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    <title>Nature Precedings - Tag feed for Vaccine</title>
    <link>http://precedings.nature.com/tags/Vaccine</link>
    <description>Recently posted documents tagged with 'Vaccine'</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
    <prism:publicationName>Nature Precedings</prism:publicationName>
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      <title>Antibody responses to a Cryptosporidium parvum rCP15/60 vaccine</title>
      <link>http://precedings.nature.com/documents/3988/version/1</link>
      <description>Cryptosporidium parvum is a zoonotic apicomplexa-protozoan pathogen that causes gastroenteritis and diarrhoea in mammals worldwide. The organism is transmitted by ingestion of oocysts, which are shed in faeces, and completes its lifecycle in a single host.1 C. parvum is ubiquitous on dairy operations worldwide and is one of the leading causes of diarrhoea in calves on these farms.2,3 Here, for the first time, we describe the antibody response in a large group of cows to a recombinant C. parvum oocyst surface protein (rCP15/60) vaccine and the antibody response in calves fed rCP15/60-immune colostrum produced by these vaccinated cows. Results of recent genotype surveys indicate that calves are the only major reservoir for C. parvum infections in humans.4 Human C. parvum infections are particularly prevalent and often fatal in neonates in developing countries and to immunocompromised people, such as AIDs patients.4 Drug therapy against cryptosporidiosis is limited and not wholly efficacious in either humans or calves5, making development of an effective vaccine of paramount importance. To date, there is no commercially available effective vaccine against C. parvum, although passive immunization utilizing different zoite surface (glyco)proteins has showed promise.6-9 All cows we vaccinated produced an antibody response to the rCP15/60 vaccine and the magnitude of response correlated strongly with the subsequent level of antibody in their colostrum. All calves fed rCP15/60-immune colostrum showed a dose-dependent absorption of antibody. Our results demonstrate that vaccination of cows with rCP15/60 successfully induces antibodies against CP15/60 in their serum and colostrum and that these antibodies are then well absorbed when fed to neonatal calves. With further research, this C. parvum vaccine may well be a practical method of conferring passive protection to calves against cryptosporidiosis. Furthermore, a specifically targeted immune-colostrum may be valuable in protection and treatment of immunocompromised human patients with cryptosporidiosis.</description>
      <guid>http://precedings.nature.com/documents/3988/version/1</guid>
      <pubDate>Fri, 20 Nov 2009 12:18:51 UTC</pubDate>
      <dc:title>Antibody responses to a Cryptosporidium parvum rCP15/60 vaccine</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3988.1</dc:identifier>
      <dc:date>2009-11-20</dc:date>
      <dc:creator>Alexandra J. Burton</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-20T12:18:51Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Immunology</prism:section>
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      <title>VO: Vaccine Ontology</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3552.1</link>
      <description>Vaccine research, as well as the development, testing, clinical trials, and commercial uses of vaccines involve complex processes with various biological data that include gene and protein expression, analysis of molecular and cellular interactions, study of tissue and whole body responses, and extensive epidemiological modeling. Although many data resources are available to meet different aspects of vaccine needs, it remains a challenge how we are to standardize vaccine annotation, integrate data about varied vaccine types and resources, and support advanced vaccine data analysis and inference. To address these problems, the community-based Vaccine Ontology (VO, http://www.violinet.org/vaccineontology) has been developed through collaboration with vaccine researchers and many national and international centers and programs, including the National Center for Biomedical Ontology (NCBO), the Infectious Disease Ontology (IDO) Initiative, and the Ontology for Biomedical Investigations (OBI). VO utilizes the Basic Formal Ontology (BFO) as the top ontology and the Relation Ontology (RO) for definition of term relationships. VO is represented in the Web Ontology Language (OWL) and edited using the Prot&#233;g&#233;-OWL. Currently VO contains more than 2000 terms and relationships. VO emphasizes on classification of vaccines and vaccine components, vaccine quality and phenotypes, and host immune response to vaccines. These reflect different aspects of vaccine composition and biology and can thus be used to model individual vaccines. More than 200 licensed vaccines and many vaccine candidates in research or clinical trials have been modeled in VO. VO is being used for vaccine literature mining through collaboration with the National Center for Integrative Biomedical Informatics (NCIBI). Multiple VO applications will be presented.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3552.1</guid>
      <pubDate>Wed, 05 Aug 2009 18:48:16 UTC</pubDate>
      <dc:title>VO: Vaccine Ontology</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3552.1</dc:identifier>
      <dc:date>2009-08-05</dc:date>
      <dc:creator>Yongqun He</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-08-05T18:48:16Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Biotechnology</prism:section>
      <prism:section>Immunology</prism:section>
      <prism:section>Microbiology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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      <title>Salmonella typhimurium harboring plasmid expressing interleukin-12 induced attenuation of infection and protective immune responses</title>
      <link>http://precedings.nature.com/documents/3413/version/1</link>
      <description>IL-12 is known to be an essential cytokine which appears to provide protective immunity against intracellular bacteria, such as Salmonella. In this study, we investigated the possibility of developing a vaccine using IL-12 against virulent Salmonella. We used the host defense system activated by cytokine IL-12. The highly virulent Salmonella strain (Salmonella typhimurium UK-1) was transformed with cytokine-expressing plasmids. These live, wild-type pathogens were used as vaccine strains without undergoing any other biological or genetic attenuating processes. The newly developed strains induced partial protection from infections (30-40%). Of note, the interleukin-12 transformed pathogen was safe upon immunization with low doses (103 CFU), induced IgG responses, and stimulated protective immune responses against Salmonella Typhimurium in mice (80-100%). These results suggest that IL-12 induced attenuation of wild-type Salmonella in the host infection stage and vaccine development using the wild-type strain harboring IL-12 secreting plasmids may be considered as an alternative process for intracellular bacterial vaccine development without the inconvenience of time-consuming attenuation processes.</description>
      <guid>http://precedings.nature.com/documents/3413/version/1</guid>
      <pubDate>Fri, 10 Jul 2009 09:38:32 UTC</pubDate>
      <dc:title>Salmonella typhimurium harboring plasmid expressing interleukin-12 induced attenuation of infection and protective immune responses</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3413.1</dc:identifier>
      <dc:date>2009-07-10</dc:date>
      <dc:creator>Yong Keun Park</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-10T09:38:32Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Biotechnology</prism:section>
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      <title>Cervical Cancer-Associated Human Papillomavirus 16 E7 Oncoprotein Inhibits Induction of Anti-Cancer Immunity by a CD4+ T Cell Dependent Mechanism </title>
      <link>http://dx.doi.org/10.1038/npre.2009.3405.1</link>
      <description>Attempts to develop therapeutic vaccines against cervical cancer have been proven difficult. One of the major causes of the failure is due to the use of the wrong mouse models based on transplantable tumours in testing the efficacy of vaccines. Now that a transgenic epithelial mouse model has been developed to closely mimic cervical cancer, the mechanisms needed to eliminate this type of cancer could be studied. The E7 oncoprotein of Human Papillomavirus (HPV) is the most expressed HPV protein in cervical cancers and its continuous production is essential to maintain the cancerous state and therefore the obvious target in the development of vaccines. Skin grafts expressing the HPV 16 E7 protein (E7 autografts) are not spontaneously rejected from an MHC matched immunocompetent host.  Interestingly, simultaneous placement of an MHC mismatched skin (allograft) next to an E7 autograft results in the E7 autograft rejection.  However when the allograft also expresses E7, the E7 autograft is rejected more slowly.  Autograft rejection requires CD8+ T cells, and is accelerated by removal of CD4+ T cells after placement of the E7 expressing allograft, suggesting induction of an E7 specific CD4+ regulatory T cell population by the E7 expressing allograft. This observation may have implications in designing effective vaccines and immunotherapy against cervical cancers in women.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3405.1</guid>
      <pubDate>Wed, 08 Jul 2009 15:57:26 UTC</pubDate>
      <dc:title>Cervical Cancer-Associated Human Papillomavirus 16 E7 Oncoprotein Inhibits Induction of Anti-Cancer Immunity by a CD4+ T Cell Dependent Mechanism </dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3405.1</dc:identifier>
      <dc:date>2009-07-08</dc:date>
      <dc:creator>Marion E. G. Brunck</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-08T15:57:26Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Cancer</prism:section>
      <prism:section>Immunology</prism:section>
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      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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    <item>
      <title>Protective vaccination in the horse against Streptococcus equi with recombinant antigens</title>
      <link>http://precedings.nature.com/documents/2985/version/1</link>
      <description>Streptococcus equi subspecies equi (S. equi) is a clonal, equine host-adapted pathogen of global importance that causes a highly contagious suppurative lymphodendopathy of the head and neck, more commonly known as Strangles. The disease is highly prevalent, can be severe and spread easily by visibly infected animals or by carrier animals that show no clinical signs of disease. Antibiotic treatment is usually ineffective. However, the majority of horses develop immunity to re-infection, suggesting that vaccination should be a feasible way to prevent the infection. Live attenuated vaccine strains of S. equi are available but adverse reactions have been reported and they suffer from a short duration of immunity. Thus, a safe and effective vaccine against S. equi is highly desirable. In this report, Welsh mountain ponies vaccinated with a combination of seven recombinant S. equi proteins, were significantly protected from experimental infection by S. equi, resembling the spontaneous disease. The protective antigens consisted of five surface localized proteins and two IgG endopeptidases. The results from a second vaccination trial indicate that the endopeptidases were important for good protection. The similarity of S. equi to other pyogenic streptococci suggests that our findings have broader implications for the prevention of streptococcal infections.</description>
      <guid>http://precedings.nature.com/documents/2985/version/1</guid>
      <pubDate>Thu, 26 Mar 2009 17:23:17 UTC</pubDate>
      <dc:title>Protective vaccination in the horse against Streptococcus equi with recombinant antigens</dc:title>
      <dc:identifier>hdl:10101/npre.2009.2985.1</dc:identifier>
      <dc:date>2009-03-26</dc:date>
      <dc:creator>Jan-Ingmar Flock</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-03-26T17:23:17Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Immunology</prism:section>
      <prism:section>Microbiology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/2985/version/1/files/npre20092985-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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    <item>
      <title>Dynamic Modeling of Vaccinating Behavior as a Function of Individual Beliefs</title>
      <link>http://precedings.nature.com/documents/2447/version/1</link>
      <description>Individual perception of vaccine safety is an important factor in determining a person&amp;#8217;s adherence to a vaccination program and its consequences for disease control. This perception, or belief, about the safety of a given vaccine, is not a static parameter but a variable subject to environmental influence. To complicate matters, perception of risk (or safety) does not correspond to actual risk. In this paper we propose a way to model the dynamics of such beliefs in the context of a realistic epidemiological scenario. The methodology proposed is based on Bayesian inference, and can be extended to model more complex belief systems associated with decision models.</description>
      <guid>http://precedings.nature.com/documents/2447/version/1</guid>
      <pubDate>Tue, 28 Oct 2008 17:13:41 UTC</pubDate>
      <dc:title>Dynamic Modeling of Vaccinating Behavior as a Function of Individual Beliefs</dc:title>
      <dc:identifier>hdl:10101/npre.2008.2447.1</dc:identifier>
      <dc:date>2008-10-28</dc:date>
      <dc:creator>Fl&#225;vio C. Coelho</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-10-28T17:13:41Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Ecology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/2447/version/1/files/npre20082447-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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    <item>
      <title>Tuberculosis vaccine strain Mycobacterium bovis BCG Russia is a natural recA mutant</title>
      <link>http://precedings.nature.com/documents/1576/version/1</link>
      <description>The current tuberculosis vaccine is a live vaccine derived from Mycobacterium bovis and attenuated by serial in vitro passaging. All vaccine substrains in use stem from one source, strain Bacille Calmette-Gu&#233;rin. However, they differ in regions of genomic deletions, antigen expression levels, immunogenicity, and protective efficacy. As a RecA phenotype increases genetic stability and may contribute restricting the ongoing evolution of the various BCG substrains, we aimed to inactivate recA by allelic replacement in BCG vaccine strains representing different phylogenetic lineages (Pasteur, Frappier, Denmark, Russia). Homologous gene replacement was successful in three out of four strains. However, only illegitimate recombination was observed in BCG substrain Russia. Sequence analyses of recA revealed that a single nucleotide insertion in the 5&amp;#8217; part of recA led to a translational frameshift with an early stop codon making BCG Russia a natural recA mutant. At the protein level BCG Russia failed to express RecA. According to phylogenetic analyses BCG Russia is an ancient vaccine strain most closely related to the parental M. bovis. Our data suggest that recA inactivation in BCG Russia occurred early and is in part responsible for its high degree of genomic stability, resulting in a substrain that has less genetic alterations than other vaccine substrains with respect to M. bovis AF2122/97 wild type.</description>
      <guid>http://precedings.nature.com/documents/1576/version/1</guid>
      <pubDate>Thu, 07 Feb 2008 18:43:58 UTC</pubDate>
      <dc:title>Tuberculosis vaccine strain Mycobacterium bovis BCG Russia is a natural recA mutant</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1576.1</dc:identifier>
      <dc:date>2008-02-07</dc:date>
      <dc:creator>Peter Sander</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-02-07T18:43:58Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Microbiology</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/1576/version/1/files/npre20081576-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin</title>
      <link>http://precedings.nature.com/documents/743/version/2</link>
      <description>The rapid evolution of the H5N1 serotype of avian influenza has been explained by a mechanism involving the selection of single nucleotide polymorphisms generated by copy errors.  The recent emergence of H5N1 Clade 2.2 in fifty countries, offered a unique opportunity to view the acquisition of new polymorphism in these evolving genomes.  We analyzed the H5N1 hemagglutinin gene from a fatal human case from Nigeria in 2007.  The newly emerged polymorphisms were present in diverse H5N1 isolates from the previous year.  The aggregation of these polymorphisms from clade 2.2 sub-clades was not supported by recent random mutations, and was most easily explained by recombination between closely related sequences.</description>
      <guid>http://precedings.nature.com/documents/743/version/2</guid>
      <pubDate>Wed, 12 Sep 2007 11:04:26 UTC</pubDate>
      <dc:title>Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin</dc:title>
      <dc:identifier>hdl:10101/npre.2007.743.2</dc:identifier>
      <dc:date>2009-03-04</dc:date>
      <dc:creator>Henry L. Niman</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-09-12T11:04:26Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/743/version/2/files/npre2007743-2.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/2.5/</creativeCommons:license>
    </item>
    <item>
      <title>Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin</title>
      <link>http://precedings.nature.com/documents/743/version/1</link>
      <description>The evolution of H5N1 has attracted significant interest 1-4 due to linkages with avian 5,6 and human infections 7,8.  The basic tenets of influenza genetics 9 attribute genetic drift to replication errors caused by a polymerase complex that lacks a proof reading function.  However, recent analysis 10 of swine influenza genes identifies regions copied with absolute fidelity for more than 25 years.  In addition, polymorphism tracing of clade 2.2 H5N1 single nucleotide polymorphisms identify concurrent acquisition 11 of the same polymorphism onto multiple genetic backgrounds in widely dispersed geographical locations.  Here we show the aggregation of regional clade 2.2 polymorphisms from Germany, Egypt, and sub-Sahara Africa onto a human Nigerian H5N1 hemagglutinin (HA), implicating recombination in the dispersal and aggregation of single nucleotide polymorphisms from closely related genomes.</description>
      <guid>http://precedings.nature.com/documents/743/version/1</guid>
      <pubDate>Thu, 16 Aug 2007 15:53:42 UTC</pubDate>
      <dc:title>Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin</dc:title>
      <dc:identifier>hdl:10101/npre.2007.743.1</dc:identifier>
      <dc:date>2007-08-16</dc:date>
      <dc:creator>Henry L. Niman</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-08-16T15:53:42Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Biotechnology</prism:section>
      <prism:section>Ecology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Immunology</prism:section>
      <prism:section>Microbiology</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/743/version/1/files/npre2007743-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/2.5/</creativeCommons:license>
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    <item>
      <title>H5N1 Clade 2.2 Polymorphism Tracing Identifies Influenza Recombination and Potential Vaccine Targets</title>
      <link>http://dx.doi.org/10.1038/npre.2007.553.2</link>
      <description>Highly pathogenic Influenza A H5N1 was first identified in Guangdong Province in 1996, followed by human cases in Hong Kong in 1997 1. The number of confirmed human cases now exceeds 300 and the associated Case Fatality Rate exceeds 60% 2. The genetic diversity of the serotype continues to increase.  Four distinct clades or sub-clades have been linked to human cases 3.4. The gradual genetic changes identified in the sub-clades have been attributed to copy errors by viral encoded polymerases that lack an editing function, thereby resulting in antigenic drift 5. We traced polymorphism acquisition in Clade 2.2 sequences. We report here the concurrent acquisition of the same polymorphism by multiple, genetically distinct, Clade 2.2 sub-clades in Egypt, Russia and Ghana. These changes are not easily explained by the current theory of &#8220;random mutation&#8221; through copy error, and are more easily explained by recombination with a common source. This conclusion is supported by additional polymorphisms shared by Clade 2.2 isolates in Egypt, Nigeria and Germany including aggregation of regional polymorphisms from each of these areas into a single Nigerian human hemagglutinin gene.</description>
      <guid>http://dx.doi.org/10.1038/npre.2007.553.2</guid>
      <pubDate>Tue, 07 Aug 2007 16:18:58 UTC</pubDate>
      <dc:title>H5N1 Clade 2.2 Polymorphism Tracing Identifies Influenza Recombination and Potential Vaccine Targets</dc:title>
      <dc:identifier>doi:10.1038/npre.2007.553.2</dc:identifier>
      <dc:date>2007-08-07</dc:date>
      <dc:creator>Henry L. Niman</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-08-07T16:18:58Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Biotechnology</prism:section>
      <prism:section>Ecology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Microbiology</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/553/version/2/files/npre2007553-2.pdf.thumb.png"/>
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