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Table 9.3. Comparison of predicted amino acid sequence for VP1 from pathogenic Cux-1 and AH-C364 and the attenuated clones P310
clone 34 and AHC140 From Schat (2009) with permission from Springer-Verlag
Amino acid changes and position
Isolate 29 75 89 125 140 141 144 251 254 265 287 321 370 376 394 413 444 447
Cux-1 a K V T I S Q D Q E N A R S L Q A Y T
P310 C 34 b R I A L S L E L G T A A S L Q A Y T
AH-C140 c R V T L A Q E R E T S A G I H S Y S
AH-C364 c R V T L A E d E R E T S A G I Q S D e S
a Meehan et al. 1992.
b Scott et al. 2001.
c Yamaguchi et al. 2001.
d One pathogenic clone had Q at this position.
e One pathogenic clone had Y at this position.
maternal antibody-free chicks often results in pathology. Infec- and house sparrows (Passer domesticus) using primers for VP2,
tion at that age in the presence of maternal antibodies prevents but sequence data were not published. Mammalian species are
virus replication. Infections after maternal antibodies have waned generally considered refractory to infection but a recent finding
normally results in subclinical infection unless the humoral of CAV in faecal samples from stray cats in China (Zhang, X. et al.,
immune response is compromised. The pathogenesis of infection 2014) raises an important question. Are these cats truly infected
in SPF chickens differs from that in conventional chickens and or are the findings the consequence of eating backyard chicks or
will be discussed separately. other birds like sparrows?
Thus far, there is no information on the susceptibility of differ-
Host range ent bird species to AGV2. Currently, a PCR assay is the only test
Chickens are the main host for CAV and the only animal model available for the detection of AGV2. Serological tests are not yet
for infection experiments. Several CAV viruses were isolated available and will need to be developed before screening of other
from commercial turkeys some of which were of low pathogenic- species can be done.
ity in chickens. MAb R2 neutralized these turkey isolates but
not several strains isolated from chickens or a pathogenic isolate Genetic resistance
from turkeys. Polyclonal chicken sera from chickens inoculated There is little experimental information on differences in genetic
with the turkey isolates neutralized chicken and turkey isolates resistance to infection or disease. Cardona et al. (2000a) vacci-
(Schrier and Jagt, 2004). These findings contrast with an earlier nated 3 SPF leghorn-type lines with known MHC haplotypes,
13 13
19 19
21 21
report that turkeys are refractory to experimental infection N2a (B B ) at 74 days of age, P2a (B B ) and S13 (B B ) at
(McNulty, 1991), the absence of antibodies in turkey sera from 4 days of age with the Nobilis CAV P4 vaccine combined with an
Northern Ireland (McNulty et al., 1988) and the absence of CAV adjuvant. At 7 weeks 100, 85 and 73% of N2a, P2a and S13 chick-
antibodies and DNA from commercial turkeys in Iran (Gholami- ens, respectively, had seroconverted. Although these differences
Ahangaran, 2015). Japanese quail are susceptible to CAV-like are highly significant, it is not clear if there is also a difference in
viruses based on the presence of VN antibodies to CAV in sera resistance to disease. Joiner et al. (2005) characterized 3-week-old
from 10/12 flocks in Japan. These flocks suffered from a number chickens from a commercial broiler breeder line ‘A’ for MHC hap-
of other diseases suggesting that CAV-induced immunosup- lotypes. Birds, selected for homozygosity for the four haplotypes
pression may have been involved (Farkas et al., 1998). Recently, present in line A, were challenged by oral inoculation at 4 weeks
Gholami-Ahangaran (2015) reported that Japanese quail in of age. Body weights and haematocrit values did not show signifi-
15/50 flocks were positive for VP2 in PCR assays, but sequence cant differences among the four groups at 5, 11, and 14 days pi.
data were not reported. Complete genomes need to be amplified At 14 days pi there were no significant differences among the four
and sequenced to confirm that these sequences are CAV or other groups in histopathology of the thymus, serology and virus titres.
related gyroviruses. Sera from ducks and pigeons were negative Male and female broilers are considered equally susceptible to
for CAV antibodies using different serological assays (McNulty CAV infection. McNulty et al. (1991) reported that subclinical
et al., 1988; Campbell, 2001) or PCR assays for VP2 (Gholami- infections had a negative effect on several economic parameters,
Ahangaran et al., 2014). Sera from Corvidae species yielded but that there was no difference between male and female broil-
conflicting data. Campbell (2001) found that sera collected in ers. Engström and Luthman (1984) found no difference in the
Ireland from jackdaws (Corvus monedula) and rooks (C. frugile- incidence of ‘blue wing disease’ (see ‘Clinical features’) between
gus) were positive for CAV antibodies. Sera collected from crows, male and female birds. On the other hand, Goryo et al. (1987a)
unfortunately without species identification, in Japan were nega- reported a much higher incidence of mortality in male than
tive for CAV antibodies (Farkas et al., 1998). Gholami-Ahangaran female chickens before 3 weeks of age. The birds were reared on
et al. (2013a,b) also reported positive PCR results in ostriches the same farm but in separate houses. Their results are difficult to

