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4 results on '"Houmeida A"'

2. Genetic variation of TLR3 gene is associated with the outcome of hepatitis b infection in mauritanian patients: case control study

Author

Tetou Soumbara, Crystel Bonnet, Cheikh Tijani Hamed, Fatimetou Veten, Mohamed Hemeyine, F-Zahra Fall-Malick, Mohamed Mahmoud El Yezid, Aichetou Diallo, Moustapha Mouhamedou Mounah, and Ahmed Houmeida

Subjects
Chronic hepatitis B virus, Single-nucleotide polymorphism, TLR3, TLR4, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Toll-Like receptors (TLRs) play an important role in the immune response during hepatitis B virus (HBV) infection. In this study, we evaluated the association between two SNP variants (TLR3 rs3775290 and TLR4 rs4986790) and susceptibility to chronic HBV infection in Mauritania. Subjects and methods : A total of 188 subjects were recruited for this study: 102 chronically infected patients and 86 individuals with spontaneously resolved HBV infection who were considered controls. Targeted PCR products were sequenced using Sanger sequencing. Results We found that TLR3 rs3775290 was significantly more frequent in patients with chronic HBV than in the control population (p = 0.03). However, no association was found between the TLR4 rs3775290 polymorphism and chronic infection. Conclusion Our results suggest that the TLR3 rs3775290 polymorphism may be a risk factor for susceptibility to chronic HBV infection in the Mauritanian population.

Published
2024
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3. Genetic variation of TLR3 gene is associated with the outcome of hepatitis b infection in mauritanian patients: case control study.

Author

Soumbara, Tetou, Bonnet, Crystel, Hamed, Cheikh Tijani, Veten, Fatimetou, Hemeyine, Mohamed, Fall-Malick, F-Zahra, El Yezid, Mohamed Mahmoud, Diallo, Aichetou, Mounah, Moustapha Mouhamedou, and Houmeida, Ahmed

Subjects
GENETIC variation, HEPATITIS B, HEPATITIS B virus, CHRONIC hepatitis B, CHRONIC active hepatitis, TOLL-like receptors
Abstract

Background: Toll-Like receptors (TLRs) play an important role in the immune response during hepatitis B virus (HBV) infection. In this study, we evaluated the association between two SNP variants (TLR3 rs3775290 and TLR4 rs4986790) and susceptibility to chronic HBV infection in Mauritania. Subjects and methods: : A total of 188 subjects were recruited for this study: 102 chronically infected patients and 86 individuals with spontaneously resolved HBV infection who were considered controls. Targeted PCR products were sequenced using Sanger sequencing. Results: We found that TLR3 rs3775290 was significantly more frequent in patients with chronic HBV than in the control population (p = 0.03). However, no association was found between the TLR4 rs3775290 polymorphism and chronic infection. Conclusion: Our results suggest that the TLR3 rs3775290 polymorphism may be a risk factor for susceptibility to chronic HBV infection in the Mauritanian population. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Splice-altering variant of PJVKgene in a Mauritanian family with non-syndromic hearing impairment

Author

Salame, Malak, Bonnet, Crystel, Singh-Estivalet, Amrit, Brahim, Selma Mohamed, Roux, Solene, Boussaty, Ely Cheikh, Hadrami, Mouna, Hamed, Cheikh Tijani, Sidi, Abdellahi M’hamed, Veten, Fatimetou, Petit, Christine, and Houmeida, Ahmed

Abstract

PJVKgene was recently shown to create hypervulnerability to sound in humans and was the first human gene implicated in non-syndromic hearing impairment due to neural defect. Targeted next-generation sequencing of over 150 known deafness genes was performed in the proband. Sanger sequencing was used to validate the PJVKvariant and confirm familial segregation of the disease. A minigene-based assay has been performed to assess the impact of the variant on splicing. We identified a novel c.550-6A > G acceptor splice-site variant in the PJVKgene in the homozygous state in a Mauritanian child with severe to profound congenital deafness. The substitution was located in intron 4. The effect of the variation was demonstrated by a minigene assay which showed that the variation, an insertion of an additional 5 bp, created a new splice site resulting in the appearance of a premature stop codon (p.Phe184Tyrfs*26) and likely a truncated protein. This result constitutes a new splice-site variant report in the PJVKgene leading to DFNB59 type associated with autosomal recessive non-syndromic hearing impairment (ARNSHI).

Published
2024
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