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
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Alleles
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Analysis of Variance
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Case-Control Studies
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Cell Adhesion Molecules / genetics*
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Communicable Diseases / genetics
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Communicable Diseases / physiopathology
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Confidence Intervals
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Cytokines / genetics
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Cytokines / metabolism
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Female
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Gene Frequency
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Genetic Predisposition to Disease*
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Humans
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Lectins, C-Type / genetics*
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Male
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Middle Aged
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Odds Ratio
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Polymorphism, Genetic*
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Probability
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Receptors, Cell Surface / genetics*
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Severe Acute Respiratory Syndrome / genetics*
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Severe Acute Respiratory Syndrome / physiopathology
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Severe acute respiratory syndrome-related coronavirus / genetics*
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Severe acute respiratory syndrome-related coronavirus / metabolism
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Tandem Repeat Sequences
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / metabolism
Substances
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CLEC4M protein, human
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Cell Adhesion Molecules
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Cytokines
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Lectins, C-Type
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Receptors, Cell Surface
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Tumor Necrosis Factor-alpha