Summary: 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. 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. Additionally, innate errors affecting the control of the response to type I interferon have been associated with pediatric multisystem inflammatory syndrome (MIS-C). Several studies have described rare errors of immunity, such as XIAP deficiency, CYBB, SOCS1, OAS1/2, and RNASEL, as underlying factors in MIS-C susceptibility. However, further investigations in expanded patient cohorts are needed to validate these findings and pave the way for new genetic approaches to MIS-C. 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. We will also discuss multisystem inflammatory syndrome in children (MIS-C). Understanding the immunological mechanisms and pathogenesis of severe COVID-19 may inform personalized patient care and population protection strategies against future serious viral infections.

Epidermodysplasia verruciformis (EV) is a rare genodermatosis caused by β-human papillomaviruses (HPV) in immunodeficient patients. EV is characterized by flat warts and pityriasis-like lesions and might be isolated or syndromic, associated with some other infectious manifestations. We report here three patients from two independent families, with syndromic EV for both of them. By whole exome sequencing, we found that the patients carry new homozygous variants in STK4, both leading to a premature stop codon. STK4 deficiency causes a combined immunodeficiency characterized by a broad infectious susceptibility to bacteria, viruses, and fungi. Auto-immune manifestations were also reported. Deep immunophenotyping revealed multiple cytopenia in the three affected patients, in particular deep CD4⁺ T cells deficiency. We report here the fourth and the fifth cases of the syndromic EV due to STK4 deficiency.

Introduction: Atopic dermatitis (AD) is driven by complex pathways that mediate inflammation and pruritus. The pathophysiology of AD’s disease involves multiple pathways. Interleukin-13 (IL-13) is considered a major cytokine in Th2-type inflammation, responsible for changing the epidermal barrier and producing chronic inflammation, whereas interleukin-31 (IL-31) is considered a major inducer of pruritus. The exact correlation of each of these cytokines with disease severity in children with AD appears to vary across studies. This study was therefore designed to evaluate whether IL-13 and IL-31 levels contribute complementarily or independently to the overall clinical severity of AD in the Moroccan pediatric population and to analyze the correlation between serum IL-13 and IL-31 levels and investigate their correlation with disease severity in a pediatric cohort. Methods: A total of 52 children with moderate to severe AD were included. The severity of the disease was measured using the SCORing Atopic Dermatitis (SCORAD) index. Serum levels of IL-13 and IL-31 were measured by Enzyme-Linked Immunosorbent Assay (ELISA). Results: The IL-13 serum level showed a considerable positive correlation with the SCORAD score (r_s = 0.7, p < 0.0001). On the other hand, IL-31 levels revealed no correlation with SCORAD (r_s = 0.07, p = 0.62) but were positively correlated with pruritus intensity (r_s = 0.91, p < 0.001). Conclusion: Our results support the presence of different pathophysiological axes in pediatric AD, where IL-13 functions as a reliable biomarker of inflammatory severity. IL-31 acts as a systemic marker of the pruritic pathway.

Acute bronchiolitis is the leading cause of infant hospitalization worldwide, with respiratory syncytial virus (RSV) historically predominating. Prospective virological data for the 2025–2026 epidemic season in Morocco were lacking. A prospective observational cohort study was conducted at the Department of Pediatric Infectious Diseases and Clinical Immunology, Casablanca Mother-Child Hospital, from August 2025 through March 2026. Consecutive infants aged 1–24 months hospitalized with acute viral bronchiolitis underwent nasopharyngeal sampling and multiplex rapid antigen testing for RSV, influenza A, influenza B, and SARS-CoV-2. A total of 131 infants were enrolled (median age 4.8 months; male-to-female ratio 0.84:1). At least one virus was identified in 63 patients (48.1%; 95% CI 39.1–57.3%). RSV predominated: 49 sole infections and 2 co-infections with influenza A, totaling 51 positives (80.9% of virus-positive cases; 38.9% of the cohort). Influenza A totaled 8 cases (12.7%), including the 2 co-infections; influenza B accounted for 2 further cases (3.2%). SARS-CoV-2 was not detected. Epidemic activity peaked in January 2026 (65 admissions), declining through February (34) and March (12). All detected pathogens have licensed preventive options, supporting the introduction of nirsevimab, maternal RSV vaccination, and seasonal influenza vaccination as public health priorities in Morocco.

Introduction. This study aims to describe the clinical and paraclinical characteristics of Multisysteminflammatory syndrome in children (MIS-C). Methods. A retrospective study encompassing 52 children diagnosed with MIS-C according to the World Health Organization criteria, over a 3-year period at Abderrahim Harrouchi Hospital in Morocco. Results. The median age was 6 years (IQR: 1-14), with a sex ratio of 1.16 (28 boys and 24 girls). Clinical manifestations were predominantly characterized by fever in all cases (100%), respiratory and gastrointestinal symptoms in 30 cases (58%) and 23 cases (44%) respectively, and shock in 9 cases (17%). We noted a myocarditis in 6 cases (12%). The treatment comprised intravenous human Immunoglobulin combined with methylprednisolone in all patients (100%). Conclusion. The characteristics of our MIS-C patients were similar to those in the literature, but more studies are needed to confirm these results.