Differential Virological and Immunological Outcome of Severe Acute Respiratory Syndrome Coronavirus Infection in Susceptible and Resistant Transgenic Mice Expressing Human Angiotensin-Converting Enzyme 2
Identifieur interne : 000216 ( PascalFrancis/Checkpoint ); précédent : 000215; suivant : 000217Differential Virological and Immunological Outcome of Severe Acute Respiratory Syndrome Coronavirus Infection in Susceptible and Resistant Transgenic Mice Expressing Human Angiotensin-Converting Enzyme 2
Auteurs : Naoko Yoshikawa [États-Unis] ; Tomoki Yoshikawa [États-Unis] ; Terence Hill [États-Unis] ; CHENG HUANG [États-Unis] ; Douglas M. Watts [États-Unis] ; Shinji Makino [États-Unis] ; Gregg Milligan [États-Unis] ; Tehsheng Chan [États-Unis] ; Clarence J. Peter [États-Unis] ; Chien-Te K. Tseng [États-Unis]Source :
- Journal of virology [ 0022-538X ] ; 2009.
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- Pascal (Inist)
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- topic : Animal transgénique, Homme.
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Abstract
We previously reported that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), were highly susceptible to SARS-CoV infection, which resulted in the development of disease of various severity and even death in some lineages. In this study, we further characterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages, AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively. The kinetics of virus replication and the inflammatory responses within the lungs and brains, as well as the clinical and pathological outcomes, were assessed in each lineage. In addition, we generated information on lymphocyte subsets and mitogen-mediated proliferation of splenocytes. We found that while both lineages were permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appeared to be more intense in AC70 than in AC22 mice, especially in the brain. Moreover, such infection was accompanied by a more profound immune suppression in the former, as evidenced by the extensive loss ofT cells, compromised responses to concanavalin A stimulation, and absence of inflammatory infiltrates within the brain. We also found that CD8+ T cells were partially effective in attenuating the pathogenesis of SARS-CoV infection in lethality-resistant AC22 mice. Collectively, our data revealed a more intense viral infection and immunosuppression in AC70 mice than in AC22 mice, thereby providing us with an immunopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Differential Virological and Immunological Outcome of Severe Acute Respiratory Syndrome Coronavirus Infection in Susceptible and Resistant Transgenic Mice Expressing Human Angiotensin-Converting Enzyme 2</title><author><name sortKey="Yoshikawa, Naoko" sort="Yoshikawa, Naoko" uniqKey="Yoshikawa N" first="Naoko" last="Yoshikawa">Naoko Yoshikawa</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Yoshikawa, Tomoki" sort="Yoshikawa, Tomoki" uniqKey="Yoshikawa T" first="Tomoki" last="Yoshikawa">Tomoki Yoshikawa</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Hill, Terence" sort="Hill, Terence" uniqKey="Hill T" first="Terence" last="Hill">Terence Hill</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Cheng Huang" sort="Cheng Huang" uniqKey="Cheng Huang" last="Cheng Huang">CHENG HUANG</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Watts, Douglas M" sort="Watts, Douglas M" uniqKey="Watts D" first="Douglas M." last="Watts">Douglas M. 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Peter</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Pathology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Center for Biodefense and Emerging Infectious Disease, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K." last="Tseng">Chien-Te K. Tseng</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Center for Biodefense and Emerging Infectious Disease, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">09-0239898</idno><date when="2009">2009</date><idno type="stanalyst">PASCAL 09-0239898 INIST</idno><idno type="RBID">Pascal:09-0239898</idno><idno type="wicri:Area/PascalFrancis/Corpus">000216</idno><idno type="wicri:Area/PascalFrancis/Curation">000772</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000216</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000216</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Differential Virological and Immunological Outcome of Severe Acute Respiratory Syndrome Coronavirus Infection in Susceptible and Resistant Transgenic Mice Expressing Human Angiotensin-Converting Enzyme 2</title><author><name sortKey="Yoshikawa, Naoko" sort="Yoshikawa, Naoko" uniqKey="Yoshikawa N" first="Naoko" last="Yoshikawa">Naoko Yoshikawa</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Yoshikawa, Tomoki" sort="Yoshikawa, Tomoki" uniqKey="Yoshikawa T" first="Tomoki" last="Yoshikawa">Tomoki Yoshikawa</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Hill, Terence" sort="Hill, Terence" uniqKey="Hill T" first="Terence" last="Hill">Terence Hill</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Cheng Huang" sort="Cheng Huang" uniqKey="Cheng Huang" last="Cheng Huang">CHENG HUANG</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Watts, Douglas M" sort="Watts, Douglas M" uniqKey="Watts D" first="Douglas M." last="Watts">Douglas M. Watts</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Pathology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Milligan, Gregg" sort="Milligan, Gregg" uniqKey="Milligan G" first="Gregg" last="Milligan">Gregg Milligan</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Pediatrics, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Chan, Tehsheng" sort="Chan, Tehsheng" uniqKey="Chan T" first="Tehsheng" last="Chan">Tehsheng Chan</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Peter, Clarence J" sort="Peter, Clarence J" uniqKey="Peter C" first="Clarence J." last="Peter">Clarence J. Peter</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Pathology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Center for Biodefense and Emerging Infectious Disease, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author><author><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K." last="Tseng">Chien-Te K. Tseng</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Center for Biodefense and Emerging Infectious Disease, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Galveston, Texas 77555-0609</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Coronavirus</term><term>Human</term><term>Infection</term><term>Mouse</term><term>Prognosis</term><term>Resistance</term><term>Severe acute respiratory syndrome</term><term>Transgenic animal</term><term>Virology</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term><term>Animal transgénique</term><term>Souris</term><term>Homme</term><term>Pronostic</term><term>Infection</term><term>Résistance</term><term>Virologie</term><term>Syndrome respiratoire aigu sévère</term><term>Angiotensin converting enzyme 2</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Animal transgénique</term><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We previously reported that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), were highly susceptible to SARS-CoV infection, which resulted in the development of disease of various severity and even death in some lineages. In this study, we further characterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages, AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively. The kinetics of virus replication and the inflammatory responses within the lungs and brains, as well as the clinical and pathological outcomes, were assessed in each lineage. In addition, we generated information on lymphocyte subsets and mitogen-mediated proliferation of splenocytes. We found that while both lineages were permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appeared to be more intense in AC70 than in AC22 mice, especially in the brain. Moreover, such infection was accompanied by a more profound immune suppression in the former, as evidenced by the extensive loss ofT cells, compromised responses to concanavalin A stimulation, and absence of inflammatory infiltrates within the brain. We also found that CD8<sup>+</sup> T cells were partially effective in attenuating the pathogenesis of SARS-CoV infection in lethality-resistant AC22 mice. Collectively, our data revealed a more intense viral infection and immunosuppression in AC70 mice than in AC22 mice, thereby providing us with an immunopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-538X</s0></fA01><fA03 i2="1"><s0>J. virol.</s0></fA03><fA05><s2>83</s2></fA05><fA06><s2>11</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Differential Virological and Immunological Outcome of Severe Acute Respiratory Syndrome Coronavirus Infection in Susceptible and Resistant Transgenic Mice Expressing Human Angiotensin-Converting Enzyme 2</s1></fA08><fA11 i1="01" i2="1"><s1>YOSHIKAWA (Naoko)</s1></fA11><fA11 i1="02" i2="1"><s1>YOSHIKAWA (Tomoki)</s1></fA11><fA11 i1="03" i2="1"><s1>HILL (Terence)</s1></fA11><fA11 i1="04" i2="1"><s1>CHENG HUANG</s1></fA11><fA11 i1="05" i2="1"><s1>WATTS (Douglas M.)</s1></fA11><fA11 i1="06" i2="1"><s1>MAKINO (Shinji)</s1></fA11><fA11 i1="07" i2="1"><s1>MILLIGAN (Gregg)</s1></fA11><fA11 i1="08" i2="1"><s1>CHAN (Tehsheng)</s1></fA11><fA11 i1="09" i2="1"><s1>PETER (Clarence J.)</s1></fA11><fA11 i1="10" i2="1"><s1>TSENG (Chien-Te K.)</s1></fA11><fA14 i1="01"><s1>Department of Microbiology and Immunology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Pathology, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Pediatrics, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>7 aut.</sZ></fA14><fA14 i1="04"><s1>Center for Biodefense and Emerging Infectious Disease, University of Texas Medical Branch</s1><s2>Galveston, Texas 77555-0609</s2><s3>USA</s3><sZ>9 aut.</sZ><sZ>10 aut.</sZ></fA14><fA20><s1>5451-5465</s1></fA20><fA21><s1>2009</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>13592</s2><s5>354000188443330150</s5></fA43><fA44><s0>0000</s0><s1>© 2009 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>40 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>09-0239898</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of virology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>We previously reported that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), were highly susceptible to SARS-CoV infection, which resulted in the development of disease of various severity and even death in some lineages. In this study, we further characterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages, AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively. The kinetics of virus replication and the inflammatory responses within the lungs and brains, as well as the clinical and pathological outcomes, were assessed in each lineage. In addition, we generated information on lymphocyte subsets and mitogen-mediated proliferation of splenocytes. We found that while both lineages were permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appeared to be more intense in AC70 than in AC22 mice, especially in the brain. Moreover, such infection was accompanied by a more profound immune suppression in the former, as evidenced by the extensive loss ofT cells, compromised responses to concanavalin A stimulation, and absence of inflammatory infiltrates within the brain. We also found that CD8<sup>+</sup> T cells were partially effective in attenuating the pathogenesis of SARS-CoV infection in lethality-resistant AC22 mice. Collectively, our data revealed a more intense viral infection and immunosuppression in AC70 mice than in AC22 mice, thereby providing us with an immunopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.</s0></fC01><fC02 i1="01" i2="X"><s0>002A05C10</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Coronavirus</s0><s2>NW</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Coronavirus</s0><s2>NW</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Coronavirus</s0><s2>NW</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Animal transgénique</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Transgenic animal</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Animal transgénico</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Souris</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Mouse</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Ratón</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Homme</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Human</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Hombre</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Pronostic</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Prognosis</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Pronóstico</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Infection</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Infection</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Infección</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Résistance</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Resistance</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Resistencia</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Virologie</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Virology</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Virología</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0><s2>NM</s2><s5>14</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0><s2>NM</s2><s5>14</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0><s2>NM</s2><s5>14</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Angiotensin converting enzyme 2</s0><s4>INC</s4><s5>79</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Coronaviridae</s0><s2>NW</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Coronaviridae</s0><s2>NW</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Coronaviridae</s0><s2>NW</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Nidovirales</s0><s2>NW</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Nidovirales</s0><s2>NW</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Nidovirales</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Pathologie de l'appareil respiratoire</s0><s5>13</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Respiratory disease</s0><s5>13</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0><s5>13</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Virose</s0></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Viral disease</s0></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Virosis</s0></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Pathologie des poumons</s0><s5>16</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Lung disease</s0><s5>16</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Pulmón patología</s0><s5>16</s5></fC07><fN21><s1>173</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Yoshikawa, Naoko" sort="Yoshikawa, Naoko" uniqKey="Yoshikawa N" first="Naoko" last="Yoshikawa">Naoko Yoshikawa</name></noRegion><name sortKey="Chan, Tehsheng" sort="Chan, Tehsheng" uniqKey="Chan T" first="Tehsheng" last="Chan">Tehsheng Chan</name><name sortKey="Cheng Huang" sort="Cheng Huang" uniqKey="Cheng Huang" last="Cheng Huang">CHENG HUANG</name><name sortKey="Hill, Terence" sort="Hill, Terence" uniqKey="Hill T" first="Terence" last="Hill">Terence Hill</name><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name><name sortKey="Milligan, Gregg" sort="Milligan, Gregg" uniqKey="Milligan G" first="Gregg" last="Milligan">Gregg Milligan</name><name sortKey="Peter, Clarence J" sort="Peter, Clarence J" uniqKey="Peter C" first="Clarence J." last="Peter">Clarence J. Peter</name><name sortKey="Peter, Clarence J" sort="Peter, Clarence J" uniqKey="Peter C" first="Clarence J." last="Peter">Clarence J. Peter</name><name sortKey="Peter, Clarence J" sort="Peter, Clarence J" uniqKey="Peter C" first="Clarence J." last="Peter">Clarence J. Peter</name><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K." last="Tseng">Chien-Te K. Tseng</name><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K." last="Tseng">Chien-Te K. Tseng</name><name sortKey="Watts, Douglas M" sort="Watts, Douglas M" uniqKey="Watts D" first="Douglas M." last="Watts">Douglas M. Watts</name><name sortKey="Yoshikawa, Tomoki" sort="Yoshikawa, Tomoki" uniqKey="Yoshikawa T" first="Tomoki" last="Yoshikawa">Tomoki Yoshikawa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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