PRAGYA SANTRA, AMITY UNIVERSITY KOLKATA
A huge part of the population worldwide has been affected due to the deadly attack of the COVID19. As per close observations and studies, it is noted that the disease becomes fatal for few and mild for others. The spread of COVID-19 is a paradox of what causes the virus to distinguish between individuals for infection rates.
Recent studies have put limelight to few instincts focusing that COVID-19 is not only a viral infection but a 10% case of critical auto-immunity. Not always the pathogen itself but at times patients own immune system misguides the defence mechanism of the body, paving opportunities for more rapid viral attack.
Whole Genome Sequencing of 659 serious COVID19 patients revealed, that the genetic flaws and mutations have led to the production of auto-antibodies attacking the interferons (IFNS), especially Type I IFNs. Type I IFNs are produced by every infected body cell which acts as the leading member in the body’s defence mechanism during pathogenesis. They launch immediate responses to alert the neighbouring healthy cells to prepare their defence system and protein production to interrupt further infection spread. But for a few patients, this concept is adjourned.
One of the two new studies focused that 10.2% of the COVID-19 patients have developed auto-antibodies ceasing the normal functioning of the IFNs; further leading to no production of proteins by uninfected cells against COVID-19, favouring the infection to spread.
According to another paper, the researchers’ also sequenced 13 proteins produced by the host body to fight against viral infections by upgrading their immune system. Out of the 3.5%, critical patients harboured mutations in 8 of those 13 protein-making genes making them unable to produce IFNs, neutralizing the first-line defence of innate immunity.
In the list of all the critically infected patients a handful of them, 5%, were females while 95% were reported to be males, which pivot a sex-related issue on the COVID-19 spread. Generally, women have a higher rate of auto-immune disorder. But a contradiction, in this case, puts light upon the X-linked recessive hypothesis. Women carrying two copies of X chromosomes do not show severe/any disease, whereas males with one copy of the X chromosome are highly affected due to the pseudo-dominance effect of the X gene.
Therapies are likely in progress to boost the function of INFs by incorporating synthetic IFNs to the patients. Besides the scientists too stated, synthetic IFNs too may fail in the patients generating the auto-antibodies and carrying the mutated version of the genes to halt the working of IFNs.
A test screening of the antibodies is still in progress to come up with new therapies and biological juggleries in the very next moment and yet many mysteries are to be solved.
Also read: Gene-editing: The Revolution has begun.
SOURCE:
- Isabelle Meyts, Giorgia Bucciol, Isabella Quinti, et al; Coronavirus Disease 2019 in patients with inborn errors of immunity: an international study; 2020; Journal of Allergy and Clinical Immunology; Vol: 10, Pg- 1016, DOI: https://doi.org/10.1016/j.jaci.2020.09.010
- Paul Bastard, Lindsey B. Rosen, Qian Zhang, et al; Auto-antibodies against type I IFNs in patients with life-threatening COVID-19; 2020; Science; Vol: 10; Pg- abe9395; DOI: https://science.sciencemag.org/content/early/2020/09/23/science.abd4585
- Julia L. McKechnie and Catherine A. Blish; The Innate Immune System: Fighting on the Front Lines or Fanning the Flames of COVID-19; 2020; Cell Host and Microbes; Volume 27, Issue 6, Pages 863-869; DOI: https://doi.org/10.1016/j.chom.2020.05.009
- Jeong Seok Lee, Seongwan Park, Hye Won Jeong, et al; Immunophenotyping of COVID-19 and influenza highlights the role of type I interferons in development of severe COVID-19; 2020; Science Immunology; Vol: 5, Issue 49, Pg: eabd1554; DOI: https://immunology.sciencemag.org/content/5/49/eabd1554
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