe disease in humans with a lethality rate of up to 60%. Since 2017, increases in YFV activity in areas of South America and Africa have been described. Although a vaccine is available, named strain 17D (Theiler and Smith, 1937), it is contraindicated for use in the elderly, expectant mothers, immunocompromised people, among others. To this day there is no antiviral treatment against YFV to reduce the severity of viral infection. Here, we used a circular polymerase extension reaction (CPER)-based reverse genetics approach to generate a full-length reporter virus (YFVhb) by introducing a small HiBit tag in the NS1 protein. The reporter virus replicates at a similar rate to the parental YFV in HuH-7 cells. Using YFVhb, we designed a high throughput antiviral screening luciferase-based assay to identify inhibitors that target any step of the viral replication cycle. We validated our assay by using a range of inhibitors including drugs, immune sera and neutralizing single chain variable fragments (scFv). In light of the recent upsurge in YFV and a potential spread of the virus, this assay is a further tool in the development of antiviral therapy against YFV.
Ricardo Sanchez-Velazquez; Giuditta de Lorenzo; Rapeepat Tandavanitj; Chayanee Setthapramote; Peter J. Bredenbeek; Leonia Bozzacco; Margaret R. MacDonald; Jordan J. Clark; Charles M. Rice; Arvind H. Patel; Alain Kohl; Margus Varjak. Generation of a reporter yellow fever virus for high throughput antiviral assays. Antiviral Research 2020, 183, 104939 .
AMA StyleRicardo Sanchez-Velazquez, Giuditta de Lorenzo, Rapeepat Tandavanitj, Chayanee Setthapramote, Peter J. Bredenbeek, Leonia Bozzacco, Margaret R. MacDonald, Jordan J. Clark, Charles M. Rice, Arvind H. Patel, Alain Kohl, Margus Varjak. Generation of a reporter yellow fever virus for high throughput antiviral assays. Antiviral Research. 2020; 183 ():104939.
Chicago/Turabian StyleRicardo Sanchez-Velazquez; Giuditta de Lorenzo; Rapeepat Tandavanitj; Chayanee Setthapramote; Peter J. Bredenbeek; Leonia Bozzacco; Margaret R. MacDonald; Jordan J. Clark; Charles M. Rice; Arvind H. Patel; Alain Kohl; Margus Varjak. 2020. "Generation of a reporter yellow fever virus for high throughput antiviral assays." Antiviral Research 183, no. : 104939.
The emergence and spread of tick-borne arboviruses pose an increased challenge to human and animal health. In Europe this is demonstrated by the increasingly wide distribution of tick-borne encephalitis virus (TBEV, Flavivirus, Flaviviridae), which has recently been found in the United Kingdom (UK). However, much less is known about other tick-borne flaviviruses (TBFV), such as the closely related louping ill virus (LIV), an animal pathogen which is endemic to the UK and Ireland, but which has been detected in other parts of Europe including Scandinavia and Russia. The emergence and potential spatial overlap of these viruses necessitates improved understanding of LIV genomic diversity, geographic spread and evolutionary history. We sequenced a virus archive composed of 22 LIV isolates which had been sampled throughout the UK over a period of over 80 years. Combining this dataset with published virus sequences, we detected no sign of recombination and found low diversity and limited evidence for positive selection in the LIV genome. Phylogenetic analysis provided evidence of geographic clustering as well as long-distance movement, including movement events that appear recent. However, despite genomic data and an 80-year time span, we found that the data contained insufficient temporal signal to reliably estimate a molecular clock rate for LIV. Additional analyses revealed that this also applied to TBEV, albeit to a lesser extent, pointing to a general problem with phylogenetic dating for TBFV. The 22 LIV genomes generated during this study provide a more reliable LIV phylogeny, improving our knowledge of the evolution of tick-borne flaviviruses. Our inability to estimate a molecular clock rate for both LIV and TBEV suggests that temporal calibration of tick-borne flavivirus evolution should be interpreted with caution and highlight a unique aspect of these viruses which may be explained by their reliance on tick vectors. Tick-borne pathogens represent a major emerging threat to public health and in recent years have been expanding into new areas. LIV is a neglected virus endemic to the UK and Ireland (though it has been detected in Scandinavia and Russia) which is closely related to the major human pathogen TBEV, but predominantly causes disease in sheep and grouse. The recent detection of TBEV in the UK, which has also emerged elsewhere in Europe, requires more detailed understanding of the spread and sequence diversity of LIV. This could be important for diagnosis and vaccination, but also to improve our understanding of the evolution and emergence of these tick-borne viruses. Here we describe the sequencing of 22 LIV isolates which have been sampled from several host species across the past century. We have utilised this dataset to investigate the evolutionary pressures that LIV is subjected to and have explored the evolution of LIV using phylogenetic analysis. Crucially we were unable to estimate a reliable molecular clock rate for LIV and found that this problem also extends to a larger phylogeny of TBEV sequences. This work highlights a previously unknown caveat of tick-borne flavivirus evolutionary analysis which may be important for understanding the evolution of these important pathogens.
Jordan J. Clark; Janice Gilray; Richard J. Orton; Margaret Baird; Gavin Wilkie; Ana Da Silva Filipe; Nicholas Johnson; Colin J. McInnes; Alain Kohl; Roman Biek. Population genomics of louping ill virus provide new insights into the evolution of tick-borne flaviviruses. PLOS Neglected Tropical Diseases 2020, 14, e0008133 .
AMA StyleJordan J. Clark, Janice Gilray, Richard J. Orton, Margaret Baird, Gavin Wilkie, Ana Da Silva Filipe, Nicholas Johnson, Colin J. McInnes, Alain Kohl, Roman Biek. Population genomics of louping ill virus provide new insights into the evolution of tick-borne flaviviruses. PLOS Neglected Tropical Diseases. 2020; 14 (9):e0008133.
Chicago/Turabian StyleJordan J. Clark; Janice Gilray; Richard J. Orton; Margaret Baird; Gavin Wilkie; Ana Da Silva Filipe; Nicholas Johnson; Colin J. McInnes; Alain Kohl; Roman Biek. 2020. "Population genomics of louping ill virus provide new insights into the evolution of tick-borne flaviviruses." PLOS Neglected Tropical Diseases 14, no. 9: e0008133.
BackgroundThe emergence and spread of tick-borne arboviruses pose an increased challenge to human and animal health. In Europe this is demonstrated by the increasingly wide distribution of tick-borne encephalitis virus (TBEV, Flavivirus, Flaviviridae), which has recently been found in the UK. However, much less is known about other tick-borne flaviviruses (TBFV), such as the closely related louping ill virus (LIV), an animal pathogen which is endemic to the UK and Ireland but which has been detected in other parts of Europe including Scandinavia and Russia. The emergence and potential spatial overlap of these viruses necessitates improved understanding of LIV genomic diversity, geographic spread and evolutionary history.Methodology/principal findingsWe sequenced a virus archive composed of 22 LIV isolates which had been sampled throughout the UK over a period of over 80 years. Combining this dataset with published virus sequences, we detected no sign of recombination and found low diversity and limited evidence for positive selection in the LIV genome. Phylogenetic analysis provided evidence of geographic clustering as well as long-distance movement, including movement events that appear recent. However, despite genomic data and an 80-year time span, we found that the data contained insufficient temporal signal to reliably estimate a molecular clock rate for LIV. Additional analyses revealed that this also applied to TBEV, albeit to a lesser extent, pointing to a general problem with phylogenetic dating for TBFV.Conclusions/significanceThe 22 LIV genomes generated during this study provide a more reliable LIV phylogeny, improving our knowledge of the evolution of tick-borne flaviviruses. Our inability to estimate a molecular clock rate for both LIV and TBEV suggests that temporal calibration of tick-borne flavivirus evolution should be interpreted with caution and highlight a unique aspect of these viruses which may be explained by their reliance on tick vectors.Author SummaryTick-borne pathogens represent a major emerging threat to public health and in recent years have been expanding into new areas. LIV is a neglected virus endemic to the UK and Ireland (though it has been detected in Scandinavia and Russia) which is closely related to the major human pathogen TBEV, but predominantly causes disease in sheep and grouse. The recent detection of TBEV in the UK, which has also emerged elsewhere in Europe, requires more detailed understanding of the spread and sequence diversity of LIV. This could be important for diagnosis and vaccination, but also to improve our understanding of the evolution and emergence of these tick-borne viruses. Here we describe the sequencing of 22 LIV isolates which have been sampled from several host species across the past century. We have utilised this dataset to investigate the evolutionary pressures that LIV is subjected to and have explored the evolution of LIV using phylogenetic analysis. Crucially we were unable to estimate a reliable molecular clock rate for LIV and found that this problem also extends to a larger phylogeny of TBEV sequences. This work highlights a previously unknown caveat of tick-borne flavivirus evolutionary analysis which may be important for understanding the evolution of these important pathogens.
Jordan J. Clark; Janice Gilray; Richard J. Orton; Margaret Baird; Gavin S. Wilkie; Ana Da Silva Filipe; Nicholas Johnson; Colin J. McInnes; Alain Kohl; Roman Biek. Population genomics of louping ill virus provide new insights into the evolution of tick-borne flaviviruses. 2020, 1 .
AMA StyleJordan J. Clark, Janice Gilray, Richard J. Orton, Margaret Baird, Gavin S. Wilkie, Ana Da Silva Filipe, Nicholas Johnson, Colin J. McInnes, Alain Kohl, Roman Biek. Population genomics of louping ill virus provide new insights into the evolution of tick-borne flaviviruses. . 2020; ():1.
Chicago/Turabian StyleJordan J. Clark; Janice Gilray; Richard J. Orton; Margaret Baird; Gavin S. Wilkie; Ana Da Silva Filipe; Nicholas Johnson; Colin J. McInnes; Alain Kohl; Roman Biek. 2020. "Population genomics of louping ill virus provide new insights into the evolution of tick-borne flaviviruses." , no. : 1.
Louping-ill (LI), caused by louping-ill virus (LIV), results in a frequently fatal encephalitis primarily affecting sheep and red grouse (Lagopus lagopus scotica), but it does occur in other species. An adult male Border collie dog was definitively diagnosed with fatal LI and the lesion profile, LIV antigen distribution and full genome sequence of the LIV responsible were investigated to determine if this differed significantly from sheep-derived LIV. No gross lesions were present. The histological lesions were confined to the central nervous system and comprised of lymphocytic perivascular cuffs, glial foci, neuronal necrosis and neuronophagia. Immunolocalization of viral antigen showed small amounts present in neurons only. These histological and immunohistochemical findings were similar to those reported in affected sheep. Compared with published full genome sequences of sheep-derived LIV, only very minor differences were present and phylogenetically the virus clustered individually between a subclade containing Scottish strains, LIV 369/T2 and G and another subclade containing an English isolate LIV A. The LIV isolated from the dog shares a common progenitor with LIV A. These findings suggest there is no canine-specific LIV strain, dogs are susceptible to sheep-associated strains of LI and with the increase in tick prevalence, and therefore exposure to LIV, a safe, effective vaccine for dogs may be required.
M.P. Dagleish; Jordan Clark; C. Robson; M. Tucker; R.J. Orton; M.S. Rocchi. A Fatal Case of Louping-ill in a Dog: Immunolocalization and Full Genome Sequencing of the Virus. Journal of Comparative Pathology 2018, 165, 23 -32.
AMA StyleM.P. Dagleish, Jordan Clark, C. Robson, M. Tucker, R.J. Orton, M.S. Rocchi. A Fatal Case of Louping-ill in a Dog: Immunolocalization and Full Genome Sequencing of the Virus. Journal of Comparative Pathology. 2018; 165 ():23-32.
Chicago/Turabian StyleM.P. Dagleish; Jordan Clark; C. Robson; M. Tucker; R.J. Orton; M.S. Rocchi. 2018. "A Fatal Case of Louping-ill in a Dog: Immunolocalization and Full Genome Sequencing of the Virus." Journal of Comparative Pathology 165, no. : 23-32.
The outbreak of Zika virus (ZIKV) in the Americas has transformed a previously obscure mosquito-transmitted arbovirus of the Flaviviridae family into a major public health concern. Little is currently known about the evolution and biology of ZIKV and the factors that contribute to the associated pathogenesis. Determining genomic sequences of clinical viral isolates and characterization of elements within these are an important prerequisite to advance our understanding of viral replicative processes and virus-host interactions. We obtained a ZIKV isolate from a patient who presented with classical ZIKV-associated symptoms, and used high throughput sequencing and other molecular biology approaches to determine its full genome sequence, including non-coding regions. Genome regions were characterized and compared to the sequences of other isolates where available. Furthermore, we identified a subgenomic flavivirus RNA (sfRNA) in ZIKV-infected cells that has antagonist activity against RIG-I induced type I interferon induction, with a lesser effect on MDA-5 mediated action. The full-length genome sequence including non-coding regions of a South American ZIKV isolate from a patient with classical symptoms will support efforts to develop genetic tools for this virus. Detection of sfRNA that counteracts interferon responses is likely to be important for further understanding of pathogenesis and virus-host interactions. The current ZIKV outbreak is a major public health concern in the Americas. To further understand the virus, and to develop tools and potentially vaccines, more information on the virus strains circulating in the Americas is required. Here we describe the full-length sequence of a ZIKV isolate from a patient with classical symptoms, including the complete non-coding regions which are missing from many currently available sequences, and put these in context. Moreover, we also demonstrate the production of an RNA molecule derived from the 3’ untranslated region that counteracts interferon responses and may therefore be important for understanding the pathogenesis of ZIKV infection.
Claire Donald; Benjamin Brennan; Stephanie L. Cumberworth; Veronica V. Rezelj; Jordan Clark; Marli T. Cordeiro; Rafael Freitas De Oliveira França; Lindomar J. Pena; Gavin S. Wilkie; Ana Cristina Da Silva Filipe; Christopher Davis; Joseph Hughes; Margus Varjak; Martin Selinger; Luíza Zuvanov; Ania M. Owsianka; Arvind H. Patel; John McLauchlan; Brett D. Lindenbach; Gamou Fall; Amadou A. Sall; Roman Biek; Jan Rehwinkel; Esther Schnettler; Alain Kohl. Full Genome Sequence and sfRNA Interferon Antagonist Activity of Zika Virus from Recife, Brazil. PLOS Neglected Tropical Diseases 2016, 10, e0005048 .
AMA StyleClaire Donald, Benjamin Brennan, Stephanie L. Cumberworth, Veronica V. Rezelj, Jordan Clark, Marli T. Cordeiro, Rafael Freitas De Oliveira França, Lindomar J. Pena, Gavin S. Wilkie, Ana Cristina Da Silva Filipe, Christopher Davis, Joseph Hughes, Margus Varjak, Martin Selinger, Luíza Zuvanov, Ania M. Owsianka, Arvind H. Patel, John McLauchlan, Brett D. Lindenbach, Gamou Fall, Amadou A. Sall, Roman Biek, Jan Rehwinkel, Esther Schnettler, Alain Kohl. Full Genome Sequence and sfRNA Interferon Antagonist Activity of Zika Virus from Recife, Brazil. PLOS Neglected Tropical Diseases. 2016; 10 (10):e0005048.
Chicago/Turabian StyleClaire Donald; Benjamin Brennan; Stephanie L. Cumberworth; Veronica V. Rezelj; Jordan Clark; Marli T. Cordeiro; Rafael Freitas De Oliveira França; Lindomar J. Pena; Gavin S. Wilkie; Ana Cristina Da Silva Filipe; Christopher Davis; Joseph Hughes; Margus Varjak; Martin Selinger; Luíza Zuvanov; Ania M. Owsianka; Arvind H. Patel; John McLauchlan; Brett D. Lindenbach; Gamou Fall; Amadou A. Sall; Roman Biek; Jan Rehwinkel; Esther Schnettler; Alain Kohl. 2016. "Full Genome Sequence and sfRNA Interferon Antagonist Activity of Zika Virus from Recife, Brazil." PLOS Neglected Tropical Diseases 10, no. 10: e0005048.