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Your search keyword '"Kerrouche, Nacim"' showing total 4 results
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4 results on '"Kerrouche, Nacim"'

1. Human TMEFF1 is a restriction factor for herpes simplex virus in the brain

Author

Chan, Yi-Hao, Liu, Zhiyong, Bastard, Paul, Khobrekar, Noopur, Hutchison, Kennen M., Yamazaki, Yasuhiro, Fan, Qing, Matuozzo, Daniela, Harschnitz, Oliver, Kerrouche, Nacim, Nakajima, Koji, Amin, Param, Yatim, Ahmad, Rinchai, Darawan, Chen, Jie, Zhang, Peng, Ciceri, Gabriele, Chen, Jia, Dobbs, Kerry, Belkaya, Serkan, Lee, Danyel, Gervais, Adrian, Aydın, Kürşad, Kartal, Ayse, Hasek, Mary L., Zhao, Shuxiang, Reino, Eduardo Garcia, Lee, Yoon Seung, Seeleuthner, Yoann, Chaldebas, Matthieu, Bailey, Rasheed, Vanhulle, Catherine, Lorenzo, Lazaro, Boucherit, Soraya, Rozenberg, Flore, Marr, Nico, Mogensen, Trine H., Aubart, Mélodie, Cobat, Aurélie, Dulac, Olivier, Emiroglu, Melike, Paludan, Søren R., Abel, Laurent, Notarangelo, Luigi, Longnecker, Richard, Smith, Greg, Studer, Lorenz, Casanova, Jean-Laurent, and Zhang, Shen-Ying

Published
2024
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3. Human inherited complete STAT2 deficiency underlies inflammatory viral diseases

Author

Bucciol, Giorgia, Moens, Leen, Ogishi, Masato, Rinchai, Darawan, Matuozzo, Daniela, Momenilandi, Mana, Kerrouche, Nacim, Cale, Catherine M., Treffeisen, Elsa R., Salamah, Mohammad Al, Saud, Bandar K. Al-, Lachaux, Alain, Duclaux-Loras, Remi, Meignien, Marie, Bousfiha, Aziz, Benhsaien, Ibtihal, Shcherbina, Anna, Roppelt, Anna, Gothe, Florian, Houhou-Fidouh, Nadhira, Hackett, Scott J., Bartnikas, Lisa M., Maciag, Michelle C., Alosaimi, Mohammed F., Chou, Janet, Mohammed, Reem W., Freij, Bishara J., Jouanguy, Emmanuelle, Zhang, Shen-Ying, Boisson-Dupuis, Stephanie, Beziat, Vivien, Zhang, Qian, Duncan, Christopher J.A., Hambleton, Sophie, Casanova, Jean- Laurent, and Meyts, Isabelle

Subjects
Genetic disorders -- Causes of -- Complications and side effects, Inflammation -- Genetic aspects -- Risk factors, STAT proteins -- Health aspects -- Genetic aspects, Virus diseases -- Risk factors -- Genetic aspects, Health care industry
Abstract

STAT2 is a transcription factor activated by type I and III IFNs. We report 23 patients with loss-of-function variants causing autosomal recessive (AR) complete STAT2 deficiency. Both cells transfected with mutant STAT2 alleles and the patients' cells displayed impaired expression of IFN-stimulated genes and impaired control of in vitro viral infections. Clinical manifestations from early childhood onward included severe adverse reaction to live attenuated viral vaccines (LAV) and severe viral infections, particularly critical influenza pneumonia, critical COVID-19 pneumonia, and herpes simplex virus type 1 (HSV-1) encephalitis. The patients displayed various types of hyperinflammation, often triggered by viral infection or after LAV administration, which probably attested to unresolved viral infection in the absence of STAT2-dependent types I and III IFN immunity. Transcriptomic analysis revealed that circulating monocytes, neutrophils, and [CD8.sup.+] memory T cells contributed to this inflammation. Several patients died from viral infection or heart failure during a febrile illness with no identified etiology. Notably, the highest mortality occurred during early childhood. These findings show that AR complete STAT2 deficiency underlay severe viral diseases and substantially impacts survival., Introduction Human type I and III IFNs operate in almost all cell types (1, 2). Type I IFNs (IFN-[alpha]/[beta]) are thought to be secreted by most, if not all, of [...]

Published
2023
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4. Autoantibodies neutralizing type I IFNs underlie severe tick-borne encephalitis in ∼10% of patients

Author

Gervais, Adrian, Marchal, Astrid, Fortova, Andrea, Berankova, Michaela, Krbkova, Lenka, Pychova, Martina, Salat, Jiri, Zhao, Shuxiang, Kerrouche, Nacim, Le Voyer, Tom, Stiasny, Karin, Raffl, Simon, Schieber Pachart, Anne, Fafi-Kremer, Samira, Gravier, Simon, Robbiani, Davide F., Abel, Laurent, MacDonald, Margaret R., Rice, Charles M., Weissmann, Gaia, Kamal Eldin, Tarek, Robatscher, Eva, Erne, Elke Maria, Pagani, Elisabetta, Borghesi, Alessandro, Puel, Anne, Bastard, Paul, Velay, Aurélie, Martinot, Martin, Hansmann, Yves, Aberle, Judith H., Ruzek, Daniel, Cobat, Aurélie, Zhang, Shen-Ying, and Casanova, Jean-Laurent

Abstract

Tick-borne encephalitis (TBE) virus (TBEV) is transmitted to humans via tick bites. Infection is benign in >90% of the cases but can cause mild (<5%), moderate (<4%), or severe (<1%) encephalitis. We show here that ∼10% of patients hospitalized for severe TBE in cohorts from Austria, Czech Republic, and France carry auto-Abs neutralizing IFN-α2, -β, and/or -ω at the onset of disease, contrasting with only ∼1% of patients with moderate and mild TBE. These auto-Abs were found in two of eight patients who died and none of 13 with silent infection. The odds ratios (OR) for severe TBE in individuals with these auto-Abs relative to those without them in the general population were 4.9 (95% CI: 1.5–15.9, P < 0.0001) for the neutralization of only 100 pg/ml IFN-α2 and/or -ω, and 20.8 (95% CI: 4.5–97.4, P < 0.0001) for the neutralization of 10 ng/ml IFN-α2 and -ω. Auto-Abs neutralizing type I IFNs accounted for ∼10% of severe TBE cases in these three European cohorts.

Published
2024
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