Page 73 - Avian Virology: Current Research and Future Trends

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were exchanged between PPMV-1 and a highly virulent NDV In enzootic countries, vaccinated poultry are considered the main
strain showed that the whole viral replication complex (N, P, and reservoir of virulent NDV (Miller et al., 2009; Alexander, 2011).
L) contributes to the virulence of NDV (Dortmans et al., 2010). Several evidences exist that support the second explanation.
A recent study that exchanged genes between a velogenic strain It has been suggested that all groups of wild bird species may
and a lentogenic strain showed that the F and HN proteins are the participate in the maintenance of virulent NDV strains and may
major contributors to virulence and the L protein as well as N and potentially be involved in the spread of these strains responsible
P proteins also contribute to virulence (Yu et al., 2017). for outbreaks in poultry (Cappelle et al., 2015). Phylogenetic
Although the studies described above have increased our analyses have also identified virulent NDV isolates recovered
understanding of NDV virulence, they were carried out between from feral pigeons and migratory cormorants as the likely source
NDV strains that may have been too divergent genetically or bio- of some NDV outbreaks in poultry (Banerjee et al., 1994; Heck-
logically to be compatible for gene swaps. Therefore, it was unclear ert et al., 1996; Ujvári et al., 2003; Aldous et al., 2004). Therefore,
whether the observed effects of the gene swaps reflected genuine infected wild birds are an important source of introduction of
virulence determinant differences versus incompatibility due to virulent NDV into poultry populations.
excessive biological or phylogenetic divergence. Therefore, a sys- The potential of low virulence NDV to become highly viru-
tematic study of NDV virulence and pathogenesis was conducted lent exists, as only few mutations at the F protein cleavage site
by exchanging the full repertoire of viral genes, individually and in is necessary to change a low virulence virus to a highly virulent
many combinations, between mesogenic strain BC and velogenic virus. However, development of a highly virulent virus from
strain GBT (Paldurai et al., 2014b). These two strains are closely a low virulence virus happens very rarely in the nature. There
related phylogenetically. They have identical genome lengths and are only two documented cases that occurred in Ireland (Col-
share 99.1% genome-wide nt sequence identity. However, the two lins et al., 1993, 1998) and in Australia (Gould et al., 2001;
strains differ greatly in virulence and pathogenicity. The results of Westbury, 2001) where it has been postulated that the virulent
this study showed that both the envelope-associated proteins and viruses originated from viruses of low virulence. It has been
the polymerase-associated proteins contribute to the virulence of experimentally shown that a virulent virus can arise from a low
NDV, with the former playing the greater role. The F and L pro- virulence waterfowl isolate by passaging in chickens (Shengqing
teins were the major individual contributors to the difference in et al., 2002; Zanetti et al., 2008). On the contrary, lentogenic
virulence between the two strains (Paldurai et al., 2014b). vaccine strains, such as LaSota and B1 have been used as live
In summary, the studies conducted to date suggest that the vaccines for more than 60 years without any alteration in viru-
aa sequence at the F protein cleavage site determines whether lence. These findings suggest that virulence enhancement of low
an NDV strain is virulent (mesogenic and velogenic) or aviru- virulence viruses by passaging in chickens may depend on the
lent (lentogenic). But the degree of virulence of an NDV strain origin of the virus. Like any other RNA virus, an NDV sample
is determined by both envelope-associated proteins (M, F and is a quasispecies mixture of avirulent and virulent genomes
HN) and internal proteins (N, P and L). The envelope-associated in different proportions, but only the majority phenotype is
proteins contribute to virulence by playing a role in the entry and expressed (Kattenbelt et al., 2010; Meng et al., 2016). A len-
spread of the virus, whereas, the internal proteins contribute to togenic NDV isolate from chicken is already well-adapted to
virulence by playing a role in the rate of replication of the virus. efficiently replicate in chicken and therefore is not under host
Among all viral proteins, the F and L proteins play greater roles in selection pressure. But when a low virulence virus isolated from
determining the virulence of NDV. a different avian species is translocated to chickens, the new
host environment imposes selective forces such that the rep-
lication of the virulent viruses is favoured over low virulence
Emergence of virulent NDV viruses (Kattenbelt et al., 2010; Meng et al., 2016). Therefore,
It is not fully understood how virulent NDV is introduced into a low virulence APMV-1 from a wild bird species can become
a geographic area. However, three possibilities have been pro- virulent after several passages in chickens.
posed to explain the emergence of virulent NDV: (1) virulent
NDV resides unnoticed in vaccinated poultry population until
development of an outbreak; (2) virulent viruses are transmitted Transmission and spread
to chickens from another species in which it shows less severe NDV is a highly infectious virus. When introduced into an avian
disease; and (3) virulent viruses arise from low virulent viruses population, NDV is rapidly transmitted among susceptible birds
by mutation (Hanson, 1972). either by inhalation or ingestion (Alexander, 1988). The virus is
The first explanation is probably true in some parts of the present at high concentrations in secretions and excretions from
world where ND is enzootic. Current vaccines may prevent actively infected birds and in all tissues of dead birds. Inhalation
clinical signs, but do not stop virus infection and shedding. This of infectious virus via aerosol is probably the major mode of trans-
allows the virulent virus to spread undetected in vaccinated birds, mission in intensively managed poultry. Transmission by ingestion
resulting in an enzootic situation. The disease becomes apparent of faeces and contaminated food and water is more common in
when immunity is not achieved due to low antibody titre, non- free range village poultry. This is also the most likely method of
vaccination or immune suppression due to infection with other transmission of avirulent enteric NDV. Vertical transmission has
agents (Capua et al., 2002; Alexander, 2011; Umali et al., 2015). not been clearly demonstrated and is not an important mode of