C.E. Gómez

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Articles (10)

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vecteur (10) Cells (9) protéine (8) gène (8) Mice (7) Expression (7) virus (6) ADN (6) Vaccinia (6) Memory (6) DNA (6) immunité (5) Deletion (5) Genes (5) T cells (5) Immunoglobulins (5) Immunity (5) Antigens (5) SIDA (4) Dendritic cells (4) Viruses (4) Strategy (4) Human beings (4) Macrophages (4) Immunization (4) Immune response (4) Viruses (4) puits (3) analyse (3) procès (3)

Documents écrit par C.E. Gómez (10) | parle de C.E. Gómez (0)

Potency and durability of T and B cell immune responses after homologous and heterologous vector delivery of a trimer-stabilized, membrane-displayed HIV-1 clade ConC Env protein.
B. Perdiguero et al. (2023)
Heterologous Combination of VSV-GP and NYVAC Vectors Expressing HIV-1 Trimeric gp145 Env as Vaccination Strategy to Induce Balanced B and T Cell Immune Responses.
B. Perdiguero et al. (2019)
Interleukin-1- and type I interferon-dependent enhanced immunogenicity of an NYVAC-HIV-1 Env-Gag-Pol-Nef vaccine vector with dual deletions of type I and type II interferon-binding proteins.
J. Delaloye et al. (2015)
Deletion of the Vaccinia Virus Gene A46R, Encoding for an Inhibitor of TLR Signalling, Is an Effective Approach to Enhance the Immunogenicity in Mice of the HIV/AIDS Vaccine Candidate NYVAC-C.
B. Perdiguero et al. (2013)
Deletion of the viral anti-apoptotic gene F1L in the HIV/AIDS vaccine candidate MVA-C enhances immune responses against HIV-1 antigens.
B. Perdiguero et al. (2012)
Systems analysis of MVA-C induced immune response reveals its significance as a vaccine candidate against HIV/AIDS of clade C.
C.E. Gómez et al. (2012)
Improved Innate and Adaptive Immunostimulation by Genetically Modified HIV-1 Protein Expressing NYVAC Vectors.
E.D. Quakkelaar et al. (2011)
Improved NYVAC-based vaccine vectors.
K.V. Kibler et al. (2011)
A Candidate HIV/AIDS Vaccine (MVA-B) Lacking Vaccinia Virus Gene C6L Enhances Memory HIV-1-Specific T-Cell Responses.
J.L. Nájera et al. (2011)
Innate immune sensing of modified vaccinia virus Ankara (MVA) is mediated by TLR2-TLR6, MDA-5 and the NALP3 inflammasome.
J. Delaloye et al. (2009)