We’re publishing today a piece by John Collis, a recently retired nurse practitioner, in which he uses the work of Professor Daniel M. Davis to explore the role of genes in the immune system and asks whether genetic diversity between individuals and groups might explain why some people are worse affected by Covid than others. Here’s the introduction:
Why are different people affected differently by a SARS-CoV-2 infection? Through this article, based on The Compatibility Gene by Professor Daniel M. Davis, I hope to be able to provide some insight. While this is a very complex subject, with the understanding of the different components and their interactions having developed over the past 60 years or so, I will set it out as clearly as I can. To simplify matters I do not discuss here the role of cytokines or other chemical signalling between cells.
The immune system is built around the body’s ability to distinguish between components that belong there (self) and those that don’t (non-self). Pathogens such as bacteria, protozoa and parasites have very different DNA and are relatively easy to identify as non-self. Viruses are different: how does the immune system distinguish between a healthy ‘self’ cell and an infected ‘self’ cell?
The part of the immune system that is responsible for this are T-cells. T-cell production is controlled by the Thymus gland located in the chest, between the lungs. Significantly, this gland is large in children, starts to shrink post puberty and is very small in older adults. Could this explain why children are less susceptible to the effects of SARS-CoV-2 infection? Could the changes in the thymus gland explain the effects being seen in teenagers and young adults? Are some of these adverse events immune system mediated?
Worth reading in full.