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The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemor...
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| Zeitschriftentitel: | Journal of Virology |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Journal of Virology, 88, 2014, 3, S. 1781-1786 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society for Microbiology
|
| Schlagwörter: |
| author_facet |
Liu, Yan Wu, Bin Paessler, Slobodan Walker, David H. Tesh, Robert B. Yu, Xue-jie Liu, Yan Wu, Bin Paessler, Slobodan Walker, David H. Tesh, Robert B. Yu, Xue-jie |
|---|---|
| author |
Liu, Yan Wu, Bin Paessler, Slobodan Walker, David H. Tesh, Robert B. Yu, Xue-jie |
| spellingShingle |
Liu, Yan Wu, Bin Paessler, Slobodan Walker, David H. Tesh, Robert B. Yu, Xue-jie Journal of Virology The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever Virology Insect Science Immunology Microbiology |
| author_sort |
liu, yan |
| spelling |
Liu, Yan Wu, Bin Paessler, Slobodan Walker, David H. Tesh, Robert B. Yu, Xue-jie 0022-538X 1098-5514 American Society for Microbiology Virology Insect Science Immunology Microbiology http://dx.doi.org/10.1128/jvi.02277-13 <jats:title>ABSTRACT</jats:title> <jats:p> Severe fever with thrombocytopenia syndrome virus (SFTSV) is a newly discovered <jats:named-content content-type="genus-species">Phlebovirus</jats:named-content> causing an emerging hemorrhagic fever in East Asia, with reported case fatality rates up to 30%. Despite the high case fatality rate and large number of persons at risk of infection, the pathobiology of the disease is unknown, and no effective animal model has been available for investigating its pathogenesis. We have studied mice and hamsters as potential small-animal models of SFTSV infection following subcutaneous, intraperitoneal, or intracerebral inoculation. Animal tissues were processed for viral load determination, histopathology, immunohistochemistry, and confocal microscopic studies. We found that immunocompetent adult mice and hamsters did not become ill after SFTSV infection. However, alpha/beta interferon receptor knockout (IFNAR <jats:sup>−/−</jats:sup> ) mice were highly susceptible to SFTSV infection, and all mice died within 3 to 4 days after subcutaneous inoculation of 10 <jats:sup>6</jats:sup> focus-forming units of SFTSV. Histologic examination of tissues of IFNAR <jats:sup>−/−</jats:sup> mice infected with SFTSV showed no detectable lesions. In contrast, by immunohistochemistry virus antigen was found in liver, intestine, kidney, spleen, lymphoid tissue, and brain, but not in the lungs. Mesenteric lymph nodes and spleen were the most heavily infected tissues. Quantitative reverse transcription-PCR (RT-PCR) confirmed the presence of virus in these tissues. Confocal microscopy showed that SFTSV colocalized with reticular cells but did not colocalize with dendritic cells, monocytes/macrophages, neutrophils, or endothelium. Our results indicate that SFTSV multiplied in all organs except for lungs and that mesenteric lymph nodes and spleen were the most heavily infected tissues. The major target cells of SFTSV appear to be reticular cells in lymphoid tissues of intestine and spleen. </jats:p> The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever Journal of Virology |
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American Society for Microbiology, 2014 |
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American Society for Microbiology, 2014 |
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| title |
The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_unstemmed |
The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_full |
The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_fullStr |
The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_full_unstemmed |
The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_short |
The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_sort |
the pathogenesis of severe fever with thrombocytopenia syndrome virus infection in alpha/beta interferon knockout mice: insights into the pathologic mechanisms of a new viral hemorrhagic fever |
| topic |
Virology Insect Science Immunology Microbiology |
| url |
http://dx.doi.org/10.1128/jvi.02277-13 |
| publishDate |
2014 |
| physical |
1781-1786 |
| description |
<jats:title>ABSTRACT</jats:title>
<jats:p>
Severe fever with thrombocytopenia syndrome virus (SFTSV) is a newly discovered
<jats:named-content content-type="genus-species">Phlebovirus</jats:named-content>
causing an emerging hemorrhagic fever in East Asia, with reported case fatality rates up to 30%. Despite the high case fatality rate and large number of persons at risk of infection, the pathobiology of the disease is unknown, and no effective animal model has been available for investigating its pathogenesis. We have studied mice and hamsters as potential small-animal models of SFTSV infection following subcutaneous, intraperitoneal, or intracerebral inoculation. Animal tissues were processed for viral load determination, histopathology, immunohistochemistry, and confocal microscopic studies. We found that immunocompetent adult mice and hamsters did not become ill after SFTSV infection. However, alpha/beta interferon receptor knockout (IFNAR
<jats:sup>−/−</jats:sup>
) mice were highly susceptible to SFTSV infection, and all mice died within 3 to 4 days after subcutaneous inoculation of 10
<jats:sup>6</jats:sup>
focus-forming units of SFTSV. Histologic examination of tissues of IFNAR
<jats:sup>−/−</jats:sup>
mice infected with SFTSV showed no detectable lesions. In contrast, by immunohistochemistry virus antigen was found in liver, intestine, kidney, spleen, lymphoid tissue, and brain, but not in the lungs. Mesenteric lymph nodes and spleen were the most heavily infected tissues. Quantitative reverse transcription-PCR (RT-PCR) confirmed the presence of virus in these tissues. Confocal microscopy showed that SFTSV colocalized with reticular cells but did not colocalize with dendritic cells, monocytes/macrophages, neutrophils, or endothelium. Our results indicate that SFTSV multiplied in all organs except for lungs and that mesenteric lymph nodes and spleen were the most heavily infected tissues. The major target cells of SFTSV appear to be reticular cells in lymphoid tissues of intestine and spleen.
</jats:p> |
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| author | Liu, Yan, Wu, Bin, Paessler, Slobodan, Walker, David H., Tesh, Robert B., Yu, Xue-jie |
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| description | <jats:title>ABSTRACT</jats:title> <jats:p> Severe fever with thrombocytopenia syndrome virus (SFTSV) is a newly discovered <jats:named-content content-type="genus-species">Phlebovirus</jats:named-content> causing an emerging hemorrhagic fever in East Asia, with reported case fatality rates up to 30%. Despite the high case fatality rate and large number of persons at risk of infection, the pathobiology of the disease is unknown, and no effective animal model has been available for investigating its pathogenesis. We have studied mice and hamsters as potential small-animal models of SFTSV infection following subcutaneous, intraperitoneal, or intracerebral inoculation. Animal tissues were processed for viral load determination, histopathology, immunohistochemistry, and confocal microscopic studies. We found that immunocompetent adult mice and hamsters did not become ill after SFTSV infection. However, alpha/beta interferon receptor knockout (IFNAR <jats:sup>−/−</jats:sup> ) mice were highly susceptible to SFTSV infection, and all mice died within 3 to 4 days after subcutaneous inoculation of 10 <jats:sup>6</jats:sup> focus-forming units of SFTSV. Histologic examination of tissues of IFNAR <jats:sup>−/−</jats:sup> mice infected with SFTSV showed no detectable lesions. In contrast, by immunohistochemistry virus antigen was found in liver, intestine, kidney, spleen, lymphoid tissue, and brain, but not in the lungs. Mesenteric lymph nodes and spleen were the most heavily infected tissues. Quantitative reverse transcription-PCR (RT-PCR) confirmed the presence of virus in these tissues. Confocal microscopy showed that SFTSV colocalized with reticular cells but did not colocalize with dendritic cells, monocytes/macrophages, neutrophils, or endothelium. Our results indicate that SFTSV multiplied in all organs except for lungs and that mesenteric lymph nodes and spleen were the most heavily infected tissues. The major target cells of SFTSV appear to be reticular cells in lymphoid tissues of intestine and spleen. </jats:p> |
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| institution | DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14 |
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| spelling | Liu, Yan Wu, Bin Paessler, Slobodan Walker, David H. Tesh, Robert B. Yu, Xue-jie 0022-538X 1098-5514 American Society for Microbiology Virology Insect Science Immunology Microbiology http://dx.doi.org/10.1128/jvi.02277-13 <jats:title>ABSTRACT</jats:title> <jats:p> Severe fever with thrombocytopenia syndrome virus (SFTSV) is a newly discovered <jats:named-content content-type="genus-species">Phlebovirus</jats:named-content> causing an emerging hemorrhagic fever in East Asia, with reported case fatality rates up to 30%. Despite the high case fatality rate and large number of persons at risk of infection, the pathobiology of the disease is unknown, and no effective animal model has been available for investigating its pathogenesis. We have studied mice and hamsters as potential small-animal models of SFTSV infection following subcutaneous, intraperitoneal, or intracerebral inoculation. Animal tissues were processed for viral load determination, histopathology, immunohistochemistry, and confocal microscopic studies. We found that immunocompetent adult mice and hamsters did not become ill after SFTSV infection. However, alpha/beta interferon receptor knockout (IFNAR <jats:sup>−/−</jats:sup> ) mice were highly susceptible to SFTSV infection, and all mice died within 3 to 4 days after subcutaneous inoculation of 10 <jats:sup>6</jats:sup> focus-forming units of SFTSV. Histologic examination of tissues of IFNAR <jats:sup>−/−</jats:sup> mice infected with SFTSV showed no detectable lesions. In contrast, by immunohistochemistry virus antigen was found in liver, intestine, kidney, spleen, lymphoid tissue, and brain, but not in the lungs. Mesenteric lymph nodes and spleen were the most heavily infected tissues. Quantitative reverse transcription-PCR (RT-PCR) confirmed the presence of virus in these tissues. Confocal microscopy showed that SFTSV colocalized with reticular cells but did not colocalize with dendritic cells, monocytes/macrophages, neutrophils, or endothelium. Our results indicate that SFTSV multiplied in all organs except for lungs and that mesenteric lymph nodes and spleen were the most heavily infected tissues. The major target cells of SFTSV appear to be reticular cells in lymphoid tissues of intestine and spleen. </jats:p> The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever Journal of Virology |
| spellingShingle | Liu, Yan, Wu, Bin, Paessler, Slobodan, Walker, David H., Tesh, Robert B., Yu, Xue-jie, Journal of Virology, The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever, Virology, Insect Science, Immunology, Microbiology |
| title | The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_full | The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_fullStr | The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_full_unstemmed | The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_short | The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| title_sort | the pathogenesis of severe fever with thrombocytopenia syndrome virus infection in alpha/beta interferon knockout mice: insights into the pathologic mechanisms of a new viral hemorrhagic fever |
| title_unstemmed | The Pathogenesis of Severe Fever with Thrombocytopenia Syndrome Virus Infection in Alpha/Beta Interferon Knockout Mice: Insights into the Pathologic Mechanisms of a New Viral Hemorrhagic Fever |
| topic | Virology, Insect Science, Immunology, Microbiology |
| url | http://dx.doi.org/10.1128/jvi.02277-13 |