When some people are exposed to
Ebola, some resist the disease, others suffer moderate to severe illness and
recover, and some who are most vulnerable succumb to bleeding, organ failure,
and shock. There is not necessarily a change to the Ebola virus itself but how
a person’s body attempts to fight the infection which determines the severity
of the disease. On October 30, 2014 Angela Rasmussen and Michael Katze
described strains of laboratory mice bred to test the role of an individual’s
genetic makeup in the course of Ebola disease. This study was hindered by the
lack of a mouse model that replicates the main characteristics of human Ebola
hemorrhagic fever. Angela Rasmussen and Michael Katze originally obtained this
genetically diverse group of inbred laboratory mice to study locations on mouse
genomes associated with influenza severity.
These scientists infected mice with
the same species of Ebola virus causing the 2014 West Africa outbreak. Initially,
conventional laboratory mice that were previously infected with this virus died
and didn’t develop symptoms of Ebola hemorrhagic fever. The present study, all
the mice lost weight in the first few days after infection. Nineteen percent of
the mice were unfazed; they survived and fully regained the weight they lost
within two weeks. They didn’t experience gross pathological evidence of disease
while their livers looked normal. Eleven percent of the mice were partially resistant
and less than half of them died. Seventy percent of the mice had greater than
50 percent mortality while 19 percent had liver inflammation without classic
symptoms of Ebola and 34 percent had blood that took too long to clot which is
a hallmark of fatal Ebola hemorrhagic fever in humans. The mice with Ebola hemorrhagic fever also
had internal bleeding, swollen spleens, and changes in liver color and texture.
The scientist correlated disease outcomes and variations in mortality rates to
specific genetic lines of mice.
The data suggested that genetic
factors play a significant role in disease outcome. When the virus infection
frenzies the genes involved in promoting blood vessel inflammation and cell
death, serious or fatal disease followed. On the other hand, survivors
experienced more activity in genes that order blood vessel repair and the
production of infection-fighting white blood cells. Rasmussen and Katze also
noted that certain specialized types of cells in the liver could also have
limited virus reproduction and put a damper on systemic inflammation and blood
clotting problems in resistant mice. Vulnerable mice had widespread liver
infection, which may have explained why they had more virus in their bodies and
poorly regulated blood clotting. Rasmussen and Katze also noticed that soleens
in the resistant and vulnerable mice took alternate routes to try to ward off
infection.
This mouse model has the potential
to be promptly implemented to find genetic markers, conduct meticulous studies on
how symptoms originated and take hold, and evaluate drugs that have broad
spectrum anti-viral activities against all Zaire Ebola viruses, including the
one responsible for the current West African epidemic.
Although this is a new study and
innovating, we don’t truly know if a person’s genes are what influence life or
death due to this virus. I guess one way to further study if genes do have a role
in survival is to test on humans but who would actually put themselves in harms
ways.
Article: http://www.sciencedaily.com/releases/2014/10/141030142206.htm
