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Béatrice Dambaya,1,2 Céline Nguefeu Nkenfou,1,3 Linda Mekue,1,4 Georges Této,1 Nicole Ngoufack,1,2 Georgia Ambada,1,2 Njiokou Flobert,1 Vittorio Colizzi,5 Ndjolo Alexis1,6 1Chantal BIYA International Reference Centre for Research on HIV/AIDS Prevention and Management (CBIRC), Yaoundé, Cameroon; 2Department of Animal Biology, Faculty of Sciences, University of Yaounde I, Yaoundé, Cameroon; 3Department of Biological Sciences, Higher Teachers’ Training College, University of Yaounde I, Yaoundé, Cameroon; 4Department of Biochemistry, Faculty of Sciences, University of Dschang, Dschang, Cameroon; 5Department of Immunology, University of Rome Tor Vergata, Rome, Italy; 6Department of Ear, Nose and Throat, Faculty of Medicine and Biomedical Sciences, University of Yaounde I, Yaoundé, CameroonCorrespondence: Céline Nguefeu NkenfouHigher Teacher Training College, University of Yaounde I, P.O. BOX 47, Yaounde, CameroonTel +675573519Email nkenfou@yahoo.comBackground: Children show various degrees of vulnerability regarding HIV infection and disease progression. This disparity presents challenges for the follow-up of infected children. Here we investigated reasons behind this variability focusing on some host-related HIV genes.Methods: We screened 570 Cameroonian children and adolescents, aged 1 to 19 years old. Among them, 137 were followed over 4 years, from 2010 to 2015. Upon signing a proxy consent, children and adolescents were classified according to their age, CD4 count, viral load and clinical symptoms as long-term non-progressors (LTNP), slow progressors (SP) and rapid progressors (RP). Their blood was collected every 6 months and used for biological and host genetic polymorphism analyses. Five genes were genotyped: Trim5α (R136Q), CCR5 promoter 59029G, CCR2-64I, SDF 3ʹA and CCR5-Δ32. Exposed non-infected (HEU) and unexposed HIV negative children (HNEU) were recruited as control groups.Results: Among the 5 genes studied, the protective allele of Trim5α (R136Q) was present in all LTNP and in 72.34% and 2.56% of SP and RP, respectively (p<0.0001). The CCR5 promoter 59029G/G was also more present in LTNP and SP than in RP (p=0.02; p=0.04). The protective CCR2-64I homozygous genotype was almost absent in all groups, only the heterozygous genotype was present with a significant difference between RP vs SP (p=0.0001), and SP vs LTNP (p=0.0002). The CCR2-∆32 was completely absent either as homozygous or heterozygous genotype. It was a monomorphic allele. SDF 3ʹA was almost present as homozygous wild-type genotype in our study population and was associated neither to disease acquisition nor to disease progression.Conclusion: Among the 5 genes described in the study, Trim 5α (R136Q), CCR5 promoter 59029G and CCR2V64I alleles were associated to the progression of HIV infection in children and adolescents.Keywords: aids related genes, infected children, disease progression