Why does the coronavirus sometimes strike young people?
It's usually clearcut. The virus only strikes people with impaired immune systems -- people who have other ailments. Old people normally have other ailments so they are very often affected by the virus.
And when young people get it, they are usually ones who are ill already. They too have other ailments. But how come there are a few cases of young people being infected who seem otherwise healthy? Why does the virus single them out? Why in their case was being young and healthy not enough to protect them?
The article from a major medical journal below shows why in at least some cases. It shows that they have a genetic defect that weakens their immune system in crucial ways. That may not be the answer in all cases but it is clearly now an in principle explanation. The vast majority of young people are safe
Presence of Genetic Variants Among Young Men With Severe COVID-19
Caspar I.van der Made et al.
Objective: To explore the presence of genetic variants associated with primary immunodeficiencies among young patients with COVID-19.
Design, Setting, and Participants: Case series of pairs of brothers without medical history meeting the selection criteria of young (age <35 12="" 16="" 2020.="" 23="" 2="" 4="" admitted="" analysis="" and="" april="" as="" available="" between="" brother="" care="" controls="" covid-19.="" date="" due="" experiments.="" families="" family="" final="" follow-up="" for="" four="" from="" functional="" genetic="" hospitals="" icus="" in="" included="" intensive="" march="" may="" members="" men="" netherlands="" of="" p="" pairs="" segregation="" severe="" the="" to="" unit="" unrelated="" variant="" was="" were="" years="">
Main Outcome and Measures: Results of rapid clinical whole-exome sequencing, performed to identify a potential monogenic cause. Subsequently, basic genetic and immunological tests were performed in primary immune cells isolated from the patients and family members to characterize any immune defects.
Results: The 4 male patients had a mean age of 26 years (range, 21-32), with no history of major chronic disease. They were previously well before developing respiratory insufficiency due to severe COVID-19, requiring mechanical ventilation in the ICU. The mean duration of ventilatory support was 10 days (range, 9-11); the mean duration of ICU stay was 13 days (range, 10-16). One patient died. Rapid clinical whole-exome sequencing of the patients and segregation in available family members identified loss-of-function variants of the X-chromosomal TLR7. In members of family 1, a maternally inherited 4-nucleotide deletion was identified (c.2129_2132del; p.[Gln710Argfs*18]); the affected members of family 2 carried a missense variant (c.2383G>T; p.[Val795Phe]). In primary peripheral blood mononuclear cells from the patients, downstream type I interferon (IFN) signaling was transcriptionally downregulated, as measured by significantly decreased mRNA expression of IRF7, IFNB1, and ISG15 on stimulation with the TLR7 agonist imiquimod as compared with family members and controls. The production of IFN-γ, a type II IFN, was decreased in patients in response to stimulation with imiquimod.
Conclusions and Relevance: In this case series of 4 young male patients with severe COVID-19, rare putative loss-of-function variants of X-chromosomal TLR7 were identified that were associated with impaired type I and II IFN responses. These preliminary findings provide insights into the pathogenesis of COVID-19
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