Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-3-25
pubmed:abstractText
Dengue disease can clinically evolve from an asymptomatic and mild disease, known as dengue fever (DF), to a severe disease known as dengue hemorrhagic fever (DHF). Recent evidence has shown how host genetic factors can be correlated with severe dengue susceptibility or protection. Many of these genes, such as CD209, TNF-a, vitamin D receptor, and FC gamma receptor IIA, are components of the innate immune system, suggesting that innate responses might have a role in dengue pathogenesis. MBL2 gene polymorphisms have been shown to modulate susceptibility or protection in many viral diseases. We investigated the involvement of MBL2 gene in the dengue clinical outcome through the analysis of MBL2 exon 1 polymorphisms (at codons 52, 54, and 57) known to be associated with reduced serum levels of the MBL protein. The genotypes of 110 well-characterized dengue-positive patients were statistically analyzed to establish possible correlations between MBL2 polymorphisms and parameters such as sex, type of infection (primary or secondary response), race/ethnicity, course of infection, and age. We found significant correlations between wild-type AA MBL2 genotype and age as associated risk factors for development of dengue-related thrombocytopenia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0198-8859
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
122-8
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
MBL2 gene polymorphisms protect against development of thrombocytopenia associated with severe dengue phenotype.
pubmed:affiliation
Virology and Experimental Therapy Laboratory, Aggeu Magalhães Research Center-CPqAM/FIOCRUZ, Recife, Brazil.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural