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Abstract
Bovine herpesvirus-1 (BoHV-1) uses many mechanisms to elude the immune system; one of them is spreading intracellularly, even in the presence of specific antiviral antibodies. Cytotoxic T lymphocytes (CTLs) are necessary to eliminate the virus. The main preventive strategy is vaccination based on inactivated virus. These vaccines are poor inducers of cellular immune responses, and complicate serological diagnosis and determination of the real prevalence [ver mas...]
dc.contributor.authorLangellotti, Cecilia Ana
dc.contributor.authorGammella, Mariela
dc.contributor.authorSoria, Ivana
dc.contributor.authorBellusci, Carolina
dc.contributor.authorQuattrocchi, Valeria
dc.contributor.authorVermeulen, Elba Monica
dc.contributor.authorMongini, Claudia
dc.contributor.authorZamorano, Patricia Ines
dc.date.accessioned2021-04-19T16:06:15Z
dc.date.available2021-04-19T16:06:15Z
dc.date.issued2021-03
dc.identifier.issn1557-8976
dc.identifier.otherhttps://doi.org/10.1089/vim.2020.0082
dc.identifier.urihttp://hdl.handle.net/20.500.12123/9126
dc.identifier.urihttps://www.liebertpub.com/doi/10.1089/vim.2020.0082
dc.description.abstractBovine herpesvirus-1 (BoHV-1) uses many mechanisms to elude the immune system; one of them is spreading intracellularly, even in the presence of specific antiviral antibodies. Cytotoxic T lymphocytes (CTLs) are necessary to eliminate the virus. The main preventive strategy is vaccination based on inactivated virus. These vaccines are poor inducers of cellular immune responses, and complicate serological diagnosis and determination of the real prevalence of infection. DNA vaccines are a good option because of the capacity of Differentiating Infected from Vaccinated Animals—(DIVA vaccine)—and may be the best way to induce cytotoxic responses. Although this type of vaccines leads to only weak “in vivo” expression and poor immune responses, incorporation of molecular and/or chemical adjuvants can improve the latter, both in magnitude and in direction. In this study, we have investigated the specific immune responses elicited in mice by DNA vaccines based on the BoHV-1 glycoprotein D (pCIgD) with and without two different adjuvants: a plasmid encoding for murine CD40L (pCD40L) or Montanide™ 1113101PR (101). Mice vaccinated with pCIgD+CD40L, pCIgD+101, and pCIgD+CD40L+101 developed significantly higher specific antibody titers against BoHV-1 than the pCIgD group (p < 0.01). The animals vaccinated with pCgD+pCD40L+101 raised significantly higher levels of IgG2a and IgG2b (p < 0.01 and p < 0.001, respectively) than mice vaccinated with pCIgD alone. On the contrary, when the activity of CTL against cells infected with BoHV-1 was measured, the vaccine pCgD+pCD40L+101 induced significantly higher levels of cytotoxicity activity (p < 0.001) than pCIgD alone. A significant increase in the CD4+ populations in the group receiving pCIgD+CD40L+101 in comparison with the pCIgD group was observed and, also, interferon gamma, interleukin (IL)-6, and IL-17A levels were higher. Considering the results obtained from this study for humoral and cellular responses in mice, the inclusion of pCD40L and 101 as adjuvants in a BoHV-1 DNA vaccine for cattle is highly recommendable.eng
dc.formatapplication/pdfes_AR
dc.language.isoenges_AR
dc.publisherMary Ann Liebertes_AR
dc.relationinfo:eu-repograntAgreement/INTA/PNBIO-1131032/AR./Desarrollo de herramientas biotecnológicas para la prevención y el control de enfermedades pecuarias: vacunas, diagnóstico y eIdemiología molecular.es_AR
dc.rightsinfo:eu-repo/semantics/restrictedAccesses_AR
dc.sourceViral Immunology 34 (2) : 68-78 (Marzo 2021)es_AR
dc.subjectBovine Herpesviruseng
dc.subjectVaccine Adjuvantseng
dc.subjectCoadyuvantes de Vacunases_AR
dc.subjectCytotoxicityeng
dc.subjectCitotoxicidades_AR
dc.subjectHerpes Virus Bovino
dc.subject.otherMice Modeleng
dc.subject.otherModelo de Ratónes_AR
dc.titleAn improved DNA vaccine against bovine herpesvirus-1 using CD40L and a chemical adjuvant induces specific cytotoxicity in micies_AR
dc.typeinfo:ar-repo/semantics/artículoes_AR
dc.typeinfo:eu-repo/semantics/articlees_AR
dc.typeinfo:eu-repo/semantics/publishedVersiones_AR
dc.description.origenInstituto de Virologíaes_AR
dc.description.filFil: Langellotti, Cecilia Ana. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Virología; Argentinaes_AR
dc.description.filFil: Langellotti, Cecilia Ana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes_AR
dc.description.filFil: Gammella, Mariela. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Virología; Argentinaes_AR
dc.description.filFil: Gammella, Mariela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes_AR
dc.description.filFil: Soria, Ivana. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Virología; Argentinaes_AR
dc.description.filFil: Soria, Ivana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes_AR
dc.description.filFil: Bellusci, Carolina. Universidad Nacional de Rio Negro. Sede Atlántica; Argentinaes_AR
dc.description.filFil: Quattrocchi, Valeria. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Virología; Argentinaes_AR
dc.description.filFil: Quattrocchi, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes_AR
dc.description.filFil: Vermeulen, Elba Monica. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental (IMEX). Laboratorio de células presentadoras de antígeno y respuesta inflamatoria; Argentinaes_AR
dc.description.filFil: Mongini, Claudia. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Virología; Argentinaes_AR
dc.description.filFil: Mongini, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes_AR
dc.description.filFil: Zamorano, Patricia Ines. Universidad del Salvador. Cátedra de Inmunología Aplicada; Argentinaes_AR
dc.subtypecientifico


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