Dengue fever is a viral infection transmitted through the bite of a mosquito. Symptoms can be mild with patients never knowing they have been infected. However, in more unfortunate cases, Dengue fever can lead to haemorrhagic tendency triggering the often-fatal Dengue Shock Syndrome. Because some people experience only limited symptoms, they can unwittingly transport the virus from the tropics back to their home country. The Dengue virus increases the permeability of blood vessels causing blood loss leading to shock. An international research team claims to have identified the enzymes, which ultimately lead to blood loss, and have established an innovative treatment strategy. Their work was recently published in Nature's EMBO Reports.
According to the team of international researchers from France, the UK and Thailand, approximately 60 to 100 million people are at risk of Dengue fever and the numbers are rising. A virus prevalent in areas also home to malaria, the most effective available prevention strategy is the elimination of the mosquito vector. In hopes of finding novel methods for eradicating the virus, the research team lead by the Institut de recherche pour le development (IRD) investigated the enzyme metalloproteinase and its effect on the cement holding blood vessels together.
They have uncovered evidence showing that metalloproteinase is responsible for effectively poking holes in the side of blood vessels by dissolving the proteins holding them together. Metalloproteinase is a naturally occurring compound involved in critical stages of embryo development and tissue repair. It has been shown to play a role in the development of certain cancers, however, and new evidence demonstrates that higher than normal concentrations can lead to haemorrhaging.
The research team was able to identify a direct relationship between cells infected by the Dengue virus and increased production of metalloproteinase. They crosschecked their findings against a series of cell cultures, and were able to confirm that raised levels of metalloproteinase were indeed responsible for the increased permeability of vascular tissue.
Once a protein inhibitor was introduced into the culture blocking the overactive metalloproteinase, natural permeability was restored. Their hypotheses concerning metalloproteinase were again supported through in vivo testing in mice.
The results uncovered by the European-led international team shed new light on Dengue's pathological strategy. Researchers now suspect that they have not only come across a defence strategy for Dengue, but for a whole range of haemorrhage-inducing viruses, such as Ebola, Marburg, or Hanta, for none of which treatment exists. Clinical trials are currently being developed taking into account these new research strategies.
Source: Bio-Bio Technology