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Dr Helena Maier
No more applications being accepted
Funded PhD Project (European/UK Students Only)
About the Project
Previous Applicants Need Not Apply.
This is a joint four year PhD project between The Pirbright Institute, at the Compton Laboratory and the Institute of Infection and Global Health at the University of Liverpool and will be co-supervised by Prof. Julian Hiscox. The student will spend contiguous time at both institutions.
A key area of research in animal disease is the development of more effective and efficient vaccines to prevent infection and transmission. To be able to achieve this objective, a better understanding of virus interaction with host cells and viral pathogenicity factors is required. The avian coronavirus infectious bronchitis virus (IBV) causes respiratory disease in chickens, and some strains cause pathology in the kidneys and reproductive tract. Virus infection results in significant losses to worldwide poultry industries due to reduced meat quality and reduced egg quality and production. Although both live attenuated and killed vaccines are available for IBV, there is poor cross protection between viral strains and the mechanism of attenuation of vaccine viruses is poorly understood. There is a real requirement for improved strategies for IBV vaccine design and understanding molecular aspects of virus replication will provide new insight for this. IBV encodes 5 accessory proteins, including the recently described gene 4b. The function of these accessory proteins is not understood. The accessory proteins of other coronaviruses including mouse hepatitis virus (MHV) and SARS-coronavirus (SARS-CoV) have been shown to play a role in replication of viral RNA, evasion of host immune responses and modulation of host cell transcription. Although genetically distinct from the accessory proteins from MHV and SARS-CoV, it is possible that the function of the IBV accessory proteins may be similar.
The objectives of this project will be to characterise more fully the function of these critically important accessory proteins on virus replication and identify host cell and viral interaction partners. This will be achieved by virological and molecular biology techniques and proteomics, initially utilising existing recombinant viruses lacking these genes and over-expression plasmids. Further genetic and RNAi experiments will be used to investigate the interaction of virus proteins with identified host cell partners. The results from this project will provide valuable information allowing attenuation of the virus as a potential avenue for vaccine development.
The student will receive specific training involving a range of virological and molecular biological skills; including general methods such as tissue culture and the growth of viruses and other general molecular biologically orientated methods to more advanced molecular virological skills including bioinformatics. In addition, the student will learn reverse genetics techniques for rescuing recombinant IBV and replication deficient adenoviruses, including virus purification. The student will also receive training in other life skill areas as part of the Pirbright and IGH PhD studentship training process, as well as the development of questioning and critical analysis skills associated with a PhD project.
Full details of the project can be found under Ref: 2013-05 HMPBJH:
http://www.pirbright.ac.uk/students/Studentships.aspx
This is a joint four year PhD project between The Pirbright Institute, at the Compton Laboratory and the Institute of Infection and Global Health at the University of Liverpool and will be co-supervised by Prof. Julian Hiscox. The student will spend contiguous time at both institutions.
A key area of research in animal disease is the development of more effective and efficient vaccines to prevent infection and transmission. To be able to achieve this objective, a better understanding of virus interaction with host cells and viral pathogenicity factors is required. The avian coronavirus infectious bronchitis virus (IBV) causes respiratory disease in chickens, and some strains cause pathology in the kidneys and reproductive tract. Virus infection results in significant losses to worldwide poultry industries due to reduced meat quality and reduced egg quality and production. Although both live attenuated and killed vaccines are available for IBV, there is poor cross protection between viral strains and the mechanism of attenuation of vaccine viruses is poorly understood. There is a real requirement for improved strategies for IBV vaccine design and understanding molecular aspects of virus replication will provide new insight for this. IBV encodes 5 accessory proteins, including the recently described gene 4b. The function of these accessory proteins is not understood. The accessory proteins of other coronaviruses including mouse hepatitis virus (MHV) and SARS-coronavirus (SARS-CoV) have been shown to play a role in replication of viral RNA, evasion of host immune responses and modulation of host cell transcription. Although genetically distinct from the accessory proteins from MHV and SARS-CoV, it is possible that the function of the IBV accessory proteins may be similar.
The objectives of this project will be to characterise more fully the function of these critically important accessory proteins on virus replication and identify host cell and viral interaction partners. This will be achieved by virological and molecular biology techniques and proteomics, initially utilising existing recombinant viruses lacking these genes and over-expression plasmids. Further genetic and RNAi experiments will be used to investigate the interaction of virus proteins with identified host cell partners. The results from this project will provide valuable information allowing attenuation of the virus as a potential avenue for vaccine development.
The student will receive specific training involving a range of virological and molecular biological skills; including general methods such as tissue culture and the growth of viruses and other general molecular biologically orientated methods to more advanced molecular virological skills including bioinformatics. In addition, the student will learn reverse genetics techniques for rescuing recombinant IBV and replication deficient adenoviruses, including virus purification. The student will also receive training in other life skill areas as part of the Pirbright and IGH PhD studentship training process, as well as the development of questioning and critical analysis skills associated with a PhD project.
Full details of the project can be found under Ref: 2013-05 HMPBJH:
http://www.pirbright.ac.uk/students/Studentships.aspx
Funding Notes
This is a fully funded project but only open to UK students or EU students who qualify for home-rated fees. See guidelines below.
http://www.bbsrc.ac.uk/web/FILES/Guidelines/studentship_eligibility.pdf.
The successful applicant will be paid the RCUK minimum of 13,590 but there may be additional funding depending upon location and degree.
Where English is not your first language evidence of IELTS level 7 must be provided.
Interested applicants must have or be predicted to obtain a good 2.1 or higher at BSc level in a relevant area, including veterinary degrees.
http://www.bbsrc.ac.uk/web/FILES/Guidelines/studentship_eligibility.pdf.
The successful applicant will be paid the RCUK minimum of 13,590 but there may be additional funding depending upon location and degree.
Where English is not your first language evidence of IELTS level 7 must be provided.
Interested applicants must have or be predicted to obtain a good 2.1 or higher at BSc level in a relevant area, including veterinary degrees.
References
Our laboratories have a strong publication record in virology:
Visualizing the autophagy pathway in avian cells and its application to studying infectious bronchitis virus.
Maier et al. Autophagy. 2013 Jan 17;9(4). PMID:23328491
Identification of a Non-Canonically Transcribed Subgenomic mRNA of Infectious Bronchitis Virus and Other Gammacoronaviruses.
Bentley et al. J Virol. 2012 Dec 5. PMID:23221558
Involvement of autophagy in coronavirus replication.
Maier HJ, Britton P. Viruses. 2012 Nov 30;4(12):3440-51. doi: 10.3390/v4123440. PMID:23202545
Coronavirus nsp6 proteins generate autophagosomes from the endoplasmic reticulum via an omegasome intermediate.
Cottam et al. Autophagy. 2011 Nov;7(11):1335-47. doi: 10.4161/auto.7.11.16642.
The replicase gene of avian coronavirus infectious bronchitis virus is a determinant of pathogenicity.
Armesto et al. PLoS One. 2009 Oct 9;4(10):e7384. doi: 10.1371/journal.pone.0007384.
Neither the RNA nor the proteins of open reading frames 3a and 3b of the coronavirus infectious bronchitis virus are essential for replication. Hodgson et al. J Virol. 2006 Jan;80(1):296-305.
Gene 5 of the avian coronavirus infectious bronchitis virus is not essential for replication.
Casais et al. J Virol. 2005 Jul;79(13):8065-78.
Wu et al. 2012. The interactome of human respiratory syncytial virus NS1 protein highlights multiple effects on host cell biology. Journal of Virology. 86:7777-7789.
Dove et al. 2012. A quantitative proteomic analysis of lung epithelial (A549) cells infected with 2009 pandemic influenza A virus using stable isotope labelling with amino acids in cell culture (SILAC). Proteomics. 12:1431-1436.
Wu et al. 2011. Characterization of the interaction between human respiratory syncytial virus and the cell cycle in continuous cell culture and primary human airway epithelial cells. Journal of Virology. 85:10300-10309.
Emmott et al. 2010. Quantitative proteomics using stable isotope labeling with amino acids in cell culture reveals changes in the cytoplasmic, nuclear, and nucleolar proteomes in vero cells infected with the coronavirus infectious bronchitis virus. Molecular and Cellular Proteomics. 9:1920-1936.
Munday et al. 2010. Quantitative proteomic analysis of A549 cells infected with human respiratory syncytial virus. Molecular and Cellular Proteomics. 9:2438-2459.
Emmott et al. 2010. Elucidation of the avian nucleolar proteome by quantitative proteomics using SILAC and changes in cells infected with the coronavirus infectious bronchitis virus. Proteomics. 10:3558-3562.
Emmott et al. 2010. Quantitative proteomics using SILAC coupled to LC-MS/MS reveals changes in the nucleolar proteome in influenza A virus-infected cells. Journal of Proteome Research. 9:5335-5345.
Visualizing the autophagy pathway in avian cells and its application to studying infectious bronchitis virus.
Maier et al. Autophagy. 2013 Jan 17;9(4). PMID:23328491
Identification of a Non-Canonically Transcribed Subgenomic mRNA of Infectious Bronchitis Virus and Other Gammacoronaviruses.
Bentley et al. J Virol. 2012 Dec 5. PMID:23221558
Involvement of autophagy in coronavirus replication.
Maier HJ, Britton P. Viruses. 2012 Nov 30;4(12):3440-51. doi: 10.3390/v4123440. PMID:23202545
Coronavirus nsp6 proteins generate autophagosomes from the endoplasmic reticulum via an omegasome intermediate.
Cottam et al. Autophagy. 2011 Nov;7(11):1335-47. doi: 10.4161/auto.7.11.16642.
The replicase gene of avian coronavirus infectious bronchitis virus is a determinant of pathogenicity.
Armesto et al. PLoS One. 2009 Oct 9;4(10):e7384. doi: 10.1371/journal.pone.0007384.
Neither the RNA nor the proteins of open reading frames 3a and 3b of the coronavirus infectious bronchitis virus are essential for replication. Hodgson et al. J Virol. 2006 Jan;80(1):296-305.
Gene 5 of the avian coronavirus infectious bronchitis virus is not essential for replication.
Casais et al. J Virol. 2005 Jul;79(13):8065-78.
Wu et al. 2012. The interactome of human respiratory syncytial virus NS1 protein highlights multiple effects on host cell biology. Journal of Virology. 86:7777-7789.
Dove et al. 2012. A quantitative proteomic analysis of lung epithelial (A549) cells infected with 2009 pandemic influenza A virus using stable isotope labelling with amino acids in cell culture (SILAC). Proteomics. 12:1431-1436.
Wu et al. 2011. Characterization of the interaction between human respiratory syncytial virus and the cell cycle in continuous cell culture and primary human airway epithelial cells. Journal of Virology. 85:10300-10309.
Emmott et al. 2010. Quantitative proteomics using stable isotope labeling with amino acids in cell culture reveals changes in the cytoplasmic, nuclear, and nucleolar proteomes in vero cells infected with the coronavirus infectious bronchitis virus. Molecular and Cellular Proteomics. 9:1920-1936.
Munday et al. 2010. Quantitative proteomic analysis of A549 cells infected with human respiratory syncytial virus. Molecular and Cellular Proteomics. 9:2438-2459.
Emmott et al. 2010. Elucidation of the avian nucleolar proteome by quantitative proteomics using SILAC and changes in cells infected with the coronavirus infectious bronchitis virus. Proteomics. 10:3558-3562.
Emmott et al. 2010. Quantitative proteomics using SILAC coupled to LC-MS/MS reveals changes in the nucleolar proteome in influenza A virus-infected cells. Journal of Proteome Research. 9:5335-5345.
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