Serological and Molecular Study of the Duffy Blood Group among Malarial Endemic Region Residents in Brazil.

Autor: Langhi Júnior D; Universidade Federal de São Paulo, Departamento de Oncologia Clínica e Experimental, São Paulo, SP, Brasil.; HHemo Hemoterapia SA, São Paulo, SP, Brasil., Albuquerque S; Fundação Hemocentro do Amazonas, Manaus, AM, Brasil., Serafim R; HHemo Hemoterapia SA, São Paulo, SP, Brasil., Duarte GC; Universidade Estadual de Campinas, Centro de Hematologia e Hemoterapia, Campinas, SP, Brasil., Covas DT; Universidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Ribeirão Preto, SP, Brasil., Bordin JO; Universidade Federal de São Paulo, Departamento de Oncologia Clínica e Experimental, São Paulo, SP, Brasil.; HHemo Hemoterapia SA, São Paulo, SP, Brasil.
Jazyk: angličtina
Zdroj: Revista da Sociedade Brasileira de Medicina Tropical [Rev Soc Bras Med Trop] 2022 Aug 05; Vol. 55, pp. e0490. Date of Electronic Publication: 2022 Aug 05 (Print Publication: 2022).
DOI: 10.1590/0037-8682-0490-2021
Abstrakt: Background: The atypical chemokine receptor 1 (ACKR1) gene encodes the Duffy blood group antigens in two allelic forms: FY*A (FY*01) and FY*B (FY*02), which define the Fy(a+b-), Fy(a-b+), and Fy(a+b+) phenotypes. FY*BES (FY*02N.01) is a single T to C substitution at nucleotide -67 that prevents the FY*B from being expressed in red blood cells (RBCs).
Methods: We evaluated 250 residents from a Brazilian malarial endemic region (RsMR). All individuals were phenotyped for Fya and Fyb antigens and genotyped for FY*A, FY*B, FY*B SE , and FY*B weak alleles.
Results: Among the 250 individuals, 209 (83.6%) reported previous malaria infection, and 41 (16.4%) did not. The Fy(a+b+) phenotype was present in 97/250 (38.8%), while the Fy(a-b-) was present in 7/250 (2.8%). The FY*A/FY*B was found in 130/250 (52%) and the FY*A/FY*A in 45/250 (18%). The c.1-67>TC was present, in homozygosity, in 11/250 (4.4%). Among 34 individuals with the Fy(a+b-) and FYA*/FYB* mutations, 4/34 (11.8%) had homozygosity for the c.1-67T>C. One individual presented the Fy(a+b-), FY*A/FY*B, and c.1-67T>C in homozygosis, whereas the other presented the Fy(a+b-), FY*A/FY*A, and c.1-67T>C in heterozygosis.
Conclusions: We reported a low prevalence of the Fy(a-b-) in persons who had previously been infected with Plasmodium vivax (67.5%). We observed that 102/141 (72.3%) individuals expressing the Fyb antigen had a P. vivax infection, indicating the importance of the Fyb antigen, silenced by a c.1-67T>C mutation in homozygosis, in preventing the P. vivax infection. We showed that the c.1-67T>C mutation in the FY*A did not silence the FY*A expression on RBCs.
Databáze: MEDLINE