Institutional members access full text with Ovid®

A nonsense mutation (428GA) in the fucosyltransferase FUT2 gene affects the progression of HIV-1 infection

Kindberg, Elina,b; Hejdeman, Boc; Bratt, Göranc; Wahren, Brittad; Lindblom, Bertila; Hinkula, Jormab,d; Svensson, Lennartb

doi: 10.1097/01.aids.0000216368.23325.bc
Basic Science: Concise Communication

Background: The human FUT2 gene encodes the α(1,2)fucosyltransferase that determines secretor status. Homozygous for the nonsense mutation are called non-secretors and are unable to express histo-blood group antigens in secretions and on mucosal surfaces. In this study we have investigated the importance of the FUT2 fucosyltransferase activity on the progress of HIV-1 infection.

Methods: Swedish blood donors (n = 276), 15 long-term non-progressors (LTNP) and 19 progressors were genotyped with respect to the nonsense mutation 428G→A in the FUT2 gene. In addition 265/276 blood donors and 19 progressors with rapid or expected progression rate were Δ32 CCR5 genotyped.

Results: Of 276 blood donors 218 (79%) were found to be secretor positive (se+), either homozygous (se+/+) wild type (30%) or heterozygous (se+/−) (49%) and 58 (21%) were homozygous non-secretors (se−/−). Five LTNP (33%) were found to be secretor-positive (se+/+, se+/−) and 10 (67%) se−/−. Of the 19 individuals with normal HIV-1 progression 15 (79 %) were found to be secretor positive and four (21%) were non-secretors. No frequency differences were found in the Δ32 CCR5 allele among the groups studied.

Conclusion: Strong association (P < 0.001) was observed between the nonsense mutation 428G→A in the FUT2 gene and a slow disease progression of HIV-1 infection.

From the aDepartment of Forensic Genetics, National Board of Forensic Medicine, University Hospital, Linköping, Sweden

bDivision of Molecular Virology, University of Linköping, Sweden

cVenhälsan, Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden

dDepartment of Virology, Swedish institute for Infectious Disease Control and MTC Karolinska Institutet, Stockholm, Sweden.

Received 6 October, 2005

Revised 30 December, 2005

Accepted 12 January, 2006

Correspondence to L. Svensson, Division of Molecular Virology, Medical Faculty (IMK), University of Linköping, 581 85 Linköping, Sweden. Tel: +46 13 228803; fax: +46 13 221375; e-mail: lensv@imk.liu.se

© 2006 Lippincott Williams & Wilkins, Inc.