Increased infectivity of Ebola virus glycoprotein from West Africa

When viruses cross species, serial transmission may lead to the selection for mutations that confer improved replication or transmission in the new host. Identifying such mutations in human viruses is extremely difficult: we cannot conduct the appropriate experiments in humans, and often do not have viral isolates spanning the time from spillover through prolonged circulation. The 2013-2016 outbreak of Ebola virus in West Africa is unique because viral genome sequences were obtained early and throughout the epidemic. The results of two new studies (link to paper one, link to paper two) suggest that some of the observed mutations increase infectivity for human cells. The impact of these mutations on infection of humans, and their role in the West African outbreak, remain unknown. Many mutations have been identified among the many hundreds of genome sequences obtained during the recent Ebola virus epidemic. One stands out: a mutation that leads to a single amino acid change in the viral glycoprotein, from alanine to valine at position 82 (A82V). This change arose early in the outbreak (it was first observed in Guinea in March 2014) and was subsequently found in most of the isolates. It has never been observed in previous Ebolavirus outbreaks. The effect of the A82V change on viral infectivity was determined by building pseudotyped viral particles – in this case, HIV particles with the Ebola virus glycoprotein. Human cells in culture were infected with pseudotyped ...
Source: virology blog - Category: Virology Authors: Tags: Basic virology Commentary Information adaptation ebola virus filovirus glycoprotein outbreak pseudotype spillover viral viruses zoonosis Source Type: blogs