Fears of the ebola virus outbreak is spreading faster than the disease itself. After killing around 4.922 people in six West African countries this year, the disease has now traveled to the United States. Panic is taking over some American households. Different measures were taken by citizens, some are even staying away from places where they thought someone who contracted the disease passed by. However, according to scientists from universities in Washington and California as well as the National Institute of Health in Montana, a person can be saved depending on his own genes.
Using mice in their experiment conducted at state-of-the-art Montana laboratory, scientists found out that the genetic variations of each animals govern how ill victims will get by after contracting the disease. They said that some mice were able to survive without contracting ebola, others had moderate illness, while others bleed heavily and fell to organ failure and shock.
"Our data suggests that genetic factors play a significant role in disease outcome," said co-author Dr Michael Katze, of Washington University's Department of Microbiology.
"We hope that medical researchers will be able to rapidly apply these findings to candidate therapeutics and vaccines."
Video by University of Washington on Publish Date October 30, 2014. Photo by University of Washington. (c) The New York Times
After the study, scientists concluded that some people could be naturally immune to the ebola virus. Authors of the research think those who survived ebola virus in West Africa have had natural immunity.
"This paper demonstrates that the genes of the host play a role in determining the outcome of Ebola infection in terms of the severity of the disease, at least in mice," said Prof Andrew Easton, Professor of Virology, University of Warwick.
We know that host genetics influences infection outcome for a range of viruses, like HIV and norovirus. We've also suspected that genetics plays a role in susceptibility to Ebola virus infection," added Prof Jonathan Ball, Professor of Molecular Virology, University of Nottingham.
"It's a reminder of how infectious diseases shape the evolution of a host; and the human host is no different to any other."
