COVID-19 and X-linked agammaglobulinemia (XLA) - insights from a monogenic antibody deficiency.
Curr Opin Allergy Clin Immunol
; 21(6): 525-534, 2021 12 01.
Article
in English
| MEDLINE | ID: covidwho-1447630
ABSTRACT
PURPOSE OF REVIEW The clinical outcomes from COVID-19 in monogenic causes of predominant antibody deficiency have pivotal implications for our understanding of the antiviral contribution of humoral immunity. This review summarizes the lessons learned from COVID-19 infection in X-linked agammaglobulinemia (XLA) due to genetic defects in Bruton's tyrosine kinase (BTK). RECENT FINDINGS:
Key molecular pathways underlying the development of severe COVID-19 are emerging, highlighting the possible contribution of BTK to hyperinflammation. SARS-CoV-2 specific T-cell responses and complement activation appear insufficient to achieve viral clearance in some B-cell deficient individuals. Whilst appearing efficacious in this group, use of convalescent plasma has been recently associated with the evolution of viral escape variants. Early data suggests individuals with XLA can mount a viral-specific T-cell vaccine response, however, the clinical significance of this is still emerging.SUMMARY:
In contrast to reports made early in the pandemic, we show XLA patients remain susceptible to severe disease. Persistent infection was common and is likely to carry a significant symptom burden and risk of novel variant evolution. COVID-19 infection in this vulnerable, antibody deficient group due to genetic, therapeutic or disease causes may require prompt and specific intervention for both patient and societal benefit.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Agammaglobulinemia
/
Genetic Diseases, X-Linked
/
Agammaglobulinaemia Tyrosine Kinase
/
SARS-CoV-2
/
COVID-19
Type of study:
Diagnostic study
/
Prognostic study
Topics:
Long Covid
/
Vaccines
/
Variants
Limits:
Humans
Language:
English
Journal:
Curr Opin Allergy Clin Immunol
Journal subject:
Allergy and Immunology
Year:
2021
Document Type:
Article
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