Role of polymorphisms of the inflammatory response genes and DC-SIGNR in genetic susceptibility to SARS and other infections

Hong Kong Med J. 2008 Aug;14 Suppl 4:31-5.

Abstract

1. A genetic risk-association study involving more than 1200 subjects showed individuals homozygous for L-SIGN tandem repeats are less susceptible to SARS infection. 2. This was supported by in vitro binding studies that demonstrated homozygous L-SIGN, compared to heterozygous, had higher binding capacity for SARS coronavirus (SARS-CoV), with higher proteasome-dependent viral degradation. In contrast, homozygous L-SIGN demonstrated lower binding capacity for HIV1-gp120.3. Genetic-association studies for single nucleotide polymorphisms of the inflammatory response genes, namely TNF-alpha, INF-alpha, INF-beta, INF-gamma, IL1-alpha, IL1-beta, IL-4, IL-6 and iNOS, failed to show a significant association with SARS clinical outcomes or susceptibility.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Alleles
  • Analysis of Variance
  • Case-Control Studies
  • Cell Adhesion Molecules / genetics*
  • Communicable Diseases / genetics
  • Communicable Diseases / physiopathology
  • Confidence Intervals
  • Cytokines / genetics
  • Cytokines / metabolism
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease*
  • Humans
  • Lectins, C-Type / genetics*
  • Male
  • Middle Aged
  • Odds Ratio
  • Polymorphism, Genetic*
  • Probability
  • Receptors, Cell Surface / genetics*
  • SARS Virus / genetics*
  • SARS Virus / metabolism
  • Severe Acute Respiratory Syndrome / genetics*
  • Severe Acute Respiratory Syndrome / physiopathology
  • Tandem Repeat Sequences
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CLEC4M protein, human
  • Cell Adhesion Molecules
  • Cytokines
  • Lectins, C-Type
  • Receptors, Cell Surface
  • Tumor Necrosis Factor-alpha