Avian influenza (AI) is a complex infection of birds, of which the ecology and epidemiology have undergone substantial changes over the last decade. Avian influenza viruses infecting poultry can be divided into two groups. The very virulent viruses cause highly pathogenic avian influenza (HPAI), with flock mortality as high as 100%. These viruses have been restricted to subtypes H5 and H7, although not all H5 and H7 viruses cause HPAI. All other viruses cause a milder, primarily respiratory, disease (low pathogenic avian influenza, LPAI), unless exacerbated by other infections or environmental conditions. Until recently, HPAI viruses were rarely isolated from wild birds, but for LPAI viruses extremely high isolation rates have been recorded in surveillance studies, particularly in feral waterfowl. In recent years, there have been costly outbreaks of HPAI in poultry in Italy, the Netherlands and Canada and in each of these countries millions of birds were slaughtered to bring the outbreaks under control. However, these outbreaks tend to have been overshadowed by the H5N1 HPAI virus, initially isolated in China, that has now spread in poultry and/or wild birds throughout Asia and into Europe and Africa, resulting in the death or culling of hundreds of millions of poultry and posing a significant zoonosis threat. Since the 1990s, AI infections due to two subtypes, LPAI H9N2 and HPAI H5N1, have been widespread in poultry across large areas of the world, resulting in a modified eco‐epidemiology and a zoonotic potential. An extraordinary effort is required to manage these epidemics from both the human and animal health perspectives.
SUMMARY Forty-four haemagglutinating viruses were isolated from the pooled tracheal/cloacal swabs of the dead birds from 170 consignments of caged birds arriving at Heathrow Airport over a period of 6 months. Two isolates were identified as Newcastle disease virus but the remaining 42 were all identified as influenza viruses with Hav 7 Neq 2 antigens. All the consignments from which influenza viruses were isolated originated in India but had widespread destinations. The NDV isolates were from birds originating in central America and destined for Japan.
Samples from a sow serum bank representative of the pig population of Great Britain collected during 1991-2, were examined for antibodies to influenza A, B and C viruses, using viruses which had been isolated from a variety of hosts. For influenza A viruses there was evidence of the continued circulation of classical swine H1N1 virus (26%) seroprevalence), and human H3N2 viruses (39%) which are antigenically most closely-related to A/Port Chalmers/1/73 virus. In addition antibodies were detected to A/swine/England/201635/92 (8%), a strain of H3N2 virus which appears to have arisen by antigenic drift from conventional H3N2 swine strains. Specific antibodies (2%) were detected to an H1N1 virus (A/swine/England/195852/92) related most closely to avian H1N1 strains. In tests with human H1N1 and H3N2 viruses, excluding isolates from pigs, the highest seroprevalence was detected to the prevailing strains from the human population. Serological tests with avian H4 and H10, human H2, equine 1 and 2 influenza A viruses were all negative. Seven pigs seropositive by haemagglutination-inhibition, virus neutralization and immunoblotting assays for antibody to influenza B virus, were randomly distributed geographically suggesting that influenza B viruses may be transmitted to pigs but fail to spread. The seroprevalence to influenza C viruses was 9.9% indicating that these viruses are widespread in pigs. These results provide further evidence that the pig can be infected by a number of influenza viruses, some of which may have significance in the epidemiology of human influenza.
An avian influenza virus, A/turkey/England/50-92/91 (H5N1), showed extremely high virulence in chickens, although its hemagglutinin (HA) cleavage site sequence (R-K-R-K-T-R), having a nonbasic (Thr) residue at the second position (P-2) from the carboxyl terminus of HA1, does not conform to the previously established consensus sequence motif, X-X-R/K-X-R/K-R (X = nonbasic residue), for highly virulent phenotype of the H5 virus. When we evaluated the HA cleavability of this strain in chicken embryo fibroblast culture, we observed that, unlike other HAs with a Thr residue at P-2, this HA was efficiently cleaved. These findings suggest that a nonbasic residue at the P-2 does not affect its recognition and catalyzation by cleavage enzymes that are otherwise influenced by steric structure around the cleavage site.
The current definitions of high-pathogenicity avian influenza (HPAI), formulated over 10 years ago, were aimed at including viruses that were overtly virulent in in vivo tests and those that had the potential to become virulent. At that time the only virus known to have mutated to virulence was the one responsible for the 1983-84 Pennsylvania epizootic. The mechanism involved has not been seen in other viruses, but the definition set a precedent for statutory control of potentially pathogenic as well as overtly virulent viruses. The accumulating evidence is that HPAI viruses arise from low-pathogenicity avian influenza (LPAI) H5 or H7 viruses infecting chickens and turkeys after spread from free-living birds. At present it can only be assumed that all H5 and H7 viruses have this potential and mutation to virulence is a random event. Therefore, the longer the presence and greater the spread in poultry the more likely it is that HPAI virus will emerge. The outbreaks in Pennsylvania, Mexico, and Italy are demonstrations of the consequences of failing to control the spread of LPAI viruses of H5 and H7 subtypes. It therefore seems desirable to control LPAI viruses of H5 and H7 subtype in poultry to limit the probability of a mutation to HPAI occurring. This in turn may require redefining statutory AI. There appear to be three options: 1) retain the current definition with a recommendation that countries impose restrictions to limit the spread of LPAI of H5 and H7 subtypes; 2) define statutory AI as an infection of birds/poultry with any AI virus of H5 or H7 subtype; 3) define statutory AI as any infection with AI virus of H5 or H7 subtype, but modify the control measures imposed for different categories of virus and/or different types of host.
Many viruses, in addition to the induction of c.p.e., produce profound biochemical alterations in the cell, particularly by the inhibition of cellular macromolecular synthesis (for review see Roizman & Spear, 1969). Reeve et al. (1971) have shown that the ability of different Newcastle disease virus (NDV) strains to inhibit cellular protein synthesis is related directly to their virulence for cells in vitro and for eggs and chickens in vivo. Certain NDV strains can also inhibit cellular RNA synthesis, but the relationship of this property to the virulence of the infecting strain is not clear (Wheelock & Tamm, 1961; choltissek & Rott, 1965; Wilson, 1968). Moore, Lomniczi & Burke (1972) examined 13 strains of NDV but were unable to establish a relationship between virulence and the inhibition of host cell RNA synthesis.
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