Scientists from The Pirbright Institute in the U.K. have used a groundbreaking approach to determine that a morbillivirus that causes disease in small ruminants such as sheep and goats — known as peste des petits ruminants (PPR), a close relative of the measles virus — could, through minor changes in a particular protein, overcome barriers that currently prevent it from entering human cells to become a human morbillivirus.

Diseases that jump from animals to people are known as zoonoses, Pirbright explained, noting that many viral pandemics start following transmission of an animal-associated virus into human populations, like with recent outbreaks of influenza virus.

In collaboration with scientists from the University of Glasgow, the University of Cambridge and other institutions, scientists from Pirbright's Viral Glycoproteins Group, led by Dr. Dalan Bailey, identified that a small change to a PPR virus protein enables it to use the human receptor SLAMF-1 to gain entry into human cells.

“Using our existing understanding of how these proteins interact and previous sequencing and structural studies, we were able to identify and confirm that a single amino acid in the [PPR virus's] hemagglutinin can allow human cell entry," Bailey explained. "It is important to note that this does not mean the virus would have the potential to cause disease in humans, as there are many other factors required for the virus to successfully replicate and cause clinical symptoms, but it does indicate that these viruses have zoonotic potential, given the right mutations and conditions.”

An equally important element of this study was the laboratory techniques the scientists used to identify these changes, the institute noted. Significantly, these approaches negated the requirement for live infectious virus and high-containment laboratories and meant that a modified live virus with potential zoonotic capability was not, and will not, be generated.

The research, published in the Journal of Virology, has important implications for monitoring virus evolution in the field, especially during eradication campaigns, the researchers said.

“In the light of these findings, we believe it is important that a sequence surveillance program, similar to that undertaken for influenza, is introduced to monitor mutations in this region,” Bailey said.

The successful eradication of rinderpest virus (a large ruminant morbillivirus) and the potential eradication of measles has led to concerns that small changes in other morbilliviruses, including PPR virus, could enable the disease to emerge in so-called "vacated ecological niches," Pirbright said. Improving the understanding of what determines host-range, particularly at the genetic and structural levels, will allow researchers to monitor the emergence of these viruses with increased accuracy.

The World Organization for Animal Health (OIE) has initiated a global strategy for eliminating PPR.

OIE said since its initial identification in Côte d’Ivoire in 1942, PPR has spread to more than 70 countries in Africa, the Near East, the Middle East and Asia and has reached new areas in recent years. In December 2016, the first reported outbreak of the disease in sheep and goats, with spillover to a wild antelope species, was observed in Mongolia, and later in June 2018, it reached the European Union, with a first-ever case reported in Bulgaria, OIE said.

While the disease is highly lethal to small ruminants, killing up to 90% of infected animals, OIE said the virus is easily preventable with inexpensive vaccines that can be administered at low cost.