A DNA vaccine expressing the E2 protein of classical swine fever virus elicits T cell responses that can prime for rapid antibody production and confer total protection upon viral challenge

Salmonella typhimurium harboring plasmid expressing interleukin-12 induced attenuation of infection and protective immune responses

“…IL-12-induced attenuation in Salmonella typhimurium higher doses could be overcome by lowering the dose of wild bacteria for immunization or by using plasmids expressing high concentrations of protein. Previous investigators suggested that an effective vaccine could be designed by plasmid DNA vaccine, prime-boost strategies and genetic alteration (Ganges et al, 2005;Jennings et al, 1998;Leroux-Roels and Leroux-Roels, 2009;Pena et al, 2008). Although rapid developments for new pathogens were limited by current vaccine technology, our results suggested that the vaccine technology using plasmid expressing IL-12 would be a rapid, easy method for new vaccine.…”

Characterization and Expression of E2 Glycoprotein of Classical Swine Fever Virus in a Eukaryotic Expression System

“…The E2 gene engineered into an expression plasmid has been evaluated as DNA vaccine against CSF [5]. E2 is one of the three envelope glycoprotein of the CSFV that is involved in virus attachment, entry to target cells, virulence and immunogenicity [16].…”

“…In animal models, DNA vaccines have been shown to elicit a broad range of immune responses similar to live vaccines [25]. Therefore, the E2 glycoprotein of CSFV is also being targeted for the specific diagnosis or immunoprophylaxis of CSF [1,5]. Although The results of the present study would be useful for the development of DNA vaccine against CSF disease.…”

Immune responses induced by a BacMam virus expressing the E2 protein of classical swine fever virus in mice

“…It has been shown that cell-mediated immunity also plays an important role in antiviral mechanisms where both CD8+ and CD4+ T-cells are essential for the control of CSFV infections [36]. There is a strong link between virus-specific CD8+ T-cell function and the efficiency of regulatory CD4+ helper T-cells [37].…”