Summary: An in-depth analysis of the SARS-CoV2 virus anatomy and physiology along with management and potential treatments.
Presenter:
Divya Reddy, MD
Department of Pulmonary Medicine
Einstein Montefiore Medical Center
Key points
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SARS-CoV2 spike protein has a S1 subunit containing a receptor binding domain that binds the ACE-2 receptor and with higher affinity than SAR-CoV1. There is polybasic cleavage site whose sequence determines viral infectivity which likely underwent mutation in humans allowing for more rapid spread. Viral dysregulation of ACE receptors may cause inflammatory imbalance, leading to ARDS.
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The highest shedding is at symptom onset compared to SARS-CoV1 which peaked later at maximum illness. Asymptomatic and post symptom resolution patients have also been shown to have high viral loads. There are 3 stages of COVID-19: viral replication, pulmonary, and hyperimmune. CT scans generally show peripheral and inferior lobe infiltrates and may be a good screening tool. Ultrasound shows b lines with pleural irregularity and correlates in severity to CT scan.
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There is no treatment currently. Chloroquine and Hydroxychloroquine are anti-viral and anti-inflammatory but there are limited in-vivo studies. Early studies of Tocilizumab and convalescent plasma show promise but the benefit of steroids during the hyperinflammatory stage is unknown. Anticoagulation may decrease mortality but overall supportive treatment is the mainstay and the ARDS protocol should be followed in mechanically ventilated patients.
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