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Potent HIV-1-specific CD8 T cell responses induced in mice after priming with a multiepitopic DNA-TMEP and boosting with the HIV vaccine MVA-B

AuthorsPerdiguero, Beatriz; Raman, Suresh C.; Sánchez-Corzo, Cristina; Sorzano, Carlos Óscar S.; Valverde, José Ramón; Esteban, Mariano; Gómez, Carmen E.
KeywordsMultiepitopic vaccine
Issue Date13-Aug-2018
PublisherMultidisciplinary Digital Publishing Institute
CitationViruses 10(8): 424 (2018)
AbstractAn effective vaccine against Human Immunodeficiency Virus (HIV) still remains the best solution to provide a sustainable control and/or eradication of the virus. We have previously generated the HIV-1 vaccine modified vaccinia virus Ankara (MVA)-B, which exhibited good immunogenicity profile in phase I prophylactic and therapeutic clinical trials, but was unable to prevent viral rebound after antiretroviral (ART) removal. To potentiate the immunogenicity of MVA-B, here we described the design and immune responses elicited in mice by a new T cell multi-epitopic B (TMEP-B) immunogen, vectored by DNA, when administered in homologous or heterologous prime/boost regimens in combination with MVA-B. The TMEP-B protein contained conserved regions from Gag, Pol, and Nef proteins including multiple CD4 and CD8 T cell epitopes functionally associated with HIV control. Heterologous DNA-TMEP/MVA-B regimen induced higher HIV-1-specific CD8 T cell responses with broader epitope recognition and higher polyfunctional profile than the homologous DNA-TMEP/DNA-TMEP or the heterologous DNA-GPN/MVA-B combinations. Moreover, higher HIV-1-specific CD4 and Tfh immune responses were also detected using this regimen. After MVA-B boost, the magnitude of the anti-VACV CD8 T cell response was significantly compromised in DNA-TMEP-primed animals. Our results revealed the immunological potential of DNA-TMEP prime/MVA-B boost regimen and supported the application of these combined vectors in HIV-1 prevention and/or therapy.
Publisher version (URL)https://doi.org/10.3390/v10080424
Appears in Collections:(CNB) Artículos
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