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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00018-008-8094-2.

Title:
Role of Nef in primate lentiviral immunopathogenesis | Cellular and Molecular Life Sciences
Description:
More than a decade ago it was established that intact nef genes are critical for efficient viral persistence and greatly accelerate disease progression in SIVmac-infected rhesus macaques and in HIV-1-infected humans. Subsequent studies established a striking number of Nef functions that evidently contribute to the maintenance of high viral loads associated with the development of immunodeficiency in the ‘evolutionary-recent’ human and the experimental macaque hosts. Recent data show that many Nef activities are conserved across different lineages of HIV and SIV. However, some differences also exist. For example, Nef alleles from most SIVs that do not cause disease in their natural monkey hosts, but not those of HIV-1 and its simian precursors, down-modulate TCR-CD3 to suppress T cell activation and programmed death. This evolutionary loss of a specific Nef function may contribute to the high virulence of HIV-1 in humans.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Telecommunications
  • Social Networks

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 8,170,236 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We see no obvious way the site makes money.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

article, nef, access, hiv, privacy, cookies, content, data, information, publish, search, primate, kirchhoff, schindler, open, author, log, journal, research, life, role, lentiviral, april, specht, viral, siv, products, discover, springer, function, optional, personal, parties, policy, find, track, cellular, molecular, sciences, immunopathogenesis, published, number, cite, arhel, münch, explore, established, persistence, disease, rhesus,

Topics {✒️}

sivmac-infected rhesus macaques species-specific host factors primate lentiviral immunopathogenesis hiv nef-mediated cd4 efficient viral persistence month download article/chapter experimental macaque hosts related subjects high viral loads privacy choices/manage cookies author correspondence full article pdf hiv-1-infected humans intact nef genes check access instant access european economic area scope submit manuscript natural monkey hosts modulate tcr-cd3 high virulence serinc5 downregulation activity heinrich pette institut specific nef function recent data show conditions privacy policy �evolutionary-recent’ human accepting optional cookies subsequent studies established immunodeficiency article cellular journal finder publish siv infection article log gene products article number 2621 1007/s00018-008-8094-2 keywords article cite personal data privacy policy life sci article kirchhoff books a nef functions nef activities nef alleles hiv hiv-1 information optional cookies

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Role of Nef in primate lentiviral immunopathogenesis
         description:More than a decade ago it was established that intact nef genes are critical for efficient viral persistence and greatly accelerate disease progression in SIVmac-infected rhesus macaques and in HIV-1-infected humans. Subsequent studies established a striking number of Nef functions that evidently contribute to the maintenance of high viral loads associated with the development of immunodeficiency in the ‘evolutionary-recent’ human and the experimental macaque hosts. Recent data show that many Nef activities are conserved across different lineages of HIV and SIV. However, some differences also exist. For example, Nef alleles from most SIVs that do not cause disease in their natural monkey hosts, but not those of HIV-1 and its simian precursors, down-modulate TCR-CD3 to suppress T cell activation and programmed death. This evolutionary loss of a specific Nef function may contribute to the high virulence of HIV-1 in humans.
         datePublished:2008-04-26T00:00:00Z
         dateModified:2008-04-26T00:00:00Z
         pageStart:2621
         pageEnd:2636
         sameAs:https://doi.org/10.1007/s00018-008-8094-2
         keywords:
            AIDS
            HIV
            SIV
            pathogenesis
            Nef
            primate lentiviruses
            immunological synapse
            viral persistence
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
         image:
         isPartOf:
            name:Cellular and Molecular Life Sciences
            issn:
               1420-9071
               1420-682X
            volumeNumber:65
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Birkhäuser-Verlag
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:F. Kirchhoff
               affiliation:
                     name:University of Ulm
                     address:
                        name:Institute of Virology, University of Ulm, Ulm, Germany
                        type:PostalAddress
                     type:Organization
               email:[email protected]
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               name:M. Schindler
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                     name:University of Ulm
                     address:
                        name:Institute of Virology, University of Ulm, Ulm, Germany
                        type:PostalAddress
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                     name:Heinrich Pette Institut
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                        name:Heinrich Pette Institut, Hamburg, Germany
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               name:A. Specht
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                     name:University of Ulm
                     address:
                        name:Institute of Virology, University of Ulm, Ulm, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:N. Arhel
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                     name:University of Ulm
                     address:
                        name:Institute of Virology, University of Ulm, Ulm, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:J. Münch
               affiliation:
                     name:University of Ulm
                     address:
                        name:Institute of Virology, University of Ulm, Ulm, Germany
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ScholarlyArticle:
      headline:Role of Nef in primate lentiviral immunopathogenesis
      description:More than a decade ago it was established that intact nef genes are critical for efficient viral persistence and greatly accelerate disease progression in SIVmac-infected rhesus macaques and in HIV-1-infected humans. Subsequent studies established a striking number of Nef functions that evidently contribute to the maintenance of high viral loads associated with the development of immunodeficiency in the ‘evolutionary-recent’ human and the experimental macaque hosts. Recent data show that many Nef activities are conserved across different lineages of HIV and SIV. However, some differences also exist. For example, Nef alleles from most SIVs that do not cause disease in their natural monkey hosts, but not those of HIV-1 and its simian precursors, down-modulate TCR-CD3 to suppress T cell activation and programmed death. This evolutionary loss of a specific Nef function may contribute to the high virulence of HIV-1 in humans.
      datePublished:2008-04-26T00:00:00Z
      dateModified:2008-04-26T00:00:00Z
      pageStart:2621
      pageEnd:2636
      sameAs:https://doi.org/10.1007/s00018-008-8094-2
      keywords:
         AIDS
         HIV
         SIV
         pathogenesis
         Nef
         primate lentiviruses
         immunological synapse
         viral persistence
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
      image:
      isPartOf:
         name:Cellular and Molecular Life Sciences
         issn:
            1420-9071
            1420-682X
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            Periodical
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      publisher:
         name:Birkhäuser-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:F. Kirchhoff
            affiliation:
                  name:University of Ulm
                  address:
                     name:Institute of Virology, University of Ulm, Ulm, Germany
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:M. Schindler
            affiliation:
                  name:University of Ulm
                  address:
                     name:Institute of Virology, University of Ulm, Ulm, Germany
                     type:PostalAddress
                  type:Organization
                  name:Heinrich Pette Institut
                  address:
                     name:Heinrich Pette Institut, Hamburg, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:A. Specht
            affiliation:
                  name:University of Ulm
                  address:
                     name:Institute of Virology, University of Ulm, Ulm, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:N. Arhel
            affiliation:
                  name:University of Ulm
                  address:
                     name:Institute of Virology, University of Ulm, Ulm, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:J. Münch
            affiliation:
                  name:University of Ulm
                  address:
                     name:Institute of Virology, University of Ulm, Ulm, Germany
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      volumeNumber:65
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      name:Birkhäuser-Verlag
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      name:University of Ulm
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         name:Institute of Virology, University of Ulm, Ulm, Germany
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      name:University of Ulm
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         name:Institute of Virology, University of Ulm, Ulm, Germany
         type:PostalAddress
      name:Heinrich Pette Institut
      address:
         name:Heinrich Pette Institut, Hamburg, Germany
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      name:University of Ulm
      address:
         name:Institute of Virology, University of Ulm, Ulm, Germany
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      name:University of Ulm
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         name:Institute of Virology, University of Ulm, Ulm, Germany
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         name:Institute of Virology, University of Ulm, Ulm, Germany
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      name:F. Kirchhoff
      affiliation:
            name:University of Ulm
            address:
               name:Institute of Virology, University of Ulm, Ulm, Germany
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:M. Schindler
      affiliation:
            name:University of Ulm
            address:
               name:Institute of Virology, University of Ulm, Ulm, Germany
               type:PostalAddress
            type:Organization
            name:Heinrich Pette Institut
            address:
               name:Heinrich Pette Institut, Hamburg, Germany
               type:PostalAddress
            type:Organization
      name:A. Specht
      affiliation:
            name:University of Ulm
            address:
               name:Institute of Virology, University of Ulm, Ulm, Germany
               type:PostalAddress
            type:Organization
      name:N. Arhel
      affiliation:
            name:University of Ulm
            address:
               name:Institute of Virology, University of Ulm, Ulm, Germany
               type:PostalAddress
            type:Organization
      name:J. Münch
      affiliation:
            name:University of Ulm
            address:
               name:Institute of Virology, University of Ulm, Ulm, Germany
               type:PostalAddress
            type:Organization
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      name:Institute of Virology, University of Ulm, Ulm, Germany
      name:Institute of Virology, University of Ulm, Ulm, Germany
      name:Heinrich Pette Institut, Hamburg, Germany
      name:Institute of Virology, University of Ulm, Ulm, Germany
      name:Institute of Virology, University of Ulm, Ulm, Germany
      name:Institute of Virology, University of Ulm, Ulm, Germany
WebPageElement:
      isAccessibleForFree:
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External Links {🔗}(33)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

4.12s.