Pathological and virological findings of type I interferon receptor knockout mice upon experimental infection with Heartland virus
Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR ) mice infected intraperitoneally with 1 × 10 tissue culture-infective dose (TCID ) of HRTV died, while those subcutaneously infected with...
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| Published in | Virus research Vol. 340; p. 199301 |
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| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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01.02.2024
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| Abstract | Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR
) mice infected intraperitoneally with 1 × 10
tissue culture-infective dose (TCID
) of HRTV died, while those subcutaneously infected with the same dose of HRTV did not. The pathophysiology of IFNAR
mice infected with HRTV and the mechanism underlying the difference in disease severity, which depends on HRTV infection route, were analyzed in this study. The liver, spleen, mesenteric and axillary lymph nodes, and gastrointestinal tract of intraperitoneally (I.P.) infected mice had pathological changes; however, subcutaneously (S.C.) infected mice only had pathological changes in the axillary lymph node and gastrointestinal tract. HRTV RNA levels in the mesenteric lymph node, lung, liver, spleen, kidney, stomach, intestine, and blood were significantly higher in I.P. infected mice than those in the S.C. infected mice. Chemokine ligand-1 (CXCL-1), tumor necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, and IL-10 levels in plasma of I.P. infected mice were higher than those of S.C. infected mice plasma. These results indicated that high levels of viral RNA and the induction of inflammatory responses in HRTV-infected IFNAR
mice may be associated with disease severity. |
|---|---|
| AbstractList | Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR
) mice infected intraperitoneally with 1 × 10
tissue culture-infective dose (TCID
) of HRTV died, while those subcutaneously infected with the same dose of HRTV did not. The pathophysiology of IFNAR
mice infected with HRTV and the mechanism underlying the difference in disease severity, which depends on HRTV infection route, were analyzed in this study. The liver, spleen, mesenteric and axillary lymph nodes, and gastrointestinal tract of intraperitoneally (I.P.) infected mice had pathological changes; however, subcutaneously (S.C.) infected mice only had pathological changes in the axillary lymph node and gastrointestinal tract. HRTV RNA levels in the mesenteric lymph node, lung, liver, spleen, kidney, stomach, intestine, and blood were significantly higher in I.P. infected mice than those in the S.C. infected mice. Chemokine ligand-1 (CXCL-1), tumor necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, and IL-10 levels in plasma of I.P. infected mice were higher than those of S.C. infected mice plasma. These results indicated that high levels of viral RNA and the induction of inflammatory responses in HRTV-infected IFNAR
mice may be associated with disease severity. Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR-/-) mice infected intraperitoneally with 1 × 107 tissue culture-infective dose (TCID50) of HRTV died, while those subcutaneously infected with the same dose of HRTV did not. The pathophysiology of IFNAR-/- mice infected with HRTV and the mechanism underlying the difference in disease severity, which depends on HRTV infection route, were analyzed in this study. The liver, spleen, mesenteric and axillary lymph nodes, and gastrointestinal tract of intraperitoneally (I.P.) infected mice had pathological changes; however, subcutaneously (S.C.) infected mice only had pathological changes in the axillary lymph node and gastrointestinal tract. HRTV RNA levels in the mesenteric lymph node, lung, liver, spleen, kidney, stomach, intestine, and blood were significantly higher in I.P. infected mice than those in S.C. infected mice. Chemokine ligand-1 (CXCL-1), tumor necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, and IL-10 levels in plasma of I.P. infected mice were higher than those of S.C. infected mice. These results indicated that high levels of viral RNA and the induction of inflammatory responses in HRTV-infected IFNAR-/- mice may be associated with disease severity.Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR-/-) mice infected intraperitoneally with 1 × 107 tissue culture-infective dose (TCID50) of HRTV died, while those subcutaneously infected with the same dose of HRTV did not. The pathophysiology of IFNAR-/- mice infected with HRTV and the mechanism underlying the difference in disease severity, which depends on HRTV infection route, were analyzed in this study. The liver, spleen, mesenteric and axillary lymph nodes, and gastrointestinal tract of intraperitoneally (I.P.) infected mice had pathological changes; however, subcutaneously (S.C.) infected mice only had pathological changes in the axillary lymph node and gastrointestinal tract. HRTV RNA levels in the mesenteric lymph node, lung, liver, spleen, kidney, stomach, intestine, and blood were significantly higher in I.P. infected mice than those in S.C. infected mice. Chemokine ligand-1 (CXCL-1), tumor necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, and IL-10 levels in plasma of I.P. infected mice were higher than those of S.C. infected mice. These results indicated that high levels of viral RNA and the induction of inflammatory responses in HRTV-infected IFNAR-/- mice may be associated with disease severity. Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR-/-) mice infected intraperitoneally with 1 × 107 tissue culture-infective dose (TCID50) of HRTV died, while those subcutaneously infected with the same dose of HRTV did not. The pathophysiology of IFNAR-/- mice infected with HRTV and the mechanism underlying the difference in disease severity, which depends on HRTV infection route, were analyzed in this study. The liver, spleen, mesenteric and axillary lymph nodes, and gastrointestinal tract of intraperitoneally (I.P.) infected mice had pathological changes; however, subcutaneously (S.C.) infected mice only had pathological changes in the axillary lymph node and gastrointestinal tract. HRTV RNA levels in the mesenteric lymph node, lung, liver, spleen, kidney, stomach, intestine, and blood were significantly higher in I.P. infected mice than those in S.C. infected mice. Chemokine ligand-1 (CXCL-1), tumor necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, and IL-10 levels in plasma of I.P. infected mice were higher than those of S.C. infected mice. These results indicated that high levels of viral RNA and the induction of inflammatory responses in HRTV-infected IFNAR-/- mice may be associated with disease severity. Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR⁻/⁻) mice infected intraperitoneally with 1 × 10⁷ tissue culture-infective dose (TCID₅₀) of HRTV died, while those subcutaneously infected with the same dose of HRTV did not. The pathophysiology of IFNAR⁻/⁻ mice infected with HRTV and the mechanism underlying the difference in disease severity, which depends on HRTV infection route, were analyzed in this study. The liver, spleen, mesenteric and axillary lymph nodes, and gastrointestinal tract of intraperitoneally (I.P.) infected mice had pathological changes; however, subcutaneously (S.C.) infected mice only had pathological changes in the axillary lymph node and gastrointestinal tract. HRTV RNA levels in the mesenteric lymph node, lung, liver, spleen, kidney, stomach, intestine, and blood were significantly higher in I.P. infected mice than those in the S.C. infected mice. Chemokine ligand-1 (CXCL-1), tumor necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, and IL-10 levels in plasma of I.P. infected mice were higher than those of S.C. infected mice plasma. These results indicated that high levels of viral RNA and the induction of inflammatory responses in HRTV-infected IFNAR⁻/⁻ mice may be associated with disease severity. • HRTV RNA levels in I.P. mice were significantly higher than those in S.C. mice. • Cytokines and chemokines levels in I.P. mice were higher than those in S.C. mice. • Infection severity is associated with viral RNA level and inflammatory responses. Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout (IFNAR - / - ) mice infected intraperitoneally with 1 × 10 7 tissue culture-infective dose (TCID 50 ) of HRTV died, while those subcutaneously infected with the same dose of HRTV did not. The pathophysiology of IFNAR - / - mice infected with HRTV and the mechanism underlying the difference in disease severity, which depends on HRTV infection route, were analyzed in this study. The liver, spleen, mesenteric and axillary lymph nodes, and gastrointestinal tract of intraperitoneally (I.P.) infected mice had pathological changes; however, subcutaneously (S.C.) infected mice only had pathological changes in the axillary lymph node and gastrointestinal tract. HRTV RNA levels in the mesenteric lymph node, lung, liver, spleen, kidney, stomach, intestine, and blood were significantly higher in I.P. infected mice than those in S.C. infected mice. Chemokine ligand-1 (CXCL-1), tumor necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, and IL-10 levels in plasma of I.P. infected mice were higher than those of S.C. infected mice. These results indicated that high levels of viral RNA and the induction of inflammatory responses in HRTV-infected IFNAR - / - mice may be associated with disease severity. |
| ArticleNumber | 199301 |
| Author | Taniguchi, Satoshi Shimojima, Masayuki Harada, Shizuko Saijo, Masayuki Ebihara, Hideki Watanabe, Shumpei Yamada, Souichi Lim, Chang Kweng Nagata, Noriyo Uda, Akihiko Takayama-Ito, Mutsuyo Kurosu, Takeshi Fujii, Hikaru Morikawa, Shigeru Maeki, Takahiro Fukushi, Shuetsu Nakayama, Eri Tani, Hideki Yoshikawa, Tomoki |
| Author_xml | – sequence: 1 givenname: Hikaru orcidid: 0000-0002-0603-7096 surname: Fujii fullname: Fujii, Hikaru – sequence: 2 givenname: Shuetsu surname: Fukushi fullname: Fukushi, Shuetsu – sequence: 3 givenname: Tomoki surname: Yoshikawa fullname: Yoshikawa, Tomoki – sequence: 4 givenname: Noriyo surname: Nagata fullname: Nagata, Noriyo – sequence: 5 givenname: Satoshi surname: Taniguchi fullname: Taniguchi, Satoshi – sequence: 6 givenname: Masayuki surname: Shimojima fullname: Shimojima, Masayuki – sequence: 7 givenname: Souichi surname: Yamada fullname: Yamada, Souichi – sequence: 8 givenname: Hideki surname: Tani fullname: Tani, Hideki – sequence: 9 givenname: Akihiko surname: Uda fullname: Uda, Akihiko – sequence: 10 givenname: Takahiro surname: Maeki fullname: Maeki, Takahiro – sequence: 11 givenname: Shizuko surname: Harada fullname: Harada, Shizuko – sequence: 12 givenname: Takeshi surname: Kurosu fullname: Kurosu, Takeshi – sequence: 13 givenname: Chang Kweng surname: Lim fullname: Lim, Chang Kweng – sequence: 14 givenname: Eri surname: Nakayama fullname: Nakayama, Eri – sequence: 15 givenname: Mutsuyo surname: Takayama-Ito fullname: Takayama-Ito, Mutsuyo – sequence: 16 givenname: Shumpei surname: Watanabe fullname: Watanabe, Shumpei – sequence: 17 givenname: Hideki surname: Ebihara fullname: Ebihara, Hideki – sequence: 18 givenname: Shigeru surname: Morikawa fullname: Morikawa, Shigeru – sequence: 19 givenname: Masayuki surname: Saijo fullname: Saijo, Masayuki |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38096954$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1016/j.blre.2020.100733 10.1126/science.8009221 10.3201/eid2212.160472 10.3201/eid1911.130792 10.1055/s-2007-985757 10.1007/s00705-020-04731-2 10.1182/blood.V99.7.2455 10.1002/ajh.25982 10.1093/cid/ciu434 10.1016/j.virol.2017.08.004 10.3389/fmicb.2017.00104 10.3390/v10090498 10.1177/1076029620938149 10.1056/NEJMoa1010095 10.3201/eid2110.150380 10.1080/22221751.2019.1710436 10.1111/j.1538-7836.2009.03584.x 10.1074/jbc.M117.805127 10.4269/ajtmh.14-0702 10.3390/v14081668 10.1038/sigtrans.2017.23 10.4269/ajtmh.13-0209 10.1128/jvi.00049-22 10.1080/1040841X.2020.1847037 10.1093/infdis/jis452 10.1093/infdis/jit603 10.1056/NEJMoa1203378 10.1128/mSphere.00061-15 10.1016/j.jcv.2018.01.017 10.1128/mSphere.00234-17 10.1097/00001721-199603000-00011 10.3201/eid2405.171802 10.3201/eid2712.211426 10.3201/eid2505.181463 10.1186/s12985-016-0677-1 |
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| Keywords | Heartland virus pathogenesis animal model IFNAR(−/−) mice |
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| Snippet | Heartland virus (HRTV) causes generalized symptoms, severe shock, and multiple organ failure. We previously reported that interferon-α/β receptor knockout... • HRTV RNA levels in I.P. mice were significantly higher than those in S.C. mice. • Cytokines and chemokines levels in I.P. mice were higher than those in S.C.... |
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| SubjectTerms | Animal model blood chemokines digestive tract disease severity Heartland virus IFNAR-/- mice interferons interleukin-10 intestines kidneys liver lungs lymph lymph nodes Pathogenesis pathophysiology RNA spleen stomach tumor necrosis factors viruses |
| Title | Pathological and virological findings of type I interferon receptor knockout mice upon experimental infection with Heartland virus |
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