Immune response to E7 protein of human papillomavirus type 16 anchored on the cell surface
Language English Country Germany Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
11904736
PubMed Central
PMC11034196
DOI
10.1007/s00262-001-0261-3
Knihovny.cz E-resources
- MeSH
- Immunity, Cellular MeSH
- Neoplasms, Experimental prevention & control MeSH
- Hemagglutinins, Viral immunology MeSH
- Interleukin-4 biosynthesis MeSH
- Rabbits MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Oncogene Proteins, Viral analysis immunology MeSH
- Papillomavirus E7 Proteins MeSH
- Antibodies, Viral biosynthesis MeSH
- Recombinant Fusion Proteins immunology MeSH
- Vaccination MeSH
- Viral Vaccines immunology MeSH
- Vaccinia virus genetics MeSH
- Animals MeSH
- Check Tag
- Rabbits MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Hemagglutinins, Viral MeSH
- Interleukin-4 MeSH
- oncogene protein E7, Human papillomavirus type 16 MeSH Browser
- Oncogene Proteins, Viral MeSH
- Papillomavirus E7 Proteins MeSH
- Antibodies, Viral MeSH
- Recombinant Fusion Proteins MeSH
- Viral Vaccines MeSH
To target the E7 protein of human papilloma virus 16 to the cell surface, a fusion gene was constructed. It encodes the signal peptide, part of the immunoglobulin (IgG)-like domain, the transmembrane anchor of vaccinia virus (VV) hemagglutinin (HA), and the complete E7-coding sequence. The fusion gene was expressed under the HA late promoter by a recombinant VV, designated VV-E7-HA. The E7-HA protein was displayed on the surface of cells infected with the recombinant virus and was more stable than unmodified E7. The biological properties of the VV-E7-HA virus were compared with those of a VV-E7 virus that expressed the unmodified E7 and with a VV expressing the Sig-E7-LAMP fusion protein. While the first two of these recombinants were based on VV strain Praha, the third was derived from the WR strain of VV. Infection of mice with the VV-E7-HA virus induced the formation of E7-specific antibodies with the predominance of the IgG2a isotype, whereas the other two viruses did not induce the formation of E7-specific antibodies. Unlike the other two viruses, VV-E7-HA did not induce a response of cytotoxic T lymphocytes or Th1 cells and did not protect mice against the growth of E7-expressing tumors. Thus, VV-E7-HA induced a differently polarized immune response to the E7 protein than the other two viruses.
References provided by Crossref.org
Attenuation of vaccinia virus by the expression of human Flt3 ligand
Mutation in the immunodominant epitope of the HPV16 E7 oncoprotein as a mechanism of tumor escape
