The two most frequent comorbidities in patients infected by coronavirus are diabetes and hypertension.
We know there are groups of population that are more vulnerable to SARS-CoV-2. Moreover, those with comorbidities (diseases) like the ones we have mentioned have higher risk of death due to the virus.
- But where is the link between metabolism and a worse infection?
- What specific mechanisms are failing or making it easier for the virus to attack people with metabolic diseases?
Metabolism and Viral Infections
As you know, SARS-COV-2 is not the first virus that has caused us problems.
Not many years ago, we witnessed the pandemic of SARS and MERS-CoV in the Middle East. Well, diabetes and hypertension were also the most frequent comorbidities in both cases.
Therefore, there must be a specific connection between a damaged metabolism and a viral infection.
You may probably think that this is not new: a metabolic disease complicates the evolution of any disease, weakening the organism in general.
Let’s explain that.
You may have probably heard the term “cytokine storm” lately.
Cytokines are messenger molecules that are neither good or bad.
However, our immune response against the SARS-COV-2 triggers a brutal increase of pro-inflammatory cytokines in the second stage of the disease. The first stage has a high viral charge, the second phase is more “immunological”, when the viral charge has dropped.
Then, what happens?
This “perfect storm” made of pro-inflammatory cytokines intensifies when we have a damaged metabolism or low systemic inflammation.
The virus enters the cells of our respiratory system by using a key on a lock.
The key is a glycoprotein with spikes and the lock is the angiotensin converting enzyme 2 or ACE2. It is located in the surface of the human cells (cells from the respiratory apparatus in this case).
Therefore, the first hypothesis for an unfavorable result is that these patients have more locks in their cells to which the virus can bind.
But that is not all
The conversion of Angiotensin II into Angiotensin 1-7 regulates the so-called renin-angiotensin-aldosterone system.
If this Angiotensin II is not transformed by the ACE2 because the virus has rendered it useless, it will increase the AGTII concentrations as well as its functions.
To sum up:
- Pro-inflammatory effect
- More aldosterone release
This will lead to hypopotassemia, which will increase the vascular permeability. In addition, it will increase the risk of RDS or respiratory distress syndrome (one of the main causes of death in these patients).
On the contrary, angiotensin 1-7 (which will drop) has an anti-inflammatory and anti-fibrotic effect by activating the receptor.
Other Metabolic Nexuses
When the virus SARS-CoV (which causes SARS, not COVID-19) joins the receptor ACE2 in the pancreatic cells, it directly damaged the pancreatic islets and reduced the insulin release.
In fact, those patients who were infected by SARS and who id not have a history of diabetes or corticosteroid treatment were compared to their healthy siblings. The study lasted three years after they were infected.
During their hospitalization, more than a 50% of the patients developed diabetes and only a 5% of them still suffered diabetes after three years (Yang et al., 2010).
Moreover, as we have seen before, DMT2 increases the ACE2 expression in other tissues like the lungs, liver and heart. This could explain why these patients run a higher risk of infection and multi-organic failure.
In addition, it would also explain why we are being so sceptical about using angiotensin-converting enzyme inhibitors (which transforms angiotensin I in II). This would actually increase the ACE2 expression in human cells.
Messages to Send Home
Nothing in human biology can escape the metabolism, it is ubiquitous.
A damaged metabolism will lower the physiological vital reserves and increases the risk of suffering multiple diseases.
Moreover, in the case of SARS-CoV-2, there are specific mechanisms that increasing the metabolic damage, affecting the progress of the virus:
- Increasing the general expression of ACE2 in the tissues.
- Increasing the actions of angiotensin II in the lung, increasing the SRDS (severe respiratory distress syndrome).
- Damaging the beta pancreatic cells directly.
- If we combine it with the metabolic damage of Obesity, the infection mechanisms can hinder the breathing mechanisms, increasing systemic inflammation,etc.
If you liked this post, we can make another one about Obesity and SARS-Cov-2.
See you in the next one!
- Bornstein, S. R., Dalan, R., Hopkins, D., Mingrone, G., & Boehm, B. O. (2020). Endocrine and metabolic link to coronavirus infection. Nature Reviews Endocrinology, 1–2.
- Yang, J. K., Lin, S. S., Ji, X. J., & Guo, L. M. (2010). Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes. Acta Diabetologica.
- Coronavirus: A Critical Approach on this link
- Why will COVID-19 change Medicine? Point of view of a physician here.