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Humans with inherited MyD88 and IRAK-4 deficiencies are predisposed to hypoxemic COVID-19 pneumonia. | LitMetric

AI Article Synopsis

  • Patients with X-linked recessive deficiency of TLR7, a crucial immune sensor, struggle to recognize SARS-CoV-2 and produce necessary type I interferons, leading to severe pneumonia cases.
  • A study included 22 unvaccinated individuals with MyD88 or IRAK-4 deficiencies from multiple countries, primarily affecting children and young adults, with a significant portion requiring hospitalization.
  • The findings highlight that these genetic deficiencies, previously linked to bacterial infections, also significantly increase vulnerability to hypoxemic pneumonia caused by COVID-19, especially as patients age.

Article Abstract

X-linked recessive deficiency of TLR7, a MyD88- and IRAK-4-dependent endosomal ssRNA sensor, impairs SARS-CoV-2 recognition and type I IFN production in plasmacytoid dendritic cells (pDCs), thereby underlying hypoxemic COVID-19 pneumonia with high penetrance. We report 22 unvaccinated patients with autosomal recessive MyD88 or IRAK-4 deficiency infected with SARS-CoV-2 (mean age: 10.9 yr; 2 mo to 24 yr), originating from 17 kindreds from eight countries on three continents. 16 patients were hospitalized: six with moderate, four with severe, and six with critical pneumonia, one of whom died. The risk of hypoxemic pneumonia increased with age. The risk of invasive mechanical ventilation was also much greater than in age-matched controls from the general population (OR: 74.7, 95% CI: 26.8-207.8, P < 0.001). The patients' susceptibility to SARS-CoV-2 can be attributed to impaired TLR7-dependent type I IFN production by pDCs, which do not sense SARS-CoV-2 correctly. Patients with inherited MyD88 or IRAK-4 deficiency were long thought to be selectively vulnerable to pyogenic bacteria, but also have a high risk of hypoxemic COVID-19 pneumonia.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9998661PMC
http://dx.doi.org/10.1084/jem.20220170DOI Listing

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