title: The nine-repeat DC-SIGNR isoform is associated with increased HIV-RNA loads and HIV sexual transmission.
abstract: OBJECTIVE
  Determine if different DC-SIGNR genotypes/alleles correlated with HIV susceptibility in the context of the HIV mode of infection, CD4+ T cell counts and blood HIV RNA loads.
  
  
  METHODS
  One hundred forty-five HIV infected individuals and 187 uninfected healthy controls were recruited to observe whether DC-SIGNR genotypes/alleles were correlated with HIV susceptibility, CD4+ T cell numbers and HIV-RNA levels.
  
  
  RESULTS
  The frequencies of DC-SIGNR genotypes/alleles in HIV-infected patients were similar to those seen in the uninfected population. However, the 9-repeat DCSIGNR allele was more frequently found in patients infected via sexual transmission compared to patients infected via blood transmission/intravenous drug use (p = 0.005). HIV RNA levels in patients with the 9- or 7-repeat DC SIGNR allele were significantly higher than the levels observed in patients with the 5-repeat DC SIGNR allele (p = 0.004, p = 0.004, respectively) and the HIV RNA levels in patients with the 9/7 genotype or with the 7/7 genotype were significantly higher than patients with the 7/5 genotype (p = 0.003, p = 0.029, respectively). There were no significant differences between CD4+ T cells in patients with different DC-SIGNR genotypes/alleles.
  
  
  CONCLUSIONS
  No DC-SIGNR genotypes/alleles were associated with reduced HIV susceptibility, however, DC-SIGNR genotypes/alleles with higher repeat numbers were associated with higher HIV-RNA blood levels, that is, the 9-repeat DC-SIGNR allele was significantly associated with increased HIV-RNA levels and HIV sexual transmission.
authors.affiliation: Clinical Center of HIV/AIDS, Fuzhou Infectious Disease Hospital, Fujian Medical University, No.315, Xihong Rd, Fuzhou City 350025, China. xuli-jun@hotmail.com
authors.forename: Lijun
authors.initials: L
authors.lastname: Xu
authors.forename: Qinguang
authors.initials: Q
authors.lastname: Li
authors.forename: Hanhui
authors.initials: H
authors.lastname: Ye
authors.forename: Qiyun
authors.initials: Q
authors.lastname: Zhang
authors.forename: Huicong
authors.initials: H
authors.lastname: Chen
authors.forename: Fan
authors.initials: F
authors.lastname: Huang
authors.forename: Ronghua
authors.initials: R
authors.lastname: Chen
authors.forename: Rui
authors.initials: R
authors.lastname: Zhou
authors.forename: Wen
authors.initials: W
authors.lastname: Zhou
authors.forename: Pincang
authors.initials: P
authors.lastname: Xia
authors.forename: Yi
authors.initials: Y
authors.lastname: Chen
authors.forename: Chen
authors.initials: C
authors.lastname: Pan
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015496:CD4-Positive T-Lymphocytes / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000235:genetics* / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006678:HIV / Q000235:genetics* / Q000254:growth & development / Q000276:immunology* / Q000472:pathogenicity; D015658:HIV Infections; D006801:Humans; D007223:Infant; D037181:Lectins, C-Type / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D020033:Protein Isoforms / Q000235:genetics; D012367:RNA, Viral / Q000032:analysis*; D011956:Receptors, Cell Surface / Q000235:genetics* / Q000378:metabolism; D012091:Repetitive Sequences, Nucleic Acid / Q000235:genetics*; D015229:Sexually Transmitted Diseases, Viral; D019562:Viral Load; D014774:Virulence / Q000235:genetics
chemical_list: C433029:CLEC4M protein, human; D015815:Cell Adhesion Molecules; D037181:Lectins, C-Type; D020033:Protein Isoforms; D012367:RNA, Viral; D011956:Receptors, Cell Surface