PhD defence A.C.M. (Anja) de Bruin

Brief summary on the aim of the doctoral thesis:

Avian influenza viruses are influenza A viruses that can be classified on basis of two proteins located on the virus surface, haemagglutinin (HA) and neuraminidase (NA). To date, sixteen different HA subtypes and nine different NA subtypes have been identified in birds, which occur in almost all possible combinations, such as H4N6 and H16N3. In addition, avian influenza viruses can be divided into severe and mild variants, or high pathogenic avian influenza (HPAI) and low pathogenic avian influenza (LPAI) viruses. LPAI viruses circulate naturally in wild waterfowl, such as ducks and gulls, and replicate mainly in the intestinal system without causing signs of disease. LPAI viruses can jump from wild waterfowl to poultry, such as chickens and turkeys, and then cause mild symptoms, such as reduced appetite and lower egg production. LPAI
viruses containing H5 or H7 HA can turn into HPAI viruses in chickens. Infection of poultry with an HPAI virus leads to severe symptoms in which mortality often up to 100%. Mortality is so high because HPAI viruses replicate in almost all organs of poultry, including blood vessels. This leads to bleeding, oedema, and multiple-organ failure. The change from LPAI to HPAI virus has been reported 51 times reported in the past 70 years, and of these, 46 cases could be directly linked to poultry. Historically, avian flu was always a disease of poultry, but that has changed since H5N1 HPAI viruses, first detected in China in 1996, jumped from poultry to wild waterfowl and spread efficiently through bird migration, among other things. The fact that wild waterfowl do not get as sick as poultry when infected with an HPAI virus contributes to this efficient spread. HPAI virus infections in wild waterfowl are often mild and the virus does not replicate in all organs or nor in blood vessels. When ducks become seriously ill, it is often accompanied by neurological symptoms. This thesis describes some of the major questions within the avian influenza research field. Why are all HPAI viruses of the H5 and H7 HA subtypes (Chapter 2 and Chapter 3)? Why do HPAI viruses not replicate in the blood vessels of ducks (Chapter 4, Chapter 5, Chapter 6)? Why do we see new HPAI viruses emerging mainly in poultry emerge and not in wild waterfowl (Chapter 7)?