Ergathon

[img]http://drupalsvn.local/%7Ejim/drupalsvn/sites/default/files/styles/large/public/assets/img/post_images/2009.11.22-114103.jpg[/img]One of the most vexing challenges in the battle against dengue virus, a mosquito-borne virus responsible for 50-100 million infections every year, is that getting infected once can put people at greater risk for a more severe infection down the road.
Now, for the first time, an international team of researchers that includes experts from the University of California, Berkeley, has pulled apart the mechanism behind changing dengue virus genetics and dynamics of host immunity, and they are reporting their findings in the Dec. 21 issue of [i]Science Translational Medicine[/i].
The virus that causes dengue disease is divided into four closely related serotypes (dengue virus 1, 2, 3 and 4), and those serotypes can be further divided into genetic variants, or subtypes.
The researchers showed that a person’s prior immune response to one serotype of dengue virus could influence the interaction with virus subtypes in a subsequent infection. How that interaction plays out could mean the difference between getting a mild fever and going into a fatal circulatory failure from dengue hemorrhagic fever or dengue shock syndrome.
The findings have implications for the efforts to combat a disease that has grown dramatically in recent decades, including the development of a first-ever dengue vaccine.
According to the World Health Organization, dengue disease is now endemic in more than 100 countries around the world, and recent estimates say some 3 billion people – almost half of the world’s population – are at risk.
It was already known that upon a person’s first infection with dengue virus, the immune system reacts normally by creating antibodies to fight the viral invaders. The problem is that those antibodies can then be confused if confronted later with one of the other three types of dengue virus, and as this new study revealed, even different subtypes within the same serotype.

“With the second infection, the antibodies sort of recognize the new type of viruses, but not well enough to clear them from the system,” said study lead author Molly OhAinle, post-doctoral fellow in infectious diseases at UC Berkeley’s School of Public Health. “Instead of neutralizing the viruses, the antibodies bind to them in a way that actually helps them invade the immune system’s other cells and spread.”
The study authors noted that this Trojan horse effect has been shown before, but the new research provides an analysis of the interplay between viral genetics and immune response with unprecedented detail, going beyond the main serotype.
Putting the puzzle pieces together required UC Berkeley’s expertise in immunology and virology, the genome analysis and biostatistical capabilities at the Broad Institute of Harvard University and Massachusetts Institute of Technology, and the epidemiological and clinical field work at Nicaragua’s National Virology Laboratory.

Both the girls and boys crew teams recently made their presence known among the holiday shoppers at Fourth Street in Berkeley.  The Annual Ergathon was held on Saturday, December 4^th. 

The girls team got things going at about 9am, followed by the boys at about noon.  This event follows the team’s fall letter writing campaign.  If you’ve received your rower’s letter, please be generous and send in your donation, as this is the team’s most important fund-raising event of the year. If you didn’t receive a letter and would like to help, please use the “Donate” button. Thanks for your help!

Sponsor a rower today!

The next time you can see the team in action will be at the Holiday Sprints at JLAC on December 19^th.  Happy Holidays!

And for more fun….check out the video of the day’s event!