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dc.contributor.authorFiorentini, Simona
dc.contributor.authorMarconi, Peggy
dc.contributor.authorAvolio, Manuela
dc.contributor.authorMarini, Elena
dc.contributor.authorGarrafa, Emirena
dc.contributor.authorCaracciolo, Sonia
dc.contributor.authorRossi, Daniele
dc.contributor.authorBozac, Alexandra
dc.contributor.authorBecker, Pablo D
dc.contributor.authorGentili, Francesca
dc.contributor.authorFacchetti, Fabio
dc.contributor.authorGuzman, Carlos A
dc.contributor.authorManservigi, Roberto
dc.contributor.authorCaruso, Arnaldo
dc.date.accessioned2008-03-05T09:45:09Z
dc.date.available2008-03-05T09:45:09Z
dc.date.issued2007-07
dc.identifier.citationReplication-deficient mutant Herpes Simplex Virus-1 targets professional antigen presenting cells and induces efficient CD4+ T helper responses. 2007, 9 (8):988-96 Microbes Infect.en
dc.identifier.issn1286-4579
dc.identifier.pmid17553721
dc.identifier.doi10.1016/j.micinf.2007.04.001
dc.identifier.urihttp://hdl.handle.net/10033/19754
dc.description.abstractBoth neutralizing antibodies and cytotoxic T-cells are necessary to control a viral infection. However, vigorous T helper responses are essential for their elicitation and maintenance. Here we show that a recombinant replication-deficient Herpes Simplex Virus (HSV)-1 vector encoding the Human Immunodeficiency Virus (HIV)-1 matrix protein p17 (T0-p17) was capable of infecting professional antigen presenting cells (APCs) in vitro and in vivo. The injection of T0-p17 in the mouse dermis generated a strong p17-specific CD4+ T helper response preceding both p17-specific humoral and effector T cell responses. Moreover, we show that T0-p17 infection did not interfere with the endogenous processing of the transgene encoded antigen, since infected APCs were able to evoke a strong recall response in vitro. Our results demonstrate that replication-deficient HSV vectors can be appealing candidates for the development of vaccines able to trigger T helper responses.
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshAntigen-Presenting Cellsen
dc.subject.meshAntigens, CD4en
dc.subject.meshCD4-Positive T-Lymphocytesen
dc.subject.meshFemaleen
dc.subject.meshGene Products, gagen
dc.subject.meshGenetic Vectorsen
dc.subject.meshHIV Antibodiesen
dc.subject.meshHIV Antigensen
dc.subject.meshHerpesvirus 1, Humanen
dc.subject.meshHumansen
dc.subject.meshImmunizationen
dc.subject.meshMacrophages, Peritonealen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred BALB Cen
dc.subject.meshMutationen
dc.subject.meshRecombination, Geneticen
dc.subject.meshT-Lymphocytes, Helper-Induceren
dc.subject.meshViral Proteinsen
dc.subject.meshVirus Replicationen
dc.subject.meshgag Gene Products, Human Immunodeficiency Virusen
dc.titleReplication-deficient mutant Herpes Simplex Virus-1 targets professional antigen presenting cells and induces efficient CD4+ T helper responses.en
dc.typeArticleen
dc.contributor.departmentDepartment of Experimental and Applied Medicine, Section of Microbiology, University of Brescia Medical School, Piazzale Spedali Civili, 1, I-25123 Brescia, Italy.en
dc.identifier.journalMicrobes and infection / Institut Pasteuren
refterms.dateFOA2018-06-13T04:07:24Z
html.description.abstractBoth neutralizing antibodies and cytotoxic T-cells are necessary to control a viral infection. However, vigorous T helper responses are essential for their elicitation and maintenance. Here we show that a recombinant replication-deficient Herpes Simplex Virus (HSV)-1 vector encoding the Human Immunodeficiency Virus (HIV)-1 matrix protein p17 (T0-p17) was capable of infecting professional antigen presenting cells (APCs) in vitro and in vivo. The injection of T0-p17 in the mouse dermis generated a strong p17-specific CD4+ T helper response preceding both p17-specific humoral and effector T cell responses. Moreover, we show that T0-p17 infection did not interfere with the endogenous processing of the transgene encoded antigen, since infected APCs were able to evoke a strong recall response in vitro. Our results demonstrate that replication-deficient HSV vectors can be appealing candidates for the development of vaccines able to trigger T helper responses.


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