Showing papers on "Avian Influenza A Virus published in 1995"

Molecular evolution of influenza viruses

Abstract: There are two different mechanisms by which influenza viruses might evolve: (1) Because the RNA genome of influenza viruses is segmented, new strains can suddenly be produced by reassortment, as happens, for example, during antigenic shift, creating new pandemic strains, (2) New viruses evolve relatively slowly by stepwise mutation and selection, for example, during antigenic or genetic drift. Influenza A viruses were found in various vertebrate species, where they form reservoirs that do not easily mix. While human influenza A viruses do not spread in birds and vice versa, the species barrier to pigs is relatively low, so that pigs might function as “mixing vessels” for the creation of new pandemic reassortants in Southeast Asia, where the probability is greatest for double infection of pigs by human and avian influenza viruses. Phylogenetic studies revealed that about 100 years ago, an avian influenza A virus had crossed the species barrier, presumably first to pigs, and from there to humans, forming the new stable human and classical swine lineages. In 1979, again, an avian virus showed up in the North European swine population, forming another stable swine lineage. The North European swine isolates from 1979 until about 1985 were genetically extremely unstable. A hypothesis is put forward stating that a mutator mutation is necessary to enable influenza virus to cross the species barrier by providing the new host with sufficient variants from which it can select the best fitting ones. As long as the mutator mutation is still present, such a virus should be able to cross the species barrier a second time, as happened about 100 years ago. Although the most recent swine isolates from northern Germany are again genetically stable, we nevertheless should be on the lookout to see if a North European swine virus shows up in the human population in the near future.

Pathogenesis of pancreatic atrophy by avian influenza a virus infection

Abstract: Summary Specific‐pathogen‐free (SPF), 2‐day‐old chicks were inoculated with type A influenza virus (A/whistling swan/Shimane/499/83/(H5N3)) into their caudal thoracic air sac. The original isolate of the virus was of low virulence (ICPI 0. 20 to 0.40), and was passaged 10 times through the respiratory organs of SPF chicks. Most of the chicks inoculated with the passaged virus (strain 499) showed respiratory and alimentary signs. Three of 30 chicks died on days 2, 6 and 7 post‐inoculation (p.i.). Almost half of the infected chicks showed poor growth, and the variation of body size in the flock became prominent from day 10 p.i. Infected chicks consistently had pathological changes in the pancreas, liver, kidneys and respiratory tracts, and occasionally in the brain, duodenum and bone marrow. Positive immunoreaction to avian influenza virus (AIV) antigen and recovery of the virus persisted for longer period in the pancreas than in other organs. The pancreatic lesions were caused by a direct, lytic virus infe...

Changes of morphological, biological and antigenic properties of avian influenza A virus haemagglutinin H2 in the course of adaptation to new host.

Abstract: The alterations of avian influenza A virus haemagglutinin (HA) H2 as a result of adaptation to mice were first investigated in this study. HA of mouse-adapted (MA) variant was somewhat different from that of the original strain in electrophoretical mobility, antigenic structure and in haemagglutination activity with mouse red blood cells.

Distribution of Antibodies to Influenza A Virus in Chickens in Japan.

Abstract: A serological surveillance was carried out to detect antibody against influenza A virus in chicken sera. A total of 8, 850 field samples were collected from 47 prefectures in Japan. Initially, all the sera were screened by agar gel immunodiffusion and those sera showing positive reaction were investigated for haemagglutination-inhibition (HI) and neuraminidase-inhibition antibodies against influenza viruses. Only 6 samples had antibodies; 4 sera had antibodies against human subtype H1N1 virus; with HI activity against strain A/PR/34; three sera had strong HI activity to strain A/Tottori/4/87, which by haemagglutination test is closely related to A/Yamagata/120/86. The remaining two chicken sera had antibodies against avian subtypes H10N4 and H3N6 viruses respectively.

[Changes in biological and physico-chemical properties of avian influenza virus A hemagglutinin H2 during adaptation to a new host].

Abstract: Avian influenza A virus with H2 hemagglutinin has been adapted to mice for the first time. Alterations in the hemagglutinin of adapted variants of the virus as a result of adaptation to a new host are described. Hemagglutinin of a highly virulent adapted variant differed from the parental avirulent strain by antigenic structure, electrophoretic mobility, and receptor activity during interactions with murine red cells.