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Chicks are most susceptible to contact infection by ALVs humans covered by the term cancer have been found to be the
during the period immediately after hatching. Although con- result of the abnormal expression of a variety of normal genes, the
genitally infected hatch mates are likely to be the main source of proto-oncogenes, or of tumour suppressor genes, that regulate
such infection, several procedures can reduce or eliminate infec- cell growth and differentiation. In the veterinary field, poultry
tion remaining from previous populations. Incubators, hatchers, geneticists have made important discoveries on understanding
brooding houses, and all equipment should be thoroughly cleaned the basis of genetic resistance to leukosis/sarcoma viruses and on
and disinfected between each use. Chick boxes should not be the nature of endogenous leukosis viruses, both areas of funda-
reused, and each farm ideally should have only one age group of mental biological significance.
chickens. The danger of introducing strains of virus not already New retroviruses and disease manifestations can arise by viral
present in the population can be eliminated if eggs or chicks from mutations. The most dramatic example was the appearance in the
different sources are not mixed, and if chicks are reared under 1980s an unusual new leukosis virus, ALV-J, in broiler breeding
isolation, conditions that will prevent cross-contamination of stocks, apparently through a rare genetic recombination between
flocks. Live vaccines used by the poultry industry are also poten- an exogenous ALV and an ancient endogenous retrovirus of the
tial sources of introduction of ALV to clean flocks (Barbosa et al., EAV family. ALV-J, associated with myeloid leukosis, spread
2008). in the 1990s to become worldwide, causing major economic
loss to the poultry industry. In some countries it has now been
Selection for genetic resistance eradicated from commercial primary broiler breeder flocks by
The frequencies of the alleles that encode cellular susceptibility the rigorous application of well-tested eradication programmes,
and resistance to infection by exogenous ALSVs vary greatly but in other countries it remains a major problem and has spread
among commercial lines of chickens (Crittenden and Motta, to layer flocks. New threats to the poultry industry from the de
1969; Motta et al., 1973) and may appear to be of value in selection novo emergence of new viruses or re-emergence of mutant viruses
of birds for disease resistance. However, with the emergence of cannot be discounted.
ALV-J infection where resistance to infection in chickens has not In recent years, there have been several reports of ALV-J
been demonstrated, the value of this approach is not clear. Never- outbreaks in parent and commercial layer flocks as well as some
theless, development of chicken lines resistant to ALV infections local breeds in China. Meanwhile, strains of ALV-A and ALV-B
using transgenesis has the potential in improving the eradica- continue to be isolated especially from the native chicken breeds,
tion methods and also preventing reinfection. Recent methods suggesting widespread distribution and complex dynamics of
of developing commercial chicken strains free of endogenous ALV infection in China. In this context, recent reports of isolation
retroviruses (Bacon et al., 2004) and the new methodologies of of ALV strains potentially belonging to a new subgroup K from
transgenesis using genetically modified primordial germ cells Chinese native chicken breeds is relevant (Wang et al., 2012; Li
(van de Lavoir et al., 2006a,b) point towards the feasibility of et al., 2016). In addition, the co-infection of ALV-A and ALV-J
using these approaches for generating ALV resistant stock in the as well as ALV-A and ALV-B viruses provide a potential oppor-
future. With the recent development of genome editing tool such tunity for recombination between different ALV subgroups (Xu
as CRISPR/Cas9 system, inducing genetic resistance to ALV will et al., 2004; Fenton et al., 2005). Although the p27 ELISA-based
be an effective adjunct for the control of these pathogens in con- screening methods used widely will detect most groups of ALV,
sideration of the pathogen diversity and for long term protection it is essential to have a continuous epizootiological surveillance
of native species of poultry. in place to detect new variants potentially escaping the current
detection methods.

Perspectives References
Work by biomedical scientists over the past few decades has Adkins, H.B., Brojatsch, J., Naughton, J., Rolls, M.M., Pesola, J.M., and
provided a deep understanding of avian L/S viruses and of the Young, J.A. (1997). Identification of a cellular receptor for subgroup E
avian leukosis virus. Proc. Natl. Acad. Sci. U.S.A. 94, 11617–11622.
molecular mechanisms by which they cause tumours. These Adkins, H.B., Brojatsch, J., and Young, J.A. (2000). Identification and
viruses and diseases have been used as model systems to further characterization of a shared TNFR-related receptor for subgroup B, D,
understand cancer in humans, and in this they have been remark- and E avian leukosis viruses reveal cysteine residues required specifically
for subgroup E viral entry. J. Virol. 74, 3572–3578.
ably successful. Much has been learnt about the viruses, leading to Adkins, H.B., Blacklow, S.C., and Young, J.A. (2001). Two functionally
new methods of virus assay and characterization, and the dynam- distinct forms of a retroviral receptor explain the nonreciprocal receptor
ics of infection, virus replication, and cell transformation, and interference among subgroups B, D, and E avian leukosis viruses. J. Virol.
this has been productively applied in the veterinary field. In more 75, 3520–3526. https://doi.org/10.1128/JVI.75.8.3520-3526.2001.
recent years, the interests of biomedical scientists have been in the Bacon, L.D. (2000). Detection of endogenous avian leukosis virus envelope
in chicken plasma using R2 antiserum. Avian Pathol. 29, 153–164.
molecular biology of the virus and the mechanisms of neoplastic https://doi.org/10.1080/03079450094180.
transformation. L/S viruses were found to either carry in their Bacon, L.D., Smith, E.J., Fadly, A.M., and Crittenden, L.B. (1996).
genome a viral oncogene derived from a cellular proto-oncogene, Development of an alloantiserum (R2) that detects susceptibility of
which they introduce into the host, or those without an oncogene chickens to subgroup E endogenous avian leukosis virus. Avian Pathol.
25, 551–568.
were found, following infection, to activate a cellular proto- Bacon, L.D., Fulton, J.E., and Kulkarni, G.B. (2004). Methods for evaluating
oncogene through insertional activation. Numerous diseases in and developing commercial chicken strains free of endogenous subgroup