Table 2.

Susceptibility, symptoms, viral replication and pathology in laboratory animals infected with SARS-CoV

Animal Species/Strain	Susceptibility and Symptoms	Viral replication/distribution in organs	Histopathological changes	Ref
African Green Monkeys (AGM), Rhesus Monkeys (RM), Cynomolgus Monkeys (CM) (infected with 106 TCID50 of SARS-CoV strain)	▪ No clinical signs of respiratory illness or fever in AGM, RM, CM (only 1/4 AGM monkey had 105oF rectal temperature on day 5) ▪ Primary infection protected from reinfection in AGM	▪ Viral replication observed in upper and lower respiratory tract of all the three species of monkeys ▪ Absence of virus in plasma, urine and fecal samples, viral RNA detected in fecal samples of AGM between day 8 and day 20 Post Inoculation(PI)	▪ Decrease of hemoglobin concentration and hematocrit in AGM but not in RM or CM ▪ Elevation of liver enzymes in AGM but not in RM or CM ▪ Focal interstitial mononuclear infiltration in lungs, edema, infiltration of macrophages in AGM	McAuliffe 2004
Common Marmosets (infection with 106 TCID50 of SARS-CoV Urbani strain)	▪ Mild symptoms of respiratory illness ▪ Significant increase in body temperature on day 4 and 7 PI ▪ Non-hemorrhagic diarrhea in 7/12 animals	▪ Viral RNA detected in lungs, tracheobronchial lymph nodes and heart ▪ No viral RNA detected in intestine and liver	▪ Multifocal atelectasis in lungs, tracheobronchial lymphadenopathy in 2/12 animals ▪ Pneumonitis and edema in lungs ▪ No gross pathological changes in heart, liver, kidneys, spleen or GI tract ▪ Multifocal hepatitis ▪ Mild diffuse colitis in 8/12 animals ▪ No renal pathology evident in any animals	Greenough, 2005
Cats (infected with 106 TCID50 of SARS-CoV strain)	▪ No clinical signs of illness	▪ Primary infected organ being the respiratory tract, lungs and intestine	▪ Multifocal pulmonary consolidation in 4/4 cats ▪ Lung histology reveals multifocal necrosis, type II pneumocyte hyperplasia, karyorrhexis, neutrophil infiltration in alveolar septa	van den Brand 2008
Ferrets (infected with 106 TCID50 of SARS-CoV strain)	▪ 4/4 animals lethargic 2-day PI ▪ 1/4 animal died on 4-day PI	▪ Primary infected organ being the respiratory tract and lungs	▪ Multifocal pulmonary consolidation in 4/4 ferret ▪ Exudative diffusive alveolar damage, infiltration of neutrophils and macrophages in alveolar septa, hypertrophy and hyperplasia in type II pneumocytes, lymphoid aggregation around pulmonary blood vessels ▪ Diffused hepatic lipidosis and congestion ▪ Lymphoid hyperplasia in trachea bronchial lymph nodes and spleen ▪ Enlarged lymph node and friable liver	van den Brand 2008
Hamsters (infected with 103/105 TCID50 of SARS-CoV strain)	▪ No weight loss or clinical signs of disease ▪ Animals recovering from primary infection protected by secondary challenge on day 28	▪ Respiratory tract and lungs ▪ Virus not distributed in liver, spleen, kidneys, GI tract or other organs	▪ Blebbing and swelling of luminal cytoplasm in bronchi, trachea and nasal tract ▪ Mono nuclear cell infiltrates in submucosal epithelium of bronchioles and nasal tract ▪ Multifocal areas of consolidation round the bronchioles ▪ Damages in nasal passage healed on 5 day PI and viral antigen not detectable in lungs 7 days PI	Roberts 2005b
BalbC mice (12-14-month old infected with 105 TCID50 SARS-CoV urbani strain)	▪ Clinical signs of disease observed like weight loss, ruffled fur, dehydration upto 7-day PI	▪ Virus detected in upper respiratory tract, lungs and liver ▪ Virus not detected in whole blood	▪ Airway epithelial necrosis, multifocal and interstitial lymphohystiocytic infiltration and proteinaceous deposition around the alveolar walls, intra-alveolar edema evident from IHC ▪ Levels of IFNα, IFNγ, TFNα elevated 2–3 day PI in infected lungs	Roberts 2005a
10 weeks old BalbC mice (infected with 104 PFU of WIV1-MA15/SARS-CoV-MA15 strains of SARS-CoV)	▪ Rapid weight loss and death in SARS-CoV-MA15 ▪ WIV1-MA15 resulted in no weight loss or lethality	▪ Viral replication reported in lungs	▪ Not reported	Subbarao 2004
C57BL6 mice (infected with 104 TCID50 SARS-CoV urbani strain )	▪ No clinical signs of disease, slow increase of body weight, no mortality ▪ Virus replicates in lungs and cleared by day-9 PI ▪ Beige, CD1−/−, RAG1−/− mice of C57BL6 background cleared the virus in a normal way	▪ Viral RNA detected in lung, liver, spleen, heart and brain but not in kidneys ▪ Viral RNA detected in epithelial lining of bronchi and terminal bronchioles but not in alveoli of lungs	▪ Less leukocyte infiltration in lungs of infected mice; no significant change in BALF of infected and mock infected mice ▪ Focal necrosis, alveolar damage, bronchiolar lining disintegration, mild endothelial swelling in lungs ▪ Significant increase in mRNA transcripts in infected mice as compared to mock infected mice ▪ Infected mice shows normal liver and kidney functions	Glass 2004
Pigs (infected with 2*106 PFU of SARS-CoV human isolate)	▪ No clinical signs of disease	▪ Viral RNA detected only in spleen	▪ Not reported	Weingartl 2004
Chickens (infected with 106 PFU of SARS-CoV human isolate)	▪ No clinical signs of disease	▪ Viral RNA detected in blood, traches, lungs and kidney but not in spleen, liver and jejunum	▪ Not reported	Weingartl 2004