Published on 21 May 2026

Blog Sara Ezzat – The bovine viral diarrhoea BVD

“The bovine viral diarrhoea virus (BVDV) is a pestivirus characterised by its ability to evade the host's immune response.”

Pestiviruses or the art of evading the immune response

Pestiviruses are viruses that primarily affect farm animals, particularly cattle and pigs, and that can cause potentially serious diseases. The bovine viral diarrhoea virus (BVDV) is such a pestivirus, one that causes gastrointestinal, respiratory and reproductive problems, leading to significant economic losses for farmers.

A distinctive feature of these viruses is their ability to evade the body's immune response. Normally, when a virus infects an animal, the immune system initially reacts by producing messenger molecules known as interferons (innate immunity). Interferons act as warning signs, directly by alerting adjacent cells to prepare for a viral infection, and indirectly by helping the adaptive immune system to mount a specific immune response against the pestivirus (T and B cell response).

But pestiviruses have developed ways to block this initial response of the immune system. A viral protein known as E^rns (one of the viral surface protein) plays an important role in this mechanism by preventing the production of interferons, thereby helping the virus to remain undetected and replicate more readily. Nevertheless, its precise mechanism of action is still not fully understood.

The Bungowannah pestivirus (BuPV; isolated from piglets in Australia) is especially useful for research because it can easily be modified in the laboratory. This means that it can serve as a model to gain a better understanding of how the E^rns protein works and, more generally, how these viruses bypass the immune system.

Interview with Dr. Sara Ezzat

• What was the aim of your doctoral thesis?

  The aim of my thesis was to advance our understanding of the role of the E^rns protein in immune evasion. To this end, I modified E^rns so as to reduce its function, investigated the impact on the innate immune response and developed a fluorescent virus to track E^rns in the cells.

• What are the main findings of your thesis?

  I was able to show that when E^rns is modified, the virus loses its ability to block the immune response, resulting in increased interferon production. In particular, the effect of E^rns is apparent not only in infected cells, but also after intercellular contact with plasmacytoid dendritic cells (immune cells capable of producing large quantities of interferon). This signifies that E^rns plays a vital role in the ability of the virus to evade the innate immune system.

  I also managed to generate a virus expressing  green fluorescent protein (GFP) fused to E^rns , which allows it to be tracked in real time in the cells while retaining the function of E^rns. Furthermore, we were able to publish an article describing the development of this virus, known as “BuPV GFP-E^rns”, that can be found online via the following link: GFP-Tagged E^rns in Bungowannah Pestivirus: A Tool for Viral Tracking and Functional Studies

• To what extent will your findings help to advance research?

  These results will give us a better understanding of the role of E^rns in immune evasion and offer new tools for studying viral infections.

• What aspect of this work are you particularly proud of?

  I am proud of having successfully modified a complex virus and confirmed the role of E^rns in the innate immune response.

• What did you especially like about working on your thesis?

  I enjoyed learning new techniques and gaining a better understanding of the complexity of working with particles as small as viruses.

• How was your time at the IVI?

  It was a very positive experience working with very friendly colleagues on rewarding projects.

• What's next for you?

  I've decided to pursue an academic career involving post-doctoral research in virology at Lausanne.