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13th International AIDS ConferenceDurban, South Africa - July 9-July 14, 2000 |
Int Conf AIDS 2000 Jul 9-14; 13:31 (abstract no.. LbPeA7001)
Sedlacek D, Subrt I
dr. E. Benese, Czech Republic. Fax: +420 19 7422691, E-mail: sedlacek@fnplzen.cz.
BACKGROUND: Chemokine receptor CCR5 is an important surface co-receptor structure which is necessary for binding of HIV-1 to target macrophage cell lines serving as reservoirs for HIV CCR5 protein is coded by CCR5 gene. It was previously reported that people with mutated CCR5 gene are HIV-1 resistant due to non-expression of CCR5. A 32-bp deletion can be found in homozygous (1-3%) or heterozygous (5-18%) form in persons of Caucasian origin. The incidence of this mutation in the population of Czech Republic has not been analysed yet. Material and
METHODS: Fifty-six randomly chosen persons (22 women, 34 men), were included in our study. Eleven people were HIV positive. Genomic DNA samples were analysed by PCR amplification of genomic DNA extracted from peripheral blood mononuclear cells or buccal cells. We used a new, original, previously non-published primer pair flanking 32-bp deletion region of CCR5 gene. Subsequent detection of wild-type and mutated allelic variants of PCR amplification products was performed on high resolution agarose gel. Laboratory method was validated using control samples obtained in co-operation with Instituto de Hematologia, Porto, Portugal.
RESULTS: 32-bp heterozygous deletion was present in 9 of 45 (20%) HIV-negative people and 5 of 11 (45%) HIV-positive patients. Homozygous form of 32-bp deletion wasn't observed.
CONCLUSIONS: Our preliminary study has validated the described method as suitable for CCR5 32-bp deletion assessment. We aim to expand the study and test 500 persons in order to obtain statistically significant results.
Copyright © 2000 - International AIDS Society (IAS). Reproduction of this abstract (other than one copy for personal reference) must be cleared through the IAS.
