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Surviving or dying from Ebola may be partly down to genes

Date: Oct-31-2014
In a highly secure, ultra-modern biocontainment safety level 4 lab in

Hamilton, MT, scientists working with Ebola-infected mice have discovered that host

genes may play an important role in deciding whether the virus infection is fatal or

not. Their findings suggest in some people, because of their genes, the virus sparks

reactions that help to limit the damage of the infection.

Reporting in the journal Science, the team hopes the new strains of mice, which

they have developed to study how host genes react to Ebola in the lab, will speed up

drug and vaccine development.

Three research centers collaborated on the project: the University of Washington in

Seattle, the National Institutes of Health's (NIH) Rocky Mountain Laboratories in Montana

and the University of North Carolina at Chapel Hill.

Severity of Ebola infection is not always due to the virus

After studying mice with different genetic features, the team found the severity of the Ebola infection and rates of death seemed to line up with specific gene patterns.

Earlier studies of people infected with Ebola have found that the diversity of

reactions is not necessarily due to the virus itself but factors in the host: some

completely resist the infection, others have a mild to moderate reaction, while those

who are most susceptible succumb to bleeding, organ failure and shock.

But what was missing in order to explore what might explain this diversity of

responses was a reliable animal model that could be used in a safe and secure lab.

The researchers behind the new study showed that the strains of mice they have

developed meet this need.

They took a genetically diverse group of inbred mice that had been developed to

study genes involved in influenza severity and used them to breed strains that

replicate the main features of human Ebola hemorrhagic fever.

In the NIH lab in Montana - which complies with federal, state, and local safety

and biosecurity regulations - they studied mice infected with a mouse version of the

Ebola strains that are currently infecting humans in the 2014 West Africa

epidemic.

Infection severity may be explained by Ebola virus effect on host genes

They found that while all the mice lost weight in the first few days of infection,

19% of them were not severely affected by the virus - not only did they survive, they

put their weight back on within 2 weeks. They showed no serious physical signs of

disease; their livers looked normal, note the authors.

Meanwhile, another 11% of the mice showed partial resistance to Ebola - less than

half of this group died - and the remaining 70% showed severe reactions - over half of

them died.

Of the 70% of mice that had a severe reaction, 19% had liver inflammation without

classic symptoms of Ebola, while 34% had blood that took a long time to clot - a

classic hallmark of fatal Ebola hemorrhagic fever in humans. These mice also showed

signs of internal bleeding, swollen spleens and their livers changed color and

texture.

When they looked at the various genetic make ups of these groups of mice, the team

found the severity of the Ebola infection and rates of death seemed to line up with

specific gene patterns.

Their results showed that in general, in the mice that suffered serious reactions and

died, the Ebola virus tended to activate genes involved in promoting blood vessel

inflammation and cell death. But in mice that survived Ebola infection, the virus

tended to activate genes that control blood vessel repair and production of immune

cells that fight infection.

Liver and spleen reactions also varied with Ebola infection severity

The team also noted there could be something happening in the livers of Ebola-resistant mice to reduce disease severity. Some specialized liver cells may have

limited virus replication and so minimized severity of systemic inflammation and

damage to blood clotting processes.

This could explain why susceptible mice suffered widespread liver infection, their

bodies having more of the virus and poor blood coagulation.

They also found that the spleens of the resistant mice took a different route to

try and ward off infection than the spleens of susceptible mice.

Lead author Dr. Angela Rasmussen, of the University of Washington (UW) microbiology

and systems biology lab, says the frequency patterns of different disease symptoms

they saw in the mice are similar to those observed in humans in the 2014 West Africa

outbreak.

Senior author Michael Katze, professor of microbiology, and head of the UW lab,

says while there may be other reasons to explain immunity in recent Ebola

survivors:

"Our data suggest that genetic factors play a significant role in disease

outcome. We hope that medical researchers will be able to rapidly apply these findings to

candidate therapeutics and vaccines."

In a letter recently published in the Lancet, some experts raise the

possibility that as it rages in West Africa, leaving many deaths in its wake,  Ebola could also quietly be immunizing many people.

Finding a reliable way to identify them, and perhaps recruit them to help with disease

control, could reduce risk of infection to those who are not immune.

Written by Catharine Paddock PhD

Not to be reproduced without permission.

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Courtesy: Medical News Today
Note: Any medical information available in this news section is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional.