Abstract

Influenza is a major human disease without any effective prophylaxis or therapy. Every year influenza inflicts enormous human suffering in the form of increased morbidity and mortality. In addition, a staggering economic loss (nearly 4 billion dollars in the USA alone) is attributed directly to influenza. The goal of this project is to elucidate the property of this virus and its behavior at the genomic level and to investigate towards developing a better immunogen for prophylaxis. Therefore, we plan to continue studying influenza genes using recombinant DNA cloning technology and elucidate the primary and secondary structure of viral proteins. Furthermore, we plan to continue expressing the cloned DNAs using appropriate vectors in mammalian cells. We also want to make specific changes at the desired location, determine precisely the function of each domain of the viral proteins and elucidate the structure-function relationship. In addition, we want to express hemagglutinin and neuraminidase genes in yeast and explore newer ways to make a better subunit vaccine.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI016348-06
Application #
3126630
Study Section
Experimental Virology Study Section (EVR)
Project Start
1980-05-01
Project End
1988-04-30
Budget Start
1985-05-01
Budget End
1986-04-30
Support Year
6
Fiscal Year
1985
Total Cost
Indirect Cost

  Institution

Name
University of California Los Angeles
Department
Type
Schools of Medicine
DUNS #
119132785
City
Los Angeles
State
CA
Country
United States
Zip Code
90095

  Publications

Nayak, Debi P; Balogun, Rilwan A; Yamada, Hiroshi et al. (2009) Influenza virus morphogenesis and budding. Virus Res 143:147-61
Barman, Subrata; Nayak, Debi P (2007) Lipid raft disruption by cholesterol depletion enhances influenza A virus budding from MDCK cells. J Virol 81:12169-78
Hui, Eric Ka-Wai; Smee, Donald F; Wong, Min-Hui et al. (2006) Mutations in influenza virus M1 CCHH, the putative zinc finger motif, cause attenuation in mice and protect mice against lethal influenza virus infection. J Virol 80:5697-707
Hui, Eric Ka-Wai; Barman, Subrata; Tang, Dominic Ho-Ping et al. (2006) YRKL sequence of influenza virus M1 functions as the L domain motif and interacts with VPS28 and Cdc42. J Virol 80:2291-308
Hui, Eric Ka-Wai; Yap, Ee Ming; An, Dong Sung et al. (2004) Inhibition of influenza virus matrix (M1) protein expression and virus replication by U6 promoter-driven and lentivirus-mediated delivery of siRNA. J Gen Virol 85:1877-84
Nayak, Debi P; Hui, Eric Ka-Wai; Barman, Subrata (2004) Assembly and budding of influenza virus. Virus Res 106:147-65
Nayak, Debi P; Hui, Eric K W (2004) The role of lipid microdomains in virus biology. Subcell Biochem 37:443-91
Barman, Subrata; Adhikary, Lopa; Chakrabarti, Alok K et al. (2004) Role of transmembrane domain and cytoplasmic tail amino acid sequences of influenza a virus neuraminidase in raft association and virus budding. J Virol 78:5258-69
Hui, Eric Ka-Wai; Ralston, Katherine; Judd, Amrit K et al. (2003) Conserved cysteine and histidine residues in the putative zinc finger motif of the influenza A virus M1 protein are not critical for influenza virus replication. J Gen Virol 84:3105-13
Barman, Subrata; Adhikary, Lopa; Kawaoka, Yoshihiro et al. (2003) Influenza A virus hemagglutinin containing basolateral localization signal does not alter the apical budding of a recombinant influenza A virus in polarized MDCK cells. Virology 305:138-52

Showing the most recent 10 out of 43 publications