A mutation of the stromal cell–derived factor 1 gene (SDF-1 30A) was shown to protect adults exposed to human immunodeficiency virus type 1 (HIV-1) from infection and to affect HIV disease progression in adults. The presence of this mutation in HIV-1–infected Kenyan children did not predict mother-to-child virus transmission. The SDF-1 30A polymorphism was studied in 256 HIV-1–infected, 118 HIV-1–exposed but uninfected, and 170 unexposed and uninfected children of Italian origin, and the frequency of SDF-1 30A heterozygosity and homozygosity in each of the 3 groups was similar. Of the 256 HIV-1–infected children, 194 were regularly followed up and were assigned to groups according to disease progression. The frequency of the SDF-1 30A allele was substantially lower among children with long-term nonprogression than among children with rapid (P ¼ .0329) or delayed (P ¼ .0375) progression. We show that the presence of the SDF-1 30A gene correlates with accelerated disease progression in HIV-1–infected children born to seropositive mothers but does not protect against mother-to-child HIV- 1 transmission.
Prognostic Value of the Stromal Cell-Derived Factor 1 3prime prime or minuteA Mutation in Pediatric Human Immunodeficiency Virus Type 1 Infection
Tresoldi E.;Crovella S.;Salvatori F.;Plebani A.;
2002
Abstract
A mutation of the stromal cell–derived factor 1 gene (SDF-1 30A) was shown to protect adults exposed to human immunodeficiency virus type 1 (HIV-1) from infection and to affect HIV disease progression in adults. The presence of this mutation in HIV-1–infected Kenyan children did not predict mother-to-child virus transmission. The SDF-1 30A polymorphism was studied in 256 HIV-1–infected, 118 HIV-1–exposed but uninfected, and 170 unexposed and uninfected children of Italian origin, and the frequency of SDF-1 30A heterozygosity and homozygosity in each of the 3 groups was similar. Of the 256 HIV-1–infected children, 194 were regularly followed up and were assigned to groups according to disease progression. The frequency of the SDF-1 30A allele was substantially lower among children with long-term nonprogression than among children with rapid (P ¼ .0329) or delayed (P ¼ .0375) progression. We show that the presence of the SDF-1 30A gene correlates with accelerated disease progression in HIV-1–infected children born to seropositive mothers but does not protect against mother-to-child HIV- 1 transmission.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
