Halima Kholaiq

Morocco

Human genetic and immunological determinants of SARS-CoV-2 infection and multisystem inflammatory syndrome in children

Halima Kholaiq1*, Yousra Abdelmoumen1, Abderrahmane Moundir1, Assiya El Kettani1,2,3, Fatima Ailal1,4, Ibtihal Benhsaien1,4, Fatima Adnane1,4, Asmaa Drissi Bourhanbour1,5, Naima Amenzoui1,4, Jalila El Bakkouri1,5,6 and Ahmed Aziz Bousfiha1,4
1. Laboratory of Clinical Immunology, Inflammation and Allergies (LICIA), Faculty of Medicine and Pharmacy, Hassan II University,
Casablanca, Morocco
2. Laboratory of Bacteriology, Virology and Hospital Hygiene, Ibn Rochd University Hospital, Casablanca, Morocco
3. Laboratory of Bacteriology and Virology, Faculty of Medicine and Pharmacy, Hassan II University, Casablanca, Morocco
4. Clinical Immunology and Infectious Pediatrics Department, Abderrahim Harouchi Hospital, Ibn Rochd University Hospital,
Casablanca, Morocco
5. Immunology Laboratory, Ibn Rochd University Hospital, Casablanca, Morocco
6. Mohammed VI University of Health Sciences (UM6SS), Casablanca, Morocco

Abstract

Background

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces pneumonia and acute respiratory failure in coronavirus disease 2019 (COVID-19) patients with inborn errors of immunity to type I interferon (IFN-I). The impact of SARS-CoV-2 infection varies widely, ranging from mild respiratory symptoms to life-threatening illness and organ failure, with a higher incidence in men than in women.

Methods

This review aims to present recent evidence from the scientific literature on genetic and immunological abnormalities predisposing individuals to critical SARS-CoV-2 infection through IFN-I.

Results

Approximately 3–5% of critical COVID-19 patients under 60 and a smaller percentage of elderly patients exhibit genetic defects in IFN-I production, including X-chromosome-linked TLR7 and autosomal TLR3 deficiencies. Around 15–20% of cases over 70 years old, and a smaller percentage of younger patients, present with preexisting autoantibodies neutralizing type I interferons.

Conclusions

Understanding the immunological mechanisms and pathogenesis of severe COVID-19 may inform personalized patient care and population protection strategies against future serious viral infections.