Enhancement of VP1-specific immune responses and protection against EMCV-K challenge by co-delivery of IL-12 DNA with VP1 DNA vaccine

Suh, You Suk; Ha, Sang‐Jun; Lee, Chu Hee; Sin, Jeong-Im; Sung, Young Chul

doi:10.1016/s0264-410x(00)00443-6

Cited by 12 publications

(10 citation statements)

References 32 publications

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“…Since this study did not include a group primed with the SIVgag plasmid DNA in the absence of plasmid IL-12, we cannot draw any formal conclusions regarding the ability of plasmid IL-12 to serve as a DNA vaccine adjuvant. However, similar studies by our group (Schadeck et al, in preparation) and others [13][14][15][16][17][18][19][20] have clearly demonstrated the adjuvant activity of plasmid IL-12. Also, it is important to note that the priming immunizations used in the current study were limited to a plasmid expressing a truncated form of SIVgag, as vectors expressing a full-length gag, as well as other important viral antigens were not available for inclusion in this study.…”

Section: Discussionsupporting

confidence: 74%

“…12 For example, a number of studies have demonstrated that plasmid-expressed interleukin-12 (IL-12) can function as a genetic adjuvant and substantially improve the efficacy of DNA vaccination. [13][14][15][16][17][18][19][20] A number of recombinant viral vectors based on modified vaccinia Ankara, [21][22][23][24][25][26] canarypox virus, 2,27-30 adenovirus, [31][32][33][34][35][36] adenoassociated virus, 37 and vesicular stomatitis virus (VSV) [38][39][40][41] are also being actively developed as candidate vaccine delivery systems for the prevention of HIV infection. Viral vectors, in contrast to naked plasmid DNA, are capable of efficiently entering host cells and expressing the encoded vaccine antigen to a relatively high level.…”

Section: Introductionmentioning

confidence: 99%

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Priming with Plasmid DNAs Expressing Interleukin-12 and Simian Immunodeficiency Virus Gag Enhances the Immunogenicity and Efficacy of an Experimental AIDS Vaccine Based on Recombinant Vesicular Stomatitis Virus

Egan

Chong

Megati

et al. 2005

AIDS Research and Human Retroviruses

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Of the various approaches being developed as prophylactic HIV vaccines, those based on a heterologous plasmid DNA prime, live vector boost vaccination regimen appear especially promising in the nonhuman primate/simian-human immunodeficiency virus (SHIV) challenge model. In this study, we sought to determine whether a series of intramuscular priming immunizations with a plasmid DNA vaccine expressing SIVgag p39, in combination with plasmid expressed rhesus IL-12, could effectively enhance the immunogenicity and postchallenge efficacy of two intranasal doses of recombinant vesicular stomatitis virus (rVSV)-based vectors expressing HIV-1 env 89.6P gp160 and SIVmac239 gag p55 in rhesus macaques. In macaques receiving the combination plasmid DNA prime, rVSV boost vaccination regimen we observed significantly increased SIVgag- specific cell-mediated and humoral immune responses and significantly lower viral loads postintravenous SHIV89.6P challenge relative to macaques receiving only the rVSV vectored immunizations. In addition, the plasmid DNA prime, rVSV boost vaccination regimen also tended to increase the preservation of peripheral blood CD4+ cells and reduce the morbidity and mortality associated with SHIV89.6P infection. An analysis of immune correlates of protection after SHIV89.6P challenge revealed that the prechallenge SHIV-specific IFN-gamma ELISpot response elicited by vaccination and the ability of the host to mount a virus-specific neutralizing antibody response postchallenge correlated with postchallenge clinical outcome. The correlation between vaccine-elicited cell-mediated immune responses and an improved clinical outcome after SHIV challenge provides strong justification for the continued development of a cytokine-enhanced plasmid DNA prime, rVSV vector boost immunization regimen for the prevention of HIV infection.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Priming with Plasmid DNAs Expressing Interleukin-12 and Simian Immunodeficiency Virus Gag Enhances the Immunogenicity and Efficacy of an Experimental AIDS Vaccine Based on Recombinant Vesicular Stomatitis Virus

Egan

Chong

Megati

et al. 2005

AIDS Research and Human Retroviruses

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“…In addition, the plasmid expressing IL-12 increases the protective efficacy of DNA vaccines in a number of other infectious models (22,23,47,48,56,60,61,68), but this is the first report of plasmid IL-23 enhancing the protective immunity of a subunit vaccine. Therefore, the addition of IL-23 and/or IL-12 may be an effective strategy for increasing the efficacy of DNA vaccines against M. tuberculosis.…”

Section: Discussionmentioning

confidence: 99%

Plasmid Interleukin-23 (IL-23), but Not Plasmid IL-27, Enhances the Protective Efficacy of a DNA Vaccine againstMycobacterium tuberculosisInfection

et al. 2006

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Protection against intracellular pathogens such asTuberculosis (TB) is a global health emergency, with an estimated nine million new cases of active disease and approximately 2 million deaths per year (11a). The development of more effective vaccines than the current vaccine Mycobacterium bovis bacillus Calmette-Guérin (BCG) may improve the control of this pandemic. New approaches to the design of TB vaccines include the preparation of recombinant BCG oversecreting mycobacterial antigens (32), attenuated strains of M. tuberculosis (54), and subunit vaccines based on DNA or protein antigens (33, 55). DNA vaccines encoding M. tuberculosis proteins, such as antigen 85A (Ag85A) or Ag85B (DNA85), induce partial protection against experimental TB (34, 36). However, the degree of protection gained from DNA vaccination alone is less than that afforded by BCG vaccination. Strategies to improve antimycobacterial immunity from subunit vaccines include the development of fusion proteins containing multiple protective antigens (46) and the use of immunostimulatory molecules as adjuvants (50).The development of acquired cellular immunity is critical for the control of M. tuberculosis infection. The key cytokine required for cell-mediated immunity is gamma interferon (IFN-␥), which functions by stimulating infected macrophages to induce phagolysosomal fusion and killing of intracellular bacteria (10,20). The heterodimeric cytokines interleukin-12 (IL-12) and IL-18 are critical for the induction of Th1-like CD4 ϩ cells and are produced primarily by dendritic cells (DCs) (44,59,67). Humans and mice lacking the p40 chain of IL-12 or its receptors are highly susceptibility to M. tuberculosis infection (6, 11). Plasmids expressing either IL-12 or IL-18 have been used as adjuvants in several infectious models (42,45,50). Coadministration of plasmids expressing IL-12 or IL-18 increased the IFN-␥ T-cell response in DNA vaccination to Ag85B, but only plasmids expressing IL-12 increased protective efficacy (62).Recently, two further cytokines, IL-23 and IL-27, have been found to contribute to the development of Th1-like CD4 ϩ T-cell responses. The heterodimeric cytokine IL-23 is secreted by activated macrophages and DCs and induces clonal expansion of memory CD4 ϩ T cells (49). IL-23 is composed of a p40 subunit, shared with IL-12, and a unique p19 subunit, signaling through the receptor IL-12R␤, and a unique IL-23R chain (49). In addition to its direct action on T cells, IL-23 also induces the secretion of IL-12 and IFN-␥ by DCs in vitro (4). This suggests that IL-23 has indirect involvement in the activation of antigen-presenting cells (APCs). Studies with genedeficient mice reveal that a number of roles that were previously accredited to IL-12 may be dependent on IL-23 (12). In

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“…Pictures were taken at 48 h post-transfection. The data shown here was one of three experiments piglets [18][19][20]. Jia et al [21] have reported that some small interfering RNA (siRNA) targeting 2C, 2B, 3C, and 3D genes could inhibit EMCV replication in BHK-21 cells.…”

Section: Discussionmentioning

confidence: 92%

Inhibition of encephalomyocarditis virus replication by shRNA targeting 1D and 3AB genes in vitro and in vivo

et al. 2011

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Encephalomyocarditis virus (EMCV) could infect many host species and cause acute myocarditis and sudden death in pre-weaned piglets. It was necessary to develop new antiviral strategies for the treatment of the virus infection. Here, four plasmids expressing shRNA (small hairpin RNA) targeted to 1D or 3AB protein genes of EMCV were constructed and their inhibition efficiency on the replication of EMCV was evaluated in both BHK21 cells and mice. The results showed that three out of those four shRNA constructs could significantly inhibit EMCV replication in BHK21 cells on the levels of viral RNA and protein. Moreover, it was found that the shRNAs could suppress significantly the load of EMCV in the brain tissue of the mice pretreated with the constructs for 6-24 h. The clinical signs and pathological lesions of the mice in the groups inoculated with the shRNA constructed were milder obviously, compared with those in pSUPER-mN3 and challenge control groups. The survival rates of mice inoculated with pSUPER-3AB-1, pSUPER-3AB-2, and pSUPER-1D-1 for 12 h was 100, 80, and 40%, respectively, while, in the control groups it was only 20%. It indicated that the vector-based shRNA targeting to 3AB and 1D genes might be a potential anti-EMCV strategy.

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Enhancement of VP1-specific immune responses and protection against EMCV-K challenge by co-delivery of IL-12 DNA with VP1 DNA vaccine

Cited by 12 publications

References 32 publications

Priming with Plasmid DNAs Expressing Interleukin-12 and Simian Immunodeficiency Virus Gag Enhances the Immunogenicity and Efficacy of an Experimental AIDS Vaccine Based on Recombinant Vesicular Stomatitis Virus

Priming with Plasmid DNAs Expressing Interleukin-12 and Simian Immunodeficiency Virus Gag Enhances the Immunogenicity and Efficacy of an Experimental AIDS Vaccine Based on Recombinant Vesicular Stomatitis Virus

Plasmid Interleukin-23 (IL-23), but Not Plasmid IL-27, Enhances the Protective Efficacy of a DNA Vaccine againstMycobacterium tuberculosisInfection

Inhibition of encephalomyocarditis virus replication by shRNA targeting 1D and 3AB genes in vitro and in vivo

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