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is disseminated to lymphoid tissues, such as spleen and thymus et al., 2017c). Genetic manipulations of infectious clones will
(Smyth et al., 1988). The primary target organ is the oviduct, the allow the definitive identification of virulence markers. Fowl
main virus replication is in the pouch shell gland at 7–20 days adenovirus 1 isolates from Japan causing gizzard erosion could
post-infection (Yamaguchi et al., 1981). The virus in the faeces be differentiated from apathogenic viruses by RFLP analysis of
probably is the result of contamination with oviduct material the fibre gene (Okuda et al., 2006), however this was not the
(Smyth et al., 1988). case for the European isolates (Marek et al., 2010b; Grafl et al.,
HEV is mainly transmitted to susceptible birds by con- 2013).
taminated faecal or litter material; the virus can persist in the No virulence markers are known for EDSV; however, few
environment for long period of time (Gross, 1967; Itakura et al., amino acid candidates were identified that might alter the tro-
1974; Pierson and Fitzgerald, 2013). After recovery, birds remain pism of a duck-derived virus for laying hens, resulting in different
persistently infected and a source of latent shedding (Beach et al., pathogenesis (Kang et al., 2017).
2009b), however no vertical transmission is reported for HEV. Differences in the sequences of some genes, such as ORF1, E3
After initial replication in the B lymphocytes of the intestine and fibre of HEV isolates suggest that these genes may play a role
the virus is transported via viraemia to the spleen and bursa of in virulence (Beach et al., 2009a).
Fabricius the main replication sites with B-lymphocytes being the
primary target. At 2–7 days post-infection HEV is present in high
amounts in the bursa of Fabricius and intestinal tract and peak Clinical features
titre is detectable in the spleen. Macrophages are also infected.
There are different hypotheses for the immunopathogenesis of Clinical signs
HEV (Fadly and Nazerian, 1982; Ossa et al., 1983; Hussain et Fowl adenoviruses are ubiquitous and can be readily isolated
al., 1993; Saunders et al., 1993; Suresh and Sharma, 1995, 1996; from birds with little or even no clinical signs. Numerous excel-
Rautenschlein et al., 2000; Rautenschlein and Sharma, 2000). lent reviews and current detailed book chapters are available on
the clinicopathology of FAdV induced diseases (McFerran and
Smyth, 2000; Hess, 2013; Schachner et al., 2018). The clini-
Virulence cal signs associated with infections with pathogenic viruses are
Fowl adenoviruses can be pathogenic and non-pathogenic, in dependent on the diseases these viruses cause (Hess, 2013).
other words can cause disease or not. Although it is established Inclusion body hepatitis is seen mainly in broilers in 3 to 7 weeks
by now that FAdVs can be primary pathogens there are many fac- of age, but it was reported in younger than 7 days old as well
tors that may influence the severity of an infection and disease (Pilkington et al., 1997). Usually sudden onset and sharp increase
outcome. Age and breed of chickens, presence of maternal anti- in mortality are noted which can be as high as 30% with a peak
bodies and other agents, especially immunosuppressive viruses, around 4–5 days after infection. The incubation period is usually
management and environmental issues among others need to be 1–2 days. The birds exhibit ruffled feathers, weakness, depres-
considered. sion and a crouching position (Howell et al., 1970; McFerran et
In spite of efforts and attempts to identify the factors and al., 1976; Philippe et al., 2005). It was shown recently that the
markers that are responsible for the virulence for FAdVs; so genetic background of the host crucially influences the clini-
far, no unambiguous data have been published. In an earlier cal outcome of IBH after experimental infection (Matos et al.,
work (Pallister et al., 1996) it was concluded that the virulence 2016a). In addition, clinical signs, for example hypoglycaemia,
of FAdV-8 is associated with the fibre protein alone. Recently, indicating metabolic disturbances due to hepatitis and pancrea-
Grgić et al. (2014) compared the fibre gene sequences of IBH titis were also demonstrated (Goodwin et al., 1993; Venne and
and non-IBH strains of serotype 8 and 11 fowl adenoviruses iso- Chorfi, 2012; Matos et al., 2016b). The clinical signs of HPS
lated in Ontario, Canada but were unable to identify virulence (or HHPS) are similar to IBH with higher mortality and more
markers. Moreover, analysis of the complete genome sequences pronounced signs (Asthana et al., 2013; Vera-Hernández et al.,
of a pathogenic and a non-pathogenic FAdV serotype 11 iso- 2016). Infection with hypervirulent Chinese FAdV-4 isolates
lates only highlighted several candidate molecular determinants could lead to 30–80% mortality, in experimentally infected birds
related to pathogenicity (Slaine et al., 2016). For strain KR5 of to 100% (Zhao et al., 2015; Li et al., 2016; Liu et al., 2016; Niu
FAdV-4 substitutions were detected on the fibre 2 gene, G to D et al., 2016). A duck origin FAdV-4 isolate caused 10% mortality
at position 219 and A to T at position 380 (Marek et al., 2012), in 35-day-old experimentally inoculated SPF chickens, but no
these substitutions were identified earlier on HHS isolates from mortality and clinical signs were recorded in similar age ducks;
Japan and Pakistan (Mase et al., 2010). Phylogenetic analysis therefore, the authors concluded that ducks could be a natural
of the fibre genes indicated that the HS-inducing strains from reservoir for fowl adenoviruses, in particular FAdV-4 (Pan et al.,
China, South America and Mexico grouped together (Liu et 2017b,c). No overt clinical signs are known for adenoviral gizzard
al., 2016). Relative to the genome of non-virulent FAdV-4 erosion (AGE), rather the economic losses due to slower growth,
viruses (KR-5 and ON1), deletions in the right end region higher mortality and condemnation associated with the infection
including a tandem repeat (TR-E) and some ORFs (ORFs 19, in mainly broilers, although layer type birds can be affected as
27, 29) are thought to be associated with virulence (Zhao et well, are important (Ono et al., 2003, 2007; Grafl et al., 2012; Lim
al., 2015; Liu et al., 2016; Vera-Hernández et al., 2016; Pan