Open access publications in the SLU publication database

Abstract

The thesis summarizes and discusses the results from studies of an influenza A virus isolated from an outbreak of pneumonia among farmed mink in Sweden. This new disease in mink was described based on clinical, serological, and pathological investigations, and the causality established by experimental infection of mink. The virus was identified and named A/mink/Sweden/84 (H10N4). Serological investigations showed that this virus was not present in mink in other areas of the country. A direct transmission of virus from birds to mink was suggested, since the subtypes H10 and N4 had previously only been isolated from birds. The genetic relationships between the mink virus and three avian derived influenza viruses of subtype H10 were analyzed by oligonucleotide mapping. The mink virus was shown to be closely related to two avianderived H10N4 viruses and less related to the prototype avian H10 strain, A/chicken/Germany/49 (H10N7). Experimental infection of mink with these four H10 influenza strains showed that all four viruses stimulated an antibody-mediated immune response. All three H10N4 viruses also caused clinical disease in mink and spread through contact, whereas the H10N7 virus only caused mild lung lesions but no clinical disease or contact transmission. Experimental aerosol infection of mink was used to study the early lesions in the respiratory tract caused by the H10N4 virus from mink and the prototype avian H10 virus. Through immunohistochemistry, morphometrical analysis of the pneumonia, histopathology and virus culture, marked differences in pathogenicity were observed between the two viruses. The H10N4 virus was reisolated from all infected mink, whereas no H10N7 virus could be reisolated. Both viruses caused a bronchointerstitial pneumonia in the infected mink. However, the spread of the virus within the respiratory tract and the area density of pneumonia peaked on day two for the H10N7 virus, whereas the H10N4 virus from mink continued to spread all through the one-week observation period, ultimately killing one of the infected mink on day seven. An additional study indicated that the differences in virus spread in vivo could be modelled in vitro in mink lung-cell cultures.