| Sample Type | n | Range | Average |
|---|---|---|---|
| Serum | 5 | 85% - 101% | 98% |
| EDTA Plasma | 5 | 86% - 99% | 93% |
| Heparin Plasma | 5 | 88% - 105% | 94% |
| Sample Type | n | 1:2 | 1:4 | 1:8 |
|---|---|---|---|---|
| Serum | 5 | 80-104% | 84-100% | 88-102% |
| EDTA Plasma | 5 | 85-104% | 86-102% | 84-98% |
| Heparin Plasma | 5 | 90-98% | 80-96% | 81-98% |
| Item | Quantity | Storage |
|---|---|---|
| Pre-Coated 96 Well Microplate | 12 x 8 Well Strips | +4°C |
| Lyopholized Standard | 2 Vials | +4°C |
| Sample Dilution Buffer | 20ml | +4°C |
| Biotinylated Detection Antibody | 120µl | +4°C |
| Antibody Dilution Buffer | 10ml | +4°C |
| HRP-Streptavidin Conjugate | 120µl | +4°C |
| SABC Dilution Buffer | 10ml | +4°C |
| TMB Substrate | 10ml | +4°C |
| Stop Solution | 10ml | +4°C |
| Wash Buffer (25X) | 30ml | +4°C |
| Plate Sealers | 5 Adhesive Strips | - |
| Foil Pouch | 1 Zip-Sealed Pouch | - |
Transmission of SARS-CoV-2 is driven by contact, fomite, and airborne transmission. The relative contribution of different transmission routes remains subject to debate. Here, we show Syrian hamsters are susceptible to SARS-CoV-2 infection through intranasal, aerosol and fomite exposure. Different routes of exposure present with distinct disease manifestations. Intranasal and aerosol inoculation causes severe respiratory pathology, higher virus loads and increased weight loss. In contrast, fomite exposure leads to milder disease manifestation characterized by an anti-inflammatory immune state and delayed shedding pattern. Whereas the overall magnitude of respiratory virus shedding is not linked to disease severity, the onset of shedding is. Early shedding is linked to an increase in disease severity. Airborne transmission is more efficient than fomite transmission and dependent on the direction of the airflow. Carefully characterized SARS-CoV-2 transmission models will be crucial to assess potential changes in transmission and pathogenic potential in the light of the ongoing SARS-CoV-2 evolution.
Pre-existing comorbidities such as obesity or metabolic diseases can adversely affect the clinical outcome of COVID-19. Chronic metabolic disorders are globally on the rise and often a consequence of an unhealthy diet, referred to as a Western Diet. For the first time in the Syrian hamster model, we demonstrate the detrimental impact of a continuous high-fat high-sugar diet on COVID-19 outcome. We observed increased weight loss and lung pathology, such as exudate, vasculitis, hemorrhage, fibrin, and edema, delayed viral clearance and functional lung recovery, and prolonged viral shedding. This was accompanied by an increased trend of systemic IL-10 and IL-6, as well as a dysregulated serum lipid response dominated by polyunsaturated fatty acid-containing phosphatidylethanolamine, recapitulating cytokine and lipid responses associated with severe human COVID-19. Our data support the hamster model for testing restrictive or targeted diets and immunomodulatory therapies to mediate the adverse effects of metabolic disease on COVID-19.
