Page 23 - Avian Virology: Current Research and Future Trends

16 | Perez et al.

can occur in the intestinal or respiratory tracts or in both. The that allows ubiquitous intracellular proteases to recognize the site
virus has been isolated from more than 200 bird species from (Swayne and Suarez, 2000). In most cases, these basic amino acids
53 families in 25 orders (Table 1.3). It is commonly accepted occur during viral mRNA transcription with the viral polymerase
that wild aquatic birds are responsible for introducing IAVs into ‘stuttering’ in the region that contains the cleavage site (similar
domestic poultry. Agricultural and commercial practices where to ‘stuttering’ during viral mRNA polyadenylation). Alternatively,
natural and non-natural hosts of influenza can become in contact, and only seen with the H7 HA subtype, recombination with
promote the interspecies transmission and emergence of IAVs host ribosomal RNA sequences or other vRNA segments leads
(Alexander, 1982). Live bird markets, backyard flocks and free- to insertions that encode polybasic amino acids. The cleavage of
range raised poultry, are few examples of such practices (Bulaga HA can also be modulated by the presence of glycosylation sites
et al., 2003; Liu et al., 2003a; Mullaney, 2003). Although the host spatially located nearby. For example, a loss of a glycosylation site
barriers that prevent IAVs from the natural reservoirs to cross to at amino acid 13 and the presence of the polybasic amino acid
poultry may be lower than for crossing to other animal species, region in the HA are pathotypic markers of the H5N2 virus that
spread and perpetuation of these viruses in poultry is expected caused the 1983–1984 outbreak in Pennsylvania (Kawaoka et al.,
to lead to adaptive changes that influence virulence, transmission, 1984; Banks and Plowright, 2003). The exact contributing factors
and host range. Additionally, it is generally well accepted that that lead to the accumulation of the polybasic amino acid region
poultry, along with other species such as pigs and (historically) at the HA cleavage site remain largely unknown, although it is
horses, can serve as intermediate hosts for influenza strains from postulated that viral adaptation to terrestrial birds plays a major
wild aquatic bird reservoir that find their way into humans and role.
can cause pandemics. The basic pathogenesis of HPAIV infection in birds starts with
initial replication in the epithelial cells of the upper respiratory
tract. Then, the virus spreads through the vascular and lymphatic
Clinical features and pathogenesis: LPAIV systems, replicates in macrophages and heterophils and dis-
and HPAIV in poultry seminate to multiple organs, where it replicates in parenchymal
In wild birds, IAV infections are mostly asymptomatic, with cells (Perkins and Swayne, 2001; Kuiken et al., 2010; Swayne et
few exceptions of outbreaks caused by the spill over of HPAIVs al., 2013). Hence, depending on the strain of HPAIV, viraemia
(Laudert et al., 1993; Chen et al., 2004; Hulse-Post et al., 2007; may or may not be associated with virus replication in endothelial
Kim et al., 2009; Marjuki et al., 2010; Reed et al., 2010; Song et cells. In the first case, the damage to the blood vessels causes typi-
al., 2011). In domestic poultry infected with LPAIVs, clinical cal disseminated haemorrhages and acute infarctions leading the
signs are usually limited to the upper respiratory tract and diges- hosts to a peracute death. In the second case, the birds survive
tive systems and less commonly to the urinary and reproductive longer, allowing more extensive virus replication in multiple
organs (Swayne and Spackman, 2013). In contrast, infection with critical organs, subsequent necrosis and subacute inflammatory
HPAIVs may lead to asymptomatic and sudden mortality to a very reaction (Kuiken et al., 2010; Swayne et al., 2013; Franca and
diverse clinical presentation depending on the virus strain and its Brown, 2014). In this latest form, death occurs at a later stage from
tissue tropism (Pantin-Jackwood and Swayne, 2009). Incubation single- or multiorgan system failure, with involvement of the pan-
period varies depending on the infectious dose, route, species, creas, brain, heart, kidney, endocrine glands (e.g. adrenal glands),
age, immune status of the host and presence of other aggravating and lymphoid system (e.g. the spleen). Turkeys are particularly
factors. For both low and high pathogenic viruses it varies from a susceptible to AIV infection and gross lesions may be unapparent,
few hours in intravenously inoculated birds to three days in natu- especially in the peracute form of disease (Swayne et al., 2013).
rally infected individual birds and up to 14 days in a flock (Swayne Considerable variations in pathogenicity have been reported for
et al., 2013; Swayne and Spackman, 2013). Respiratory signs can the Eurasian H5 subtype of HPAIV in both natural outbreaks and
be mild to severe and include signs such as coughing, sneezing, experimentally inoculated birds (Lee et al., 2004; Mundt et al.,
rales, rattles, and excessive lacrimation. In layers and breeders 2009; Bertran et al., 2016, 2017; Spackman et al., 2016; Stoute et
there may be a sudden drop in egg production. Generalized clini- al., 2016; Carnaccini et al., 2017; Pantin-Jackwood et al., 2017).
cal signs include huddling, ruffled feathers, listlessness, decreased These differences are related to multiple factors such as viral fit-
activity, lethargy, decreased feed and water consumption, and ness, adaptation and virulence, host species and immunity, age
occasionally diarrhoea (Swayne et al., 2013). at infection, infection route, infectious dose, and the presence of
In theory, viruses of all HA subtypes have the potential to cause other concomitant infections.
severe disease. However, only H5 and H7 subtypes have been his- Anatomopathological presentation varies greatly depending
torically linked to HPAI outbreaks; although not all viruses that on the host species, viral strain and pathotype, infectious dose
belong to these two subtypes are highly pathogenic. Viruses of and presence of opportunistic infections. The most virulent
any other subtype can cause a mild, primarily respiratory disease forms of HPAIV are characterized by a highly fatal systemic
in poultry, which may be exacerbated by secondary infections or infection that spreads to most organ systems including the car-
environmental conditions. An H5 or H7 virus can present itself as diovascular and nervous systems (Acland et al., 1984; Gross et al.,
a low pathogenic virus to later mutate without warning to become 1986; Slemons et al., 1991; Perkins and Swayne, 2002a,b, 2003).
highly pathogenic. Highly virulent H5 and H7 viruses possess Morbidity and mortality can be as high as 100%, particularly in
multiple basic amino acids at the cleavage site of the HA (Fig. 1.1) gallinaceous species. The incubation period is usually between