Page 242 - Avian Virology: Current Research and Future Trends

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Exogenous and endogenous avian leukosis EV21 ALV by the ev21 locus, which is linked with the sex-linked
viruses slow-feathering gene K, on the Z chromosome, has a tolerizing
On the basis of the way in which they are transmitted naturally, effect on response to exogenous ALV, and has been associated
ALV can also be classified as exogenous or endogenous viruses with an increased incidence of lymphoid leukosis in the field and
(reviewed by Crittenden, 1981; Payne, 1987). The former spread experimentally.
as infectious virions, either vertically (congenitally) from dam
to progeny through the egg, or horizontally from bird to bird.
Viruses of subgroups A, B, C, D and J spread in this way, and of Transmission and epizootiology
these A, B and J occur commonly in the field; C and D appear Exogenous ALVs are almost ubiquitous in commercial chickens
to be rare. Endogenous viruses are integrated into the genome of on a world-wide basis, although many primary egg-type and
normal birds as proviral sequences that are transmitted geneti- meat-type breeding companies have successfully instituted ALV
cally as Mendelian genes, either as complete viral genomes able eradication schemes. Chickens are the natural hosts for all viruses
to code for infectious virus of subgroup E, or more usually, as of L/S group (Payne, 1987); these viruses have not been isolated
incomplete (defective) genomes able to code for certain retro- from other avian species except pheasants, partridges, and quail.
viral products (e.g. gs-antigen) only. The sites of integration of Exogenous ALVs are transmitted in two ways: vertically from
these endogenous viruses are termed ‘ev loci’. Endogenous ALVs infected hens to their offspring through the egg and horizontally
are apparently non-oncogenic although they may influence the from bird to bird by direct or indirect contact (Payne, 1992;
response of the bird to infection by exogenous ALVs by inducing Payne and Nair, 2012). Although usually only a small percent-
immunological tolerance or immunity. Apart from the family of age of chicks are infected vertically, this route of transmission is
ev endogenous viruses closely related to exogenous ALV, other important in transmitting the infection from one generation to
more distantly related endogenous families have been discovered the next, and in providing a source of contact infection to other
in the normal genome, namely: EAV (endogenous avian virus), chicks. Most chickens become infected by close contact with
ART-CH (avian retrotransposon from chicken genome) and CR1 congenitally infected birds. Sources of virus from infected birds
(chicken repeat 1). The EAV family is of particular interest, since include faeces, saliva and desquamated skin. The period of sur-
members designed EAV-HP (or ev/J) appear to be the source of vival of ALV outside the body is relatively short (a few hours),
the envelope gene of subgroup J ALV (Sacco et al., 2000). and consequently ALV is not highly contagious. Although verti-
The origin, evolutionary relationships and biological sig- cal transmission is important in the maintenance of the infection,
nificance of these elements are not clearly understood. In horizontal infection may also be necessary to maintain a rate
evolutionary terms, the CR1 retrotransposon elements appear of vertical transmission sufficient to prevent the infection from
to be the most ancient and the ev genes the most recent. These dying out (Payne and Bumstead, 1982). The infection does not
types of elements are examples of retroelements (retroposons, spread readily from between birds through indirect contact (in
retrotransposons) that are found in an extremely broad range of separate pens or cages), probably because of the relatively short
organisms, including fungi, plants, protozoa, and animals, and life of the virus outside the birds. However, contact exposure at
that are concerned with the mobility of genes within the genome hatch was shown to be an effective method of spread of ALV-J
of organisms. These elements are believed to be the evolution- among broiler breeder chickens (Fadly and Smith, 1999; Witter,
ary precursors of retroviruses; that is, genetic elements that have 2000; Witter et al., 2000) and was prevented by small group rear-
acquired the ability to exist as infectious entities outside of cells. ing (Witter and Fadly, 2001).
Even so, it is considered that some endogenous viruses, such as
the ev loci, may represent exogenous viruses that have become
reintegrated on an evolutionary scale into the germline. Most Flock infection
endogenous viruses are genetically defective in that they do not Four classes of ALV infection statuses are recognized in mature
possess the full complement of retroviral genes necessary for the chicken flocks: (1) no viraemia, no antibody (V-A-); (2) no virae-
production of infectious virions. However, some do and they mia, with antibody (V-A+); (3) with viraemia, with antibody
give rise to subgroup E ALV, of which RAV-0 is the prototype. (V+A+); and (4) with viraemia, no antibody (V+A-) reviewed
Unlike viruses of the other subgroups, subgroup E ALV do not by (Payne, 1992; Payne and Nair, 2012; Nair and Fadly, 2013).
induce neoplasms, evidently because the LTR has weak gene Birds in an infection-free flock and genetically resistant birds
promoter activity. The biological value of endogenous viruses in a susceptible flock fall into the category V-A-. Genetically
is not clear. It has been argued that because they persist, they susceptible birds in an infected flock fall into one of the other
must be of value. More specifically, the presence of ev2 or ev3 has three categories. Most are V-A+, and a minority, usually less than
been reported to protect birds from a non-neoplastic syndrome 10%, is V+A–. Most V+A– hens transmit ALV to a varying but
caused by infection with subgroup A ALV (Crittenden et al., relatively high proportion of their progeny (Payne, 1992; Payne
1982, 1984). However, in certain circumstances they can be det- and Nair, 2012). A small proportion of V-A+ hens transmit the
rimental. Thus, embryonic infection with RAV-0 causes a more virus congenitally and do so more intermittently; the tendency
persistent viraemia and more neoplasms following infection for congenital transmission of ALV in this category was found to
with exogenous ALV, apparently due to depression of humoral be more frequent in hens with low antibody titre (Tsukamoto et
immunity (Crittenden et al., 1987). Similarly, expression of al., 1992). Congenitally infected embryos develop immunologic