title: Periodontal attachment loss in HIV-infected patients is associated with the major histocompatibility complex 8.1 haplotype (HLA-A1,B8,DR3).
abstract: Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals.
authors.affiliation: Department of Clinical Immunology, Royal Perth Hospital, Australia. pprice@cyllene.uwa.edu.au
authors.forename: P
authors.initials: P
authors.lastname: Price
authors.forename: D M
authors.initials: DM
authors.lastname: Calder
authors.forename: C S
authors.initials: CS
authors.lastname: Witt
authors.forename: R J
authors.initials: RJ
authors.lastname: Allcock
authors.forename: F T
authors.initials: FT
authors.lastname: Christiansen
authors.forename: G R
authors.initials: GR
authors.lastname: Davies
authors.forename: P U
authors.initials: PU
authors.lastname: Cameron
authors.forename: M
authors.initials: M
authors.lastname: Rogers
authors.forename: K
authors.initials: K
authors.lastname: Baluchova
authors.forename: C B
authors.initials: CB
authors.lastname: Moore
authors.forename: M A
authors.initials: MA
authors.lastname: French
mesh_terms: D000328:Adult; D000483:Alleles; D015658:HIV Infections / Q000150:complications* / Q000235:genetics / Q000276:immunology*; D006680:HLA Antigens / Q000235:genetics / Q000276:immunology*; D015788:HLA-A1 Antigen / Q000235:genetics / Q000276:immunology; D015795:HLA-B8 Antigen / Q000235:genetics / Q000276:immunology; D015803:HLA-DR3 Antigen / Q000235:genetics / Q000276:immunology; D006239:Haplotypes; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics; D008297:Male; D017622:Periodontal Attachment Loss / Q000235:genetics / Q000276:immunology* / Q000821:virology*; D010641:Phenotype; D011110:Polymorphism, Genetic; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D006680:HLA Antigens; D015788:HLA-A1 Antigen; D015795:HLA-B8 Antigen; D015803:HLA-DR3 Antigen; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha