COVID-19 newsletter

Published: 03/05/2020

By May 1, The World Health Organization reported 3,175,207 confirmed COVID-19 cases and 224,172 deaths. For a moment there are more information available to understand severe acute respiratory syndrome (SARS) coronavirus.

Initially, an infected person may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches. If immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus moving down the respiratory tract and attacks the lungs. The thinner, distant branches of the bronchial tree (alveoli) lined by cells having ACE2 receptors. They are the points where virus comes in touch with lung cells (1).

ACE2 receptors (angiotensin-converting type 2) play significant role in regulating of blood pressure. There are drugs called “inhibitors of ACE receptors”. Many people taking them routinely, to control blood pressure. Fortunately, still there are no evidence that new virus interacts somehow with these drugs, so patients with COVID-19 may continue to take ACE inhibitors.

When the immune system starts to battle the virus, immune cells release inflammatory molecules (cytokines). This battle leaves “corpses” and fragments of our cells. Other immune cells arrive to help and to “clear the battlefield”, launching chain reaction. Dead and alive cells block very thin blood vessels coming to alveoli and erythrocytes can’t reach point where it is possible to release carbon dioxide and capture oxygen. Peculiarity of SARS-Cov-2 (it is a name of the new virus, COVID-19 is a name of the disease) – switching on unusually severe immune response in small part of population. It looks like allergic reaction though from medical point it is not. The body itself, not the virus, damages own organs and systems.

The blood itself is also influenced by the virus. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one third already had clots (2). Blood clots also block vessels, incl. small lung arterioles (“pulmonary embolism”). «The more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19» says Behnood Bikdeli from Columbia University Irving Medical Center.

There are still a lot of question in the pathophysiology of COVID-19 patients but now we have more information comparing to the start of epidemic.

We wish you stay safe and healthy.

DISCLAIMER: The text below is the review of the information that is publicly available. AIDA International isn’t responsible for assessment and/ or ranking of scientific evidence of presented data. An individual should follow the recommendations of local authorities and treating physician(s).

 

References

 

  1. Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol. 2004;203(2):631‐637. doi:10.1002/1570https://pubmed.ncbi.nlm.nih.gov/15141377/
  2. Klok FA, Kruip MJHA, van der Meer NJM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19 [published online ahead of print, 2020 Apr 10]. Thromb Res. 2020;S0049-3848(20)30120-1. doi:10.1016/j.thromres.2020.04.013

https://www.thrombosisresearch.com/article/S0049-3848(20)30120-1/fulltext