Page 256 - Avian Virology: Current Research and Future Trends

Chicken Infectious Anaemia Virus

Karel A. Schat* 9

Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.

*Correspondence: kas24@cornell.edu
https://doi.org/10.21775/9781912530106.09

Abstract the presence of antibodies to CAV in chicken sera which were
Chicken anaemia virus (CAV) is the only member of the genus banked in 1959. Based on the pathogenesis of CAV infection in
Gyrovirus of the family Anelloviridae. It has a single-stranded, SPF chickens (see section ‘Transmission of CAV in SPF flocks’)
covalently linked circular DNA genome of 2.3 kb coding for three Miller and Schat (2004) suggested that CAV is most likely an
viral proteins (VPs). VP1 forms the capsid and is the only protein ancient pathogen that has been present in jungle fowl for a long
in the virus particles. VP2 has multiple functions, which are essen- time.
tial for the formation of the virus particles. VP3 causes apoptosis Virus isolation was originally performed by serial passage in
in vitro and in vivo. VP3, also known as Apoptin, is investigated 1-day-old chicks until it was learned that the Marek’s Disease-
as a potential anticancer treatment for human tumours. The pro- derived, lymphoblastoid Chicken Cell line (MDCC)-MSB1
moter/enhancer region resembles oestrogen response elements could be used for isolation and propagation of CAV (Yuasa,
and transcription can be activated by oestrogen and repressed 1983). Since then, CAV isolations and the presence of CAV
by chicken ovalbumin upstream promoter transcription factor antibodies have been reported from all continents with a poultry
1. Viral DNA can remain present in the gonads of chickens with industry. CAV infection is important for the poultry industry
or without virus-neutralizing (VN) antibodies. Transfer of viral for several reasons. First of all, infection of newly hatched chicks
DNA through the embryo can occur independently of the pres- lacking maternal antibodies causes severe anaemia and mortality.
ence of VN antibodies. Infection of 1-day-old chicks without Secondly, infection after 2 to 3 weeks of age can result in sub-
maternal antibodies causes apoptosis of the haematopoietic cells clinical immunosuppression leading to increased susceptibility to
in the bone marrow and thymocytes in the thymus cortex causing other diseases and decreased responses to vaccinations. Finally,
anaemia and immunosuppression. Infection after 2 to 3 weeks CAV has been, and still is, a major problem for the SPF industry,
of age does not cause clinical disease but may cause subclinical and by extension for vaccine producers, with breaks occurring
immunosuppression. Vaccination of pullets between 9 and 15 after the development of sexual maturity.
weeks of age prevents clinical disease in newly hatched chickens
by the transfer of maternal antibodies.
Infectious agent

Introduction and history Classification
Chicken infectious anaemia virus (CAV or CIAV) was first The classification of CAV has been changed several times since
described by Yuasa et al. (1979). This small virus (< 25 nm) 1979. Originally, CAV was named chicken anaemia agent (CAA)
was obtained from a flock of chickens, which were vaccinated because at that time it did not fit in any known virus family
with Marek’s disease (MD) vaccine contaminated with reticu- (Yuasa et al., 1979). Gelderblom et al. (1989) found that CAA
loendotheliosis virus (REV) (Yuasa et al., 1976) in addition structurally resembled porcine circovirus (PCV), a contaminant
to CAV. It is not uncommon that research and commercial in the porcine kidney cell line PK15 (Tischer et al., 1982). They
specific-pathogen-free (SPF) flocks are contaminated with CAV proposed renaming CAA as CAV or perhaps avian circovirus. In
(McNulty et al., 1989; Fadly et al., 1994; Cardona et al., 2000b; addition to structural similarities, both viruses possess a cova-
Schat and Van Santen, 2013). Although CAV was first described lently closed circular single-stranded DNA genome (Claessens et
in 1979, the virus has been around for a long time. Jakowski et al., 1991; Noteborn et al., 1991; Meehan et al., 1992). Ritchie et al.
al. (1970) reported a case of haematopoietic destruction in MD (1989) isolated a virus from cockatoos with psittacine beak and
virus (MDV) infected chickens. Years later, Wellenstein (personal feather disease (PBFD) with similar characteristics: 14–16 nm in
communication, 1989; quoted in Schat and Van Santen, 2013) diameter with an icosahedral structure and a covalently closed
isolated a CAV strain from original tumour material saved from circular single-stranded DNA genome. The similarities between
this case. Using banked chicken sera, Toro et al. (2006) reported PCV, CAV and PBDF virus (PBFDV) led Studdert (1993) to