Post by mr potatohead on Mar 30, 2020 10:56:41 GMT
Here's an excerpt of a report from 2010 about SARS-CoV-1, which was just labeled "SARS-CoV" back then (2003) since there was no ".......-2" until now.
Further down in the report, I noticed a mention of protease inhibitors.
Understanding the past may help to understand the present.
Further down in the report, I noticed a mention of protease inhibitors.
Understanding the past may help to understand the present.
Human Cases of SARS
Clinical Features
Common symptoms of SARS include fever, a nonproductive cough, myalgia, and dyspnea. Poor outcomes are associated with the presence of comorbidities, male sex, age over 60 years, high neutrophil counts, and severe biochemical abnormalities.
The incubation period may vary from 1 to 14 days (mean, 4–6 days). A prospective study of one outbreak found that the clinical progression of SARS was mostly uniform and followed a triphasic pattern.49
Fever, myalgia, coughing, and a sore throat characterized the first week, followed in the second week by frequent recurrence of fever, diarrhea, and hypoxemia. Half the patients had abnormal chest radiographs. Virus shedding from the respiratory tract peaked on the 10th day after onset and was excreted in the feces from 12 to 14 days after onset. Immuno globulin G seroconversion occurred 10 to 15 days after onset and correlated with a decreased viral load.
Some patients showed clinical worsening at this stage and developed acute respiratory distress syndrome by week 3, although this can develop within the first week.
The most severe cases died between 4 and 108 days after the onset of symptoms.
Research suggests that immunopathologic damage from an overexuberant host immune response, rather than uncontrolled viral replication, was the major cause of lung damage at this stage.48,50,69,77
Pathologic Changes
The autopsy results of some SARS patients have been released since the first outbreak, in 2003. The major pathologic finding in these cases was diffuse alveolar damage (DAD). This acute lung injury was associated with viral replication and immuno- pathogenic factors. Histopathologically, the lungs of SARS victims showed various stages of DAD that are related to the duration of the illness, such as exudation, regeneration, and repair.
During the early phase of the illness (7–10 days after the onset of symptoms), the lungs showed signs of severe damage, including hyaline membrane formation, extensive edema, fibrin exudation, and some infiltration by inflammatory cells (Fig. 1). Cellular infiltration by macrophages has been observed, as has a combination of macrophages and lymphocytes, with or without neutrophils.6,8,17-19,48,58,69 Large multi-nucleated cells identified as macrophages and pneumocytes by immunohistochemistry are frequently observed in the lungs of SARS patients. Bronchiolitis obliterans organizing pneumonia,48 hemophagocytosis in the mononuclear cells residing in pulmonary tissues,48 and apoptosis of epithelial cells, monocytes/macrophages, lymphocytes and pneumocytes17 are also seen.
In some cases, coinfections by Aspergillus sp, Mucor sp, Pseudomonas aeruginosa, Klebsiella sp, methicillin-resistant Staphylococcus aureus, a-hemolytic Streptococcus sp, and cytomegalovirus have been reported.6,19 In situ hybridization and immunohistochemistry studies have identified viral nucleic acid and/or antigen in epithelial cells from bronchi,
bronchioles, trachea, and alveoli and in multinucleated cells and alveolar macrophages.16,17,47,58,66,75 Investigation of the cytokine and chemokine profiles of SARS patients has suggested that severe SARS-related lung injury might be attributed to an excessive host immune response — particularly, the deregulation of proinflammatory cytokine production.48,50,68,77
Clinical Features
Common symptoms of SARS include fever, a nonproductive cough, myalgia, and dyspnea. Poor outcomes are associated with the presence of comorbidities, male sex, age over 60 years, high neutrophil counts, and severe biochemical abnormalities.
The incubation period may vary from 1 to 14 days (mean, 4–6 days). A prospective study of one outbreak found that the clinical progression of SARS was mostly uniform and followed a triphasic pattern.49
Fever, myalgia, coughing, and a sore throat characterized the first week, followed in the second week by frequent recurrence of fever, diarrhea, and hypoxemia. Half the patients had abnormal chest radiographs. Virus shedding from the respiratory tract peaked on the 10th day after onset and was excreted in the feces from 12 to 14 days after onset. Immuno globulin G seroconversion occurred 10 to 15 days after onset and correlated with a decreased viral load.
Some patients showed clinical worsening at this stage and developed acute respiratory distress syndrome by week 3, although this can develop within the first week.
The most severe cases died between 4 and 108 days after the onset of symptoms.
Research suggests that immunopathologic damage from an overexuberant host immune response, rather than uncontrolled viral replication, was the major cause of lung damage at this stage.48,50,69,77
Pathologic Changes
The autopsy results of some SARS patients have been released since the first outbreak, in 2003. The major pathologic finding in these cases was diffuse alveolar damage (DAD). This acute lung injury was associated with viral replication and immuno- pathogenic factors. Histopathologically, the lungs of SARS victims showed various stages of DAD that are related to the duration of the illness, such as exudation, regeneration, and repair.
During the early phase of the illness (7–10 days after the onset of symptoms), the lungs showed signs of severe damage, including hyaline membrane formation, extensive edema, fibrin exudation, and some infiltration by inflammatory cells (Fig. 1). Cellular infiltration by macrophages has been observed, as has a combination of macrophages and lymphocytes, with or without neutrophils.6,8,17-19,48,58,69 Large multi-nucleated cells identified as macrophages and pneumocytes by immunohistochemistry are frequently observed in the lungs of SARS patients. Bronchiolitis obliterans organizing pneumonia,48 hemophagocytosis in the mononuclear cells residing in pulmonary tissues,48 and apoptosis of epithelial cells, monocytes/macrophages, lymphocytes and pneumocytes17 are also seen.
In some cases, coinfections by Aspergillus sp, Mucor sp, Pseudomonas aeruginosa, Klebsiella sp, methicillin-resistant Staphylococcus aureus, a-hemolytic Streptococcus sp, and cytomegalovirus have been reported.6,19 In situ hybridization and immunohistochemistry studies have identified viral nucleic acid and/or antigen in epithelial cells from bronchi,
bronchioles, trachea, and alveoli and in multinucleated cells and alveolar macrophages.16,17,47,58,66,75 Investigation of the cytokine and chemokine profiles of SARS patients has suggested that severe SARS-related lung injury might be attributed to an excessive host immune response — particularly, the deregulation of proinflammatory cytokine production.48,50,68,77