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Chicken Anaemia Virus


Higher order taxa

Viruses; ssDNA viruses; Circoviridae; Gyrovirus NCBI


NCBI: Taxonomy

Chicken Anaemia Virus

Description and significance

Chicken Anaemia Virus (CAV) when transmitted by the transovarian route, can result in severe disease in progeny characterized by anemia, subcutaneous hemorrhage, and a decreased resistance to secondary bacterial diseases. Affected chickens, if coinfected with infectious bursal disease virus, may develop a profound immunosuppression with enhanced susceptibility to a wide range of viral and bacterial pathogens. Infections with CAV are considered to be economically significant because of the clinical disease associated with vertical transmission and because of its potential for inducing immune dysfunction alone on in combination with other pathogens.(3)

Genome structure

The virion is a small DNA virus with a circular, covalently linked, single negative-strand genome. (5) The CAV genome has been shown to incorporate three overlapping open reading frames (ORFs) which code for three viral proteins designated VP1, VP2 and VP3, all of which are expressed in CAV infected cells. (8)

The capsid of CAV consists of a single type of protein VP1, which encapsidates a negative-strand genome of about 2,300 bases. VP1 (50 kDa), has an extremely basic N-terminal region of about 50 amino acids that is likely to interact with the packaged DNA. The C-terminal region of the protein carries motifs associated with rolling circle replication (RCR) of DNA, suggesting that VP1 has both structural and functional roles. (1) Thus, it is the only structural protein. (6)

VP2 (24 kDa) is a dual-specificity protein phosphatase and has been shown to interact with VP1, possibly helping VP1 assemble to conform stability. (6) and (8) When the cell is infected, the VP3 protein (13 kDA) colocalizes with the cellular chromatin and forms aggregates, thus, the cells become apoptotic. VP2 and VP3 are non-structural proteins.(8)

Cell structure and metabolism

The capsid is formed from 12 pentagonal trumpet-shaped capsomeres, indicating a T=1 surface lattice containing 60 subunits when the CAV computed from cryomicrographs.(1) The intact virion is icosahedral with an average diameter of approximately 25 nm. (3)

Information on metabolism could not be provided.


CAV has a narrow host range infecting chickens reared for the meat and egg industry worldwide. Economic losses can be very high as a consequence of outbreaks that cause mortality and morbidity due to secondary infections, and reduction in broiler weight. The apoptin protein induces apoptosis in infected chicken cells. Additionally, it was shown to cause apoptosis in human tumor cells, but not in normal human cells (6)


The virus causes aplastic anaemia, generalized lymphoid atrophy and increased mortality after infection of day-old susceptible chickens. Infection of older birds with CAV results in subclinical disease and reduced resistance to other pathogens. Dual infection of chickens with other immunosuppressive viruses increases the severity of CAV signs and decreases the resistance of older birds to infection. (9) Disease usually occurs during the first 3 wk of life resulting from vertical transmission or contact exposure close to hatch. (3) CAV can be transmitted between chickens by both the horizontal and vertical routes. Horizontal spread usually occurs via the oral–faecal route, but infection via the respiratory route has also been demonstrated in experimentally infected birds. Vertical spread through hatched chickens is considered to be the most important means of dissemination of the virus. (9)

Current Research

• A study shows that CAV proteins can be expressed in plants as an alternative for recombinant protein production in animal cells. Also, the effect of VP3 expression was tested to evaluate possible involvement in programmed cell death in plants. Current expression levels of VP1 may be too low to be exploited as an oral vaccine, but optimizing expression level in plant cells to obtain recombinant VP1 protein capable of inducing neutralizing antibodies, most likely by co-expression with VP2, represents an attractive low cost strategy towards novel, affordable vaccines against CAV. (6)

The CAV genes were cloned in binary vectors with the Green fluorescent protein (GFP) as N terminal fusion, and into a Potato virus X (PVX) and Tobacco Mosaic Virus (TMV)-based vectors. (6)

• The aim of the work reported the potential of chicken anaemia virus (CAV) mutants as CAV vaccine strains. Seventy 1-day-old chickens were divided into seven groups of 10 birds, and at 1 day old birds were inoculated subcutaneously with RPMI medium, with mutants S77N, Q131P, D186G or R/K/K150/151/152G/A/A, or with wild-type CAV. A serum neutralization assay, based on viral detection using a quantitative polymerase chain reaction assay, was used to determine the neutralizing antibody titres in blood samples collected at day 35 p.i. Mutant E186G induced the highest post-challenge neutralizing antibody titres, followed by mutants Q131P, S77N and R/K/K150/151/152G/A/A. These studies have shown that mutant E186G is an appropriate candidate mutant CAV vaccine strain. (7)

• This study has established that VP2 is an effective target for attenuation through site-directed mutagenesis and is the first study to demonstrate attenuation of viral effects in vivo through modification of VP2. This is in contrast to previous studies examining virus constructs mutated in VP3, which were not replication competent. The mechanism by which VP2 mutagenesis attenuates virulence remains unknown. It is probable that VP2 has multiple functions and that directed mutagenesis that maintains infectivity may maintain functions necessary to replication, whilst modifying functions associated with virulence. (2)

• This report is the first time a method to detect both infected and transfected MDCC-MSB1 cells by flow cytometry has been utilised. It is also the first study that demonstrates silencing of CAV mRNA expression is possible with single or multiple shRNA molecules. As the CAV genome sequence is highly conserved amongst strains, developing shRNAs targeting this virus should be highly efficient at cross-strain protection. It will now be essential to determine whether these shRNAs are able to protect chickens from a productive CAV infection. (4)


1. Allan, G.M., Berriman, J. A., Crowther, R. A., Curran, W. L., Todd, D., 2003, Comparison of the structures of three circoviruses: Chicken Anemia Virus, Porcine Circovirus Type 2, and Beak and Feather Disease Virus, Journal of Virology, 77, p. 13036–13041.

2. Browning, G.F., Crabb, B.S., Peters, M.A., Tivendale, K.A., 2007, Attenuation of chicken anemia virus by site-directed mutagenesis of VP2, Journal of General Virology, v. 88, p. 2168-2175.

3. Cloud, S.S., Rosenberger, J.K, 1998, Chicken Anemia Virus, Poultry Science, v. 77, p. 1190-1192.

4. Doran, T. J, Hinton, T. M., 2008, Inhibition of Chicken Anaemia Virus replication using multiple short-hairpin RNAs, Antiviral Research, v. 80, p. 143-149.

5. Giap, T.C., Hailemariam, Z., Hair-Bejo, M., Omar, A. R., 2008, Detection and characterization of chicken anemia virus from commercial broiler breeder chickens, Virology Journal, v. 5: 128.

6. Goldbach, R., Lacorte, C., Lohuis, H., Prins, M., 2007, Assessing the expression of chicken anemia virus proteins in plants, Virus Research, v: 129, p. 80-86.

7. Kaffashi, A., Shrestha, S., 2008, Evaluation of Chicken Anaemia Virus mutants as potential vaccine strains in 1-day-old chickens, Avian Pathology, v. 37, p. 109-114.

8. Noteborn, Mathieu H. M., Koch, G., 1995, Chicken anaemia virus infection: Molecular basis of pathogenicity, Avian Pathology, v. 24:1, p. 11-31.

9. Tan, J, Tannock, G.A., 2005, Role of Viral load in the pathogenesis of chicken anemia virus, Journal of General Virology, v: 86, p-1327-1333.

Edited by student of Emily Lilly at University of Massachusetts Dartmouth.