As part of considering why some people are more prone to contracting the SARS-CoV-2 coronavirus than others, it is important to factor in how the virus spreads. The primary way is through water or mucus droplets, which are passed from person to person. Second to this is direct contact – from hand to infected surface, and then to the nose, mouth or eyes. Viral RNA can be recovered from a variety of surfaces, including plastic and steel several days after it was originally deposited.
The issue that is less clear cut is transmission via aerosols. Here scientists at the U.S. National Institute of Allergy and Infectious Diseases indicated that the found the virus is also stable in aerosols for up to three hours. There are different factors that may affect this as we’ve also looked at in another video. Another study by researchers in China found that higher temperatures and humidity are probably influential factors for viral survival.
In relation to the infectivity of the virus, research relating to the SARS-CoV-2 spike indicate that it is between 10 and 20 times more likely to bind to the ACE2 on human cells than the spike from the SARS-CoV virus. ACE2 is the doorways as to how the virus gets into a cell.
Cells in the lung have the ACE2 receptor and this is what the S-proteins on the spikes of the coronavirus use to attach to the receptor. The spikes on the coronavirus are what gives the virus its name – as they resemble the rays emitting from corona of the Sun.
Once docked, another protein in the cell membrane called serine protease helps to internalise the virus. Essentially in allows the messenger RNA in the virus to enter and infect the cell.
This greater binding helps to explain why SARS-CoV-2 can spread more readily between people compared with the original than SARS coronavirus between 2002 and 2003. ACE2 was the same receptor that allowed the original SARS into the cell.
Medically, there is some research on-going into blood pressure medications and greater infectivity, since common blood pressure medications increase the number of ACE2 receptors on certain cells (these medications are angiotensin converting enzyme inhibitors (ACE-i) or Angiotensin Receptor Blockers (ARBs)). Therefore, more AEC2 receptors potentially provide more entry points for the virus.
Further information about this appears in an article published in The Lancet titled ‘Are patients with hypertension and diabetes mellitus at increased risk of COVID-19 infection?’
The authors suggest that “patients with cardiac diseases, hypertension, or diabetes, who are treated with ACE2-increasing drugs, are at higher risk for severe COVID-19 infection and, therefore, should be monitored.”
However, this is not supported by all scientists, including the European Society for Cardiology, which do not find any evidence that drugs to combat high blood pressure increase infection rates. The European review concludes: “This speculation about the safety of ACE-i or ARB treatment in relation to COVID-19 does not have a sound scientific basis or evidence to support it.”
Currently it seems that the jury is out on this one (signalling the complex biology of the virus and how much more there is to learn about the infectious agent). Importantly no one should stop taking any medication, and all courses of medication should be discussed with a medical professional.
