From U Colorado: “CU-Boulder study reveals evolutionary arms race between Ebola virus, bats”

U Colorado

University of Colorado Boulder.

December 22, 2015
Sara Sawyer, 303-735-0531

Trent Knoss, CU-Boulder media relations, 303-735-0528

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The Ebola virus, isolated in November 2014 from patient blood samples obtained in Mali. The virus was isolated on Vero cells in a BSL-4 suite at Rocky Mountain Laboratories. Credit: NIAID

The Ebola virus and fruit bats have been waging a molecular battle for survival that may have started at least 25 million years ago, according to a study led by researchers at the University of Colorado Boulder, Albert Einstein College of Medicine and the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID).

The findings, published today in the journaleLife [no link], shed new light on the biological factors that determine which bat species may harbor the virus in between outbreaks in humans and how bats may transmit the virus to people.

The researchers showed that a single amino acid change in the Ebola virus could overcome the resistance of the African straw-colored fruit bat cells to infection. These findings hint at one way in which Ebola and other highly infectious filoviruses can evolve to better infect a host.

“There seems to be a low barrier for Ebola virus to establish itself in this type of bat,” said co-lead author Sara Sawyer, an associate professor in CU-Boulder’s Molecular, Cellular, and Developmental Biology and the BioFrontiers Institute. “One has to wonder why that has not happened yet.”

To learn more, the researchers exposed cells from four types of African bats (two of them previously linked to Ebola) to several filoviruses, including Ebola. Cells from only one type of bat proved resistant to Ebola virus infection: the African straw-colored fruit bat, which is commonly hunted for bushmeat in West Africa and migrates long distances.

Outbreaks of Ebola virus disease among humans are thought to begin when a person comes into contact with a wild animal carrying Ebola virus.

“We knew from our previous research that Ebola virus infects host cells by attaching its surface glycoprotein to a host cell receptor called NPC1,” said Kartik Chandran, an associate professor of microbiology and immunology at Albert Einstein College of Medicine in New York and a co-lead author of the study. “Here, we show how bats have evolved to resist Ebola infection and how, in turn, the virus could have evolved to overcome that resistance.”

“Identifying potential animal reservoir hosts for Ebola virus will provide a crucial guide for public health prevention and response programs going forward,” said Maryska Kaczmarek, a graduate researcher in Sawyer’s lab at CU-Boulder and a co-author of the study.

There are currently no FDA-approved treatments or vaccines for the Ebola virus. The 2014 Ebola outbreak in West Africa was the world’s deadliest to date, infecting an estimated 28,000 people and killing more than 11,000, according to the Centers for Disease Control and Prevention.

The study was co-authored by Melinda Ng, Esther Ndungo, Rohit Jangra and Rohan Biswas, all at Albert Einstein; John Hawkins and Ann Demogines, all at University of Texas at Austin; Andrew Herbert, Ana Kuehne and Rebekah James, all at USAMRIID; Tabea Binger and Marcel Müller at University of Bonn Medical Center; Robert Gifford at University of Glasgow; Meng Yu and Lin-Fa Wang at Duke-NUS Graduate Medical School; Thijn Brummelkamp at Netherlands Cancer Institute; Christian Drosten at the German Centre for Infectious Diseases Research; and Jens Kuhn at the National Institutes of Health’s Integrated Research Facility at Fort Detrick.

This research was supported by grants from National Institutes of Health, the Defense Threat Reduction Agency, European Union FP-7 Antigone, the EBOKON Project, and the National Research Foundation Singapore.

See the full article here .

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