Researchers in South East Asia have identified two genetic variants that offer clues to how the body responds to dengue infection.
The study, funded by the Wellcome Trust and the Agency for Science, Technology, and Research (A*STAR), Singapore, compared genomes of about 2,000 children with severe dengue against population controls.
Changes in the DNA code within two codes – MICB on chromosome 6 and PLCE1 on chromosome 10 – seemed to increase a child’s susceptibility to dengue shock syndrome.
MICB is known to play a role in the body’s immune system and variants of this gene may affect the activation of natural killer cells or CD8 T-cells, two types of cells that play a key role in combating viral infection.
If these cells are not properly functioning, the body cannot entirely fight off the dengue virus.
Mutations in PLCE1 have previously been linked to nephrotic syndrome, a childhood disease characterised by impairment of the normal barrier and blood filtering functions of cells in the kidney.
Researchers believe mutations in PLCE1 could result in leakage from the blood vessels, which is consistent with dengue shock syndrome.
The findings are published today in the scientific journal Nature Genetics.
Professor Cameron Simmons, senior author of the study from the Oxford University Clinical Research Unit, Vietnam, said: “Our study confirms epidemiological evidence that some people are naturally more susceptible to severe forms of the disease than others.”
Dengue is globally the most common mosquito-borne infection after malaria, with an estimated 100 million infections occurring annually.
No clinically-approved vaccine or specific treatments exist for the disease.