Genetic analysis of CR1 (the C3b complement receptor, CD35) expression on erythrocytes of HIV-infected individuals.
The number of C3b receptor (CR1) molecules on erythrocytes is genetically determined by two codominant autosomal alleles. The genetic polymorphism of CR1 expression correlates with a Hind III restriction fragment length polymorphism (RFLP) of the CR1 gene. The relative frequency of individuals homozygous for the allele coding for low CR1 numbers is approximately 5% of the normal population. CR1 numbers/erythrocytes are significantly decreased in symptomatic HIV-infected individuals. Decreased CR1 expression correlates with the severity of disease. The present study investigated the CR1 genomic Hind III RFLP-related polymorphism in 79 HIV-infected individuals and 84 healthy subjects. Allele frequencies were found to be similar in both populations. Thus, there is no susceptibility nor resistance to HIV-infected linked to the CR1 gene. Defective expression of CR1 in HIV-infected patients is acquired through central and/or peripheral mechanisms.
Cohen
J H
JH
Laboratoire d'Immunologie, Hôpital R. Debré, Reims, Paris, France.
Geffriaud
C
C
Caudwell
V
V
Kazatchkine
M D
MD
D000163:Acquired Immunodeficiency Syndrome / Q000235:genetics / Q000276:immunology; D000483:Alleles; D015139:Blotting, Southern; D004912:Erythrocytes / Q000378:metabolism*; D005838:Genotype; D006679:HIV Seropositivity / Q000235:genetics* / Q000276:immunology; D015497:HIV-1; D006801:Humans; D012150:Polymorphism, Restriction Fragment Length; D011951:Receptors, Complement / Q000096:biosynthesis / Q000235:genetics*; D017463:Receptors, Complement 3b
D011951:Receptors, Complement; D017463:Receptors, Complement 3b