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Polymorphisms at GLUT1 gene are not associated with the development of TSP/HAM in Brazilian HTLV‐1 infected individuals and the discovery of a new polymorphism at GLUT1 gene
Author(s) -
Costa Giselle Calasans Souza,
Azevedo Rochele,
Gadelha Sandra Rocha,
Kashima Simone Haddad,
Muricy Gabriel,
Olavarria Viviaila,
Covas Dimas Tadeu,
Takayanagui Osvaldo Massaiti,
GalvãoCastro Bernardo,
Alcantara Luiz Carlos Júnior
Publication year - 2009
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.21421
Subject(s) - provirus , genotype , glut1 , biology , single nucleotide polymorphism , asymptomatic carrier , virology , snp , population , allele , asymptomatic , gene , immunology , genetics , glucose transporter , medicine , genome , environmental health , endocrinology , insulin
The development of HTLV‐1 associated clinical manifestations, such as TSP/HAM and ATLL, occur in 2–4% of the infected population and it is still unclear why this infection remains asymptomatic in most infected carriers. Recently, it has been demonstrated that HTLV uses the Glucose transporter type 1 (GLUT1) to infect T‐CD4 + lymphocytes and that single nucleotide polymorphisms (SNP) in the GLUT1 gene are associated with diabetic nephropathy in patients with diabetes mellitus in different populations. These polymorphisms could contribute to a higher GLUT1 protein expression on cellular membrane, facilitating the entry of HTLV and its transmission cell by cell. This could result in a higher provirus load and consequently in the development of TSP/HAM. To evaluate the role of GLUT1 gene polymorphisms in the development of TSP/HAM in HTLV‐1 infected individuals, the g.22999G > T, g.15339T > C and c.‐2841A > T sites were analyzed by PCR/RFLP or sequencing in 244 infected individuals and 102 normal controls. The proviral load of the HTLV‐1 infected patients was also analyzed using Real Time Quantitative PCR. Genotypic and allelic frequencies of the three sites did not differ significantly between controls and HTLV‐1 infected individuals. There was no difference in genotypic and allelic distributions among patients as to the presence or absence of HTLV‐1 associated clinic manifestations. As regards the quantification of the provirus load, we observed a significant reduction in the asymptomatic individuals compared with the oligosymptomatic and TSP/HAM individuals. These results suggest that g.22999G > T, g.15339T > C, and c.‐2841A > T SNP do not contribute to HTLV‐1 infection nor to the genetic susceptibility of TSP/HAM in Brazilian HTLV‐1 infected individuals. J. Med. Virol. 81:552–557, 2009. © 2009 Wiley‐Liss, Inc.