We encourage you to republish this article online and in print, it’s free under our creative commons attribution license, but please follow some simple guidelines:
  1. You have to credit our authors.
  2. You have to credit SciDev.Net — where possible include our logo with a link back to the original article.
  3. You can simply run the first few lines of the article and then add: “Read the full article on SciDev.Net” containing a link back to the original article.
  4. If you want to also take images published in this story you will need to confirm with the original source if you're licensed to use them.
  5. The easiest way to get the article on your site is to embed the code below.
For more information view our media page and republishing guidelines.

The full article is available here as HTML.

Press Ctrl-C to copy

Genetic factors could determine who is at risk from the virus that causes dengue fever, according to research published in the current issue of Nature Genetics.

Having a particular variant of a gene called CD209 protects some people from dengue fever, says the study. But this variant provides no protection against the more severe, and often fatal, form known as dengue haemorrhagic fever.

The researchers, led by Cécile Julier of France's Pasteur Institute knew that CD209 makes a molecule called DC-SIGN1, which the dengue virus attaches to when attacking human cells.

Julier's team investigated whether people with different forms of the gene have different levels of susceptibility to the virus.

The researchers analysed the genetic profile of more than 1,300 Thai children, 606 of whom had been admitted to hospital with dengue fever, and 696 who were healthy.

One variant of the gene was highly protective — those with it were five times less likely to develop dengue fever than were those who had a different version.

But the researchers found that variation of the gene played no role in determining whether people developed the severe form of the disease. They suggest that this is because in the more severe form, the virus finds another way to enter cells — one that doesn't involve DC-SIGN1.

This, they say, is important for researchers studying ways to tackle both forms of the disease. For example, tests for potential vaccines or treatments will need to take this difference into account.

DC-SIGN1 is also important for other viruses that attack our cells such as Ebola, HIV and SARS (severe acute respiratory syndrome).

Variation in the CD209 gene might also affect people's susceptibility to these other viruses, say the scientists.

Dengue virus is mainly transmitted to people by the bite of a mosquito species called Aedes aegypti, which occurs in the tropics and subtropics.

Around two-fifths of the world's population are thought to be at risk getting dengue fever.

Nature Genetics 37, 507 (2005)

Related topics