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The Dengue Virus Unplugged

The manner of transmission of mosquito-borne viruses is well known; a bite on the body that allows the virus to make an entry into the blood stream. But what happens next that causes the virus //to multiply and take hold of its victim. Researchers led by a Howard Hughes Medical Institute (HHMI) international scholar in Argentina have been able to point at a genetic element which helps the dengue virus multiply, which is the main cause of the potentially fatal illness termed as dengue hemorrhagic fever.

In the August 15, 2006, issue of the journal Genes & Development, published online August 1, 2006, virologist Andrea Gamarnik and colleagues at Leloir Institute Foundation in Buenos Aires, describe how a viral enzyme recognizes and amplifies the genetic material needed to assemble new dengue viruses. Their findings provide the first model for RNA replication in the family of viruses that includes West Nile, St. Louis encephalitis, and hepatitis C.

These viruses, known as flaviviruses, cause millions of cases of human illness each year, but no vaccines or antiviral drugs exist to control most of the infections. Dengue fever is endemic in many tropical and subtropical regions, causing a severe, flu-like illness that sickens more than 50 million people and kills 25,000 each year.

Once a virus enters a host cell, its top priority is to copy its genetic code so that it can make more virus. Flaviviruses are so efficient at this task that they can churn out tens of thousands of copies of their genome--which is composed of ribonucleic acid, or RNA--within hours of infecting a cell.

For dengue and other flaviviruses, the first step is to produce viral proteins, including an enzyme that can copy RNA. But the viral RNA is not the only RNA in an infected cell. So once the enzyme, called RNA-dependent RNA polymerase (RdRp), is produced, it finds itself surrounded by cellular RNA, creating a dilemma: How does RdRp distinguish vir
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