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Rapid genome sequencing identifies novel variants in complement factor I
Journal article   Open access   Peer reviewed

Rapid genome sequencing identifies novel variants in complement factor I

Katherine M Rodriguez, Jordan Vaught, Michelle Dilley, Kataryzna Ellsworth, Alaina Heinen, Edsel M Abud, Yuzhou Zhang, Richard J H Smith, Robert Sheets, Bob Geng, …
Cold Spring Harbor molecular case studies, Vol.8(7), p.a006239
12/2022
DOI: 10.1101/mcs.a006239
PMCID: PMC9808552
PMID: 36577522
url
https://doi.org/10.1101/mcs.a006239View
Published (Version of record) Open Access

Abstract

Complement factor I deficiency (CFID; OMIM #610984) is a rare immunodeficiency caused by deficiencies in the serine protease complement factor I (CFI). CFID is characterized by predisposition to severe pneumococcal infection, often in infancy. We report a previously healthy adolescent male who presented with respiratory failure secondary to pneumococcal pneumonia and severe systemic inflammatory response. Rapid genome sequencing (rGS) identified compound heterozygous variants in in the proband, with a novel maternally inherited likely pathogenic variant, a single nucleotide deletion resulting in premature stop (c.1646del; p.Asn549ThrfsTer25) and a paternally inherited novel likely pathogenic deletion (Chr 4:110685580-110692197del).
Adolescent Chromosome Mapping Complement Factor I Genotype Humans Male

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