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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID 		Ace2tm1Pngr
targeted mutation 1, Josef M Penninger
MGI:2661723
Summary 11 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
 		Ace2tm1Pngr/Ace2tm1Pngr B6.129P2-Ace2tm1Pngr/J MGI:6402915
hm2
 		Ace2tm1Pngr/Ace2tm1Pngr involves: 129P2/OlaHsd MGI:6402529
hm3
 		Ace2tm1Pngr/Ace2tm1Pngr involves: 129P2/OlaHsd * C57BL/6 MGI:2661729
hm4
 		Ace2tm1Pngr/Ace2tm1Pngr involves: 129P2/OlaHsd * C57BL/6J MGI:6402565
cx5
 		Acetm1Unc/Acetm1Unc
Ace2tm1Pngr/Y 		involves: 129P2/OlaHsd MGI:2661733
cx6
 		Acetm1Unc/Acetm1Unc
Ace2tm1Pngr/Ace2tm1Pngr 		involves: 129P2/OlaHsd MGI:2661736
cx7
 		Ace2tm1Pngr/Y
Pik3cgtm1Pngr/Pik3cgtm1Pngr 		involves: 129P2/OlaHsd * C57BL/6 MGI:5912245
ot8
 		Ace2tm1Pngr/Y B6.129P2-Ace2tm1Pngr/J MGI:5912243
ot9
 		Ace2tm1Pngr/Y involves: 129P2/OlaHsd MGI:6402530
ot10
 		Ace2tm1Pngr/Y involves: 129P2/OlaHsd * C57BL/6 MGI:2661730
ot11
 		Ace2tm1Pngr/Y involves: 129P2/OlaHsd * C57BL/6J MGI:6402568


Genotype
MGI:6402915
hm1
Allelic
Composition		 Ace2tm1Pngr/Ace2tm1Pngr
Genetic
Background		 B6.129P2-Ace2tm1Pngr/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
immune system
decreased susceptibility to Coronaviridae infection ( J:286299 )
• mice show decreased susceptibility to intranasal infection with severe acute respiratory syndrome coronavirus (SARS-CoV; Beijing strain, PUMC01 isolate) , showing lower levels of infectious virus in the lungs, reduced copy numbers of the SARS-CoV Spike RNA, and reduced pathologic alterations in lungs compared to infected wild-type mice




Genotype
MGI:6402529
hm2
Allelic
Composition		 Ace2tm1Pngr/Ace2tm1Pngr
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
abnormal susceptibility to injury induced morbidity/mortality ( J:100334 )
• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
increased susceptibility to bacterial infection induced morbidity/mortality ( J:282139 )
• mice exhibit decreased survival following P. aeruginosa infection

growth/size/body
increased susceptibility to weight loss ( J:282139 )
• mice infected with P. aeruginosa show a greater decrease in body weight than wild-type mice

homeostasis/metabolism
pulmonary edema ( J:100334 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
increased angiotensin II level ( J:100334 )
• acid-treated mice show a greater increase in angiotensin II levels in the lungs than similarly treated controls
increased circulating angiotensin II level ( J:100334 )
• acid-treated mice show a greater increase in angiotensin II levels in plasma than similarly treated controls
abnormal susceptibility to injury induced morbidity/mortality ( J:100334 )
• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
increased susceptibility to injury ( J:100334 )
• mice exhibit enhanced acute lung injury after acid aspiration, cecal ligation and perforation (CLP), or endotoxin challenge compared to controls
• mice exposed to acid aspiration show worsened oxygenation, massive lung edema, increased inflammatory cell infiltration and hyaline membrane formation compared to controls
• CLP-treated mutant mice show worsening of lung function, increased edema, and leukocyte accumulation
• pharmacological inhibition of angiotensin II type 1 receptor with Losartan attenuates the severity of acid-induced lung injury
• however, inhibition of angiotensin II type 2 receptor with PD123.319 has no effect on the acute lung injury

hematopoietic system
increased neutrophil cell number ( J:282139 )
• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs

immune system
increased neutrophil cell number ( J:282139 )
• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs
lung inflammation ( J:100334 , J:282139 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation, respectively, compared to controls (J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils (J:282139)
increased susceptibility to bacterial infection ( J:282139 )
• mice infected with P. aeruginosa exhibit weight loss, enhanced lung permeability, increased neutrophil infiltration into the lungs, reduced bacterial outgrowth in bronchoalveolar lavage fluid, and exaggerated lung inflammation and lung injury compared to controls
increased susceptibility to bacterial infection induced morbidity/mortality ( J:282139 )
• mice exhibit decreased survival following P. aeruginosa infection

respiratory system
pulmonary edema ( J:100334 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
lung inflammation ( J:100334 , J:282139 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation, respectively, compared to controls (J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils (J:282139)
increased susceptibility to pulmonary hyaline membrane formation ( J:100334 )
• mice exposed to acid aspiration show hyaline membrane formation
increased lung elastance ( J:100334 )
• mice exposed to acid aspiration, CLP or endotoxin challenge to induce acute lung injury show greater lung elastance compared to controls

cardiovascular system
increased vascular permeability ( J:100334 )
• mice exposed to acid aspiration show greatly increased pulmonary vascular permeability




Genotype
MGI:2661729
hm3
Allelic
Composition		 Ace2tm1Pngr/Ace2tm1Pngr
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
decreased cardiac muscle contractility ( J:77232 )
• less severe than in age matched mutant male mice

muscle
decreased cardiac muscle contractility ( J:77232 )
• less severe than in age matched mutant male mice




Genotype
MGI:6402565
hm4
Allelic
Composition		 Ace2tm1Pngr/Ace2tm1Pngr
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
increased susceptibility to Orthomyxoviridae infection induced morbidity/mortality ( J:277074 )
• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls

immune system
lung inflammation ( J:277074 )
• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
increased susceptibility to Orthomyxoviridae infection ( J:277074 )
• mice show increased susceptibility to H5N1 avian flu virus (A/chicken/Jilin/9/2004) infection, showing higher viral load in lungs 5 days after infection and greater lung injury, including increased alveolar wall thickness, formation of hyaline membranes, and proteinaceous debris filling the airspaces
increased susceptibility to Orthomyxoviridae infection induced morbidity/mortality ( J:277074 )
• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls

homeostasis/metabolism
pulmonary edema ( J:277074 )
• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls

respiratory system
pulmonary edema ( J:277074 )
• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls
lung inflammation ( J:277074 )
• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
increased susceptibility to pulmonary hyaline membrane formation ( J:277074 )
• H5N1 virus-infected mice show formation of hyaline membranes




Genotype
MGI:2661733
cx5
Allelic
Composition		 Acetm1Unc/Acetm1Unc
Ace2tm1Pngr/Y
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
Acetm1Unc mutation (1 available); any Ace mutation (57 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
hypotension ( J:77232 )
• similar to Acetm1Unc homozygotes however normal cardiac contractility is seen at 6 months of age unlike in Acetm1Unc homozygotes

homeostasis/metabolism
decreased angiotensin II level ( J:100334 )
• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in lung compared to single Ace2tm1Pngr mutants
decreased circulating angiotensin II level ( J:100334 )
• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in plasma compared to single Ace2tm1Pngr mutants
decreased susceptibility to injury ( J:100334 )
• mice show rescue of severe lung failure, edema formation, and histological lung changes induced by acid aspiration in single Ace2tm1Pngr mutants
• mice show rescue of the severe lung impairments seen in single Ace2tm1Pngr mutants with endotoxin-induced acute lung injury

renal/urinary system
abnormal kidney morphology ( J:77232 )
• similar to Acetm1Unc homozygotes




Genotype
MGI:2661736
cx6
Allelic
Composition		 Acetm1Unc/Acetm1Unc
Ace2tm1Pngr/Ace2tm1Pngr
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
Acetm1Unc mutation (1 available); any Ace mutation (57 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
hypotension ( J:77232 )
• similar to Acetm1Unc homozygotes however normal cardiac contractility is seen unlike Acetm1Unc homozygotes

homeostasis/metabolism
decreased angiotensin II level ( J:100334 )
• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in lung compared to single Ace2tm1Pngr mutants
decreased circulating angiotensin II level ( J:100334 )
• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in plasma compared to single Ace2tm1Pngr mutants
decreased susceptibility to injury ( J:100334 )
• mice show rescue of severe lung failure, edema formation, and histological lung changes induced by acid aspiration in single Ace2tm1Pngr mutants
• mice show rescue of the severe lung impairments seen in single Ace2tm1Pngr mutants with endotoxin-induced acute lung injury

renal/urinary system
abnormal kidney morphology ( J:77232 )
• similar to Acetm1Unc homozygotes




Genotype
MGI:5912245
cx7
Allelic
Composition		 Ace2tm1Pngr/Y
Pik3cgtm1Pngr/Pik3cgtm1Pngr
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
Pik3cgtm1Pngr mutation (0 available); any Pik3cg mutation (59 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
increased cardiac muscle contractility ( J:124548 )
• increase in basal myocardial contractility
• mice exhibit a partial reversal of myocardial hypertrophy, prevention of neutrophil infiltration into myocardial tissue, and prevention of systolic function deterioration

muscle
increased cardiac muscle contractility ( J:124548 )
• increase in basal myocardial contractility
• mice exhibit a partial reversal of myocardial hypertrophy, prevention of neutrophil infiltration into myocardial tissue, and prevention of systolic function deterioration




Genotype
MGI:5912243
ot8
Allelic
Composition		 Ace2tm1Pngr/Y
Genetic
Background		 B6.129P2-Ace2tm1Pngr/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
cardiovascular system phenotype ( J:124548 )
N
• heart angiotensin II levels are not elevated and superoxide production is normal indicating lack of oxidative stress in aged mice

immune system
decreased susceptibility to Coronaviridae infection ( J:286299 )
• mice show decreased susceptibility to intranasal infection with severe acute respiratory syndrome coronavirus (SARS-CoV; Beijing strain, PUMC01 isolate) , showing lower levels of infectious virus in the lungs, reduced copy numbers of the SARS-CoV Spike RNA, and reduced pathologic alterations in lungs compared to infected wild-type mice




Genotype
MGI:6402530
ot9
Allelic
Composition		 Ace2tm1Pngr/Y
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
abnormal susceptibility to injury induced morbidity/mortality ( J:100334 )
• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
increased susceptibility to bacterial infection induced morbidity/mortality ( J:282139 )
• mice exhibit decreased survival following P. aeruginosa infection

growth/size/body
increased susceptibility to weight loss ( J:282139 )
• mice infected with P. aeruginosa show a greater decrease in body weight than wild-type mice

homeostasis/metabolism
pulmonary edema ( J:100334 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
increased angiotensin II level ( J:100334 )
• acid-treated mice show a greater increase in angiotensin II levels in the lungs than similarly treated controls
increased circulating angiotensin II level ( J:100334 )
• acid-treated mice show a greater increase in angiotensin II levels in plasma than similarly treated controls
abnormal susceptibility to injury induced morbidity/mortality ( J:100334 )
• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
increased susceptibility to injury ( J:100334 )
• CLP-treated mutant mice show worsening of lung function, increased edema, and leukocyte accumulation
• mice exposed to acid aspiration show worsened oxygenation, massive lung edema, increased inflammatory cell infiltration and hyaline membrane formation compared to controls
• mice exhibit enhanced acute lung injury after acid aspiration, cecal ligation and perforation (CLP), or endotoxin challenge compared to controls
• pharmacological inhibition of angiotensin II type 1 receptor with Losartan attenuates the severity of acid-induced lung injury
• however, inhibition of angiotensin II type 2 receptor with PD123.319 has no effect on the acute lung injury

hematopoietic system
increased neutrophil cell number ( J:282139 )
• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs

immune system
increased neutrophil cell number ( J:282139 )
• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs
lung inflammation ( J:100334 , J:282139 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation compared to controls (J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils (J:282139)
increased susceptibility to bacterial infection ( J:282139 )
• mice infected with P. aeruginosa exhibit weight loss, enhanced lung permeability, increased neutrophil infiltration into the lungs, reduced bacterial outgrowth in bronchoalveolar lavage fluid, and exaggerated lung inflammation and lung injury compared to controls
increased susceptibility to bacterial infection induced morbidity/mortality ( J:282139 )
• mice exhibit decreased survival following P. aeruginosa infection

respiratory system
pulmonary edema ( J:100334 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
lung inflammation ( J:100334 , J:282139 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation compared to controls (J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils (J:282139)
increased susceptibility to pulmonary hyaline membrane formation ( J:100334 )
• mice exposed to acid aspiration show hyaline membrane formation
increased lung elastance ( J:100334 )
• mice exposed to acid aspiration, CLP, or endotoxin challenge to induce acute lung injury show greater lung elastance compared to controls

cardiovascular system
increased vascular permeability ( J:100334 )
• mice exposed to acid aspiration show greatly increased pulmonary vascular permeability




Genotype
MGI:2661730
ot10
Allelic
Composition		 Ace2tm1Pngr/Y
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
cardiac hypertrophy ( J:124548 )
• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• hearts show upregulation of hypertrophic disease markers ANF and BNP
decreased heart left ventricle wall thickness ( J:77232 )
• slight thinning of the left ventricular wall resulting in mild dilation, 6 months of age
dilated heart ventricle ( J:124548 )
• ventricular dilation at 6 and 12 months of age
dilated heart left ventricle ( J:124548 )
• progressive left ventricular dilation and reduced systolic function with increasing age
abnormal cardiovascular system physiology ( J:124548 )
• age-dependent and progressive decline in cardiac function
dilated cardiomyopathy ( J:124548 )
• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• young mice treated with the specific AT1 receptor blocker, irbesartan, until 12 months of age prevents the development of dilated cardiomyopathy at 6 months and persists until 12 months of age
decreased cardiac muscle contractility ( J:77232 , J:124548 )
• more severe at 6 months of age than at 3 months of age (J:77232)
• more severe in 6 month old males than in age matched female mutant mice (J:77232)
• decrease in fractional shortening and velocity of circumferential shortening corrected for heart rate, decreased peak aortic velocity corrected for heart rate (J:124548)
• rightward displacement of the pressure-volume curve indicating reduced systolic function (J:124548)
abnormal heart echocardiography feature ( J:124548 )
• echocardiography indicates increased left ventricular end diastolic and systolic dimension, decreased fractional shortening, decreased velocity of circumferential shortening corrected for heart rate, decreased peak aortic velocity corrected for heart rate, increased left ventricle end diastolic pressure, and decreased maximum and minimum first derivative of the left ventricle pressure (+dP/dt and dP/dt)
increased left ventricle diastolic pressure ( J:124548 )
• increase in left ventricle end diastolic pressure
hypotension ( J:77232 )
• reduced blood pressure observed at 6 months of age
• blood pressure was normal at 3 months of age
heart inflammation ( J:124548 )
• 4-fold increase in neutrophil infiltration in the myocardium of aged mice
• however, no macrophage infiltration into the myocardium is seen
• treatment with irbesartan prevents neutrophil infiltration in the myocardium

growth/size/body
cardiac hypertrophy ( J:124548 )
• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• hearts show upregulation of hypertrophic disease markers ANF and BNP

cellular
oxidative stress ( J:124548 )
• myocardial aldehyde levels are increased in mice indicating chronic myocardial oxidative damage
• treatment with irbesartan normalizes myocardial aldehyde levels

homeostasis/metabolism
abnormal cytokine level ( J:124548 )
• increase in expression of inflammatory cytokines, IL-1beta, IL-6, and MCP-1 in aged mice
• treatment with irbesartan prevents increased expression of inflammatory cytokines
increased NAD(P)H oxidase activity ( J:124548 )
• NADPH oxidase activity is increase in the left ventricle of 6 month old mice
• mice treated with irbesartan to block AT1 suppresses the increase in NADPH oxidase activity

muscle
dilated cardiomyopathy ( J:124548 )
• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• young mice treated with the specific AT1 receptor blocker, irbesartan, until 12 months of age prevents the development of dilated cardiomyopathy at 6 months and persists until 12 months of age
decreased cardiac muscle contractility ( J:77232 , J:124548 )
• more severe at 6 months of age than at 3 months of age (J:77232)
• more severe in 6 month old males than in age matched female mutant mice (J:77232)
• decrease in fractional shortening and velocity of circumferential shortening corrected for heart rate, decreased peak aortic velocity corrected for heart rate (J:124548)
• rightward displacement of the pressure-volume curve indicating reduced systolic function (J:124548)

immune system
heart inflammation ( J:124548 )
• 4-fold increase in neutrophil infiltration in the myocardium of aged mice
• however, no macrophage infiltration into the myocardium is seen
• treatment with irbesartan prevents neutrophil infiltration in the myocardium
abnormal cytokine level ( J:124548 )
• increase in expression of inflammatory cytokines, IL-1beta, IL-6, and MCP-1 in aged mice
• treatment with irbesartan prevents increased expression of inflammatory cytokines

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
congestive heart failure DOID:6000 J:124548




Genotype
MGI:6402568
ot11
Allelic
Composition		 Ace2tm1Pngr/Y
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ace2tm1Pngr mutation (1 available); any Ace2 mutation (66 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
increased susceptibility to Orthomyxoviridae infection induced morbidity/mortality ( J:277074 )
• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls

immune system
lung inflammation ( J:277074 )
• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
increased susceptibility to Orthomyxoviridae infection ( J:277074 )
• mice show increased susceptibility to H5N1 avian flu virus (A/chicken/Jilin/9/2004) infection, showing higher viral load in lungs 5 days after infection and greater lung injury, including increased alveolar wall thickness, formation of hyaline membranes, and proteinaceous debris filling the airspaces
increased susceptibility to Orthomyxoviridae infection induced morbidity/mortality ( J:277074 )
• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls

homeostasis/metabolism
pulmonary edema ( J:277074 )
• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls

respiratory system
pulmonary edema ( J:277074 )
• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls
lung inflammation ( J:277074 )
• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
increased susceptibility to pulmonary hyaline membrane formation ( J:277074 )
• H5N1 virus-infected mice show formation of hyaline membranes




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Send questions and comments to User Support. 		last database update
11/12/2024
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