Page 271 - Avian Virology: Current Research and Future Trends

264 | Schat

Figure 9.9 (A) Thymus of chicken infected with chicken anaemia virus with atrophy of lobules and loss of distinction between medulla
and cortex. (B) Uninfected control hatch-mate H&E, 9.5 ×. Source: From Shivaprasad and Lucio, 1994, with permission from the American
Association of Avian Pathologists

fully susceptible to infection resulting in a significant reduction The division of CAV isolates into four clusters (see ‘Genome
+
+
+
of CT1 , CD4 and CD8 thymocytes (Hu et al., 1993a). These structure and organization’) has limited practical importance
results support the hypothesis that age-related resistance to because all isolates still belong to the same serotype. Moreover,
disease is based on the development of antibodies prior to the there is no clear pattern of divergence that is linked to differences
development of disease and not on the disappearance of suscep- in pathogenicity. For example, Connor et al. (1991) compared
tible target cells. When chickens are infected at one day of age the pathogenicity of two Australian isolates, 3711 and 3713,
other tissues may undergo changes which are mostly associated with Cux-1 and Gifu-1 and concluded that the Australian strains
with lymphocyte aggregations. However, swelling of hepatocytes did not differ significantly from Cux-1 and Gifu-1. Isolate 3711
has also been mentioned (Goryo et al., 1989a) even when chicks is placed in genotype I together with another Australian isolate.
are infected at 4 weeks of age (Haridy et al., 2012). Genotype I strains are the most divergent isolates compared with
B cells are considered refractory to infection, although there genotype II and III isolates (e.g. Kye et al., 2013). Differences in
are several reports of atrophy of the bursa of Fabricius using bird- pathogenicity have been reported but can only properly be evalu-
propagated CAV (e.g. Goryo et al., 1985; Lucio et al., 1990) or ated when experiments are performed within the same laboratory
virus passaged 10 times in MSB1 cells (e.g. Goryo et al., 1989a; and the absence of infectious bursal disease virus is confirmed
Haridy et al., 2012). In these cases, the medulla of the bursal fol- (see also ‘Immunosuppression’).
licles showed mild to moderate lymphoid depletion. In the case The genetics of attenuated viruses has been reviewed by Schat
of bird-propagated virus it remains possible that infectious bursal (2009) and was also discussed in sections ‘Viral protein 1’ and
disease virus (IBDV) was present in the inoculum although Lucio ‘Viral protein 2’. Table 9.3 compares the amino acid sequence of
et al. (1990) used inoculum after filtration through 50 nm filters. VP1 for the pathogenic Cux-1 and clone AH-C364 (Yamaguchi et
The presence of IBDV is less likely when CAV has been passaged al., 2001) and the attenuated clones AH-C140 (Yamaguchi et al.,
10 times in MSB1 cells. Possible explanations other than the pres- 2001) and P310 C 34 (Scott et al., 2001). Yamaguchi et al. (2001)
ence of IBDV include differences in virus strains and virus dose as stated that histidine at position 394 was linked to attenuation
well as indirect effect by infected T-cells in the bursa of Fabricius while glutamine was present in all pathogenic clones. However,
resulting in cytokine alterations (Adair, 2000). the attenuated clone P310 C 34 had glutamine at position 394.
Clearly, other changes in VP1 and or VP2 are also involved in
attenuation. A similar lack of consensus showing the importance
Genetics of changes in VP2 for attenuation was discussed in the section
As mentioned in the section ‘Genome structure and organiza- Viral protein 2.
tion’ all CAV isolates reported thus far belong to the same species
within the genus Gyrovirus. In general, the divergence for ORF1
of all CAV isolates is less than 5% at the nt level, which is clearly Pathogenesis
within the guidelines proposed by ICTV for a species in the
Anelloviridae (Biagini, 2015). This holds true for recent isolates Introduction
from commercial and backyard poultry and SPF flocks (e.g. Kye The pathogenesis of CAV infection in conventional chickens
et al., 2013; Nayabian and Mardani, 2013; Ganar et al., 2017; Li depends on the combination of age at infection and the presence
et al., 2016, 2017) and older isolates (reviewed by Schat, 2009). of maternal antibodies. Infection before 7 to 14 days of age in