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Chicken Infectious Anaemia Virus |   265

          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
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          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
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