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(Kung and Maihle, 1987; Kung and Liu, 1997) will lead to onco- enzyme will dephosphorylate adenosine triphosphate, and this
genic transformation. activity can be used for virus assay and purification. Cells without
Some laboratory strains and field isolates of ALV also possess this enzyme, such as fibroblasts, release virus that is devoid of this
one (or rarely two) viral oncogene(s) inserted within the genome. activity.
Such viruses have acquired the oncogene by transduction of a
cellular oncogene during oncogenesis. These ‘acutely transform-
ing’ viruses are usually genetically defective due to the deletions Virus replication
within the genome and require the presence of co-infecting As with other retroviruses, replication of ALSV is characterized
non-defective ‘helper viruses’ to enable replication (Maeda et al., by the formation, under the direction of reverse transcriptase, of
2008). Acquisition of a viral oncogene usually is accompanied a DNA provirus that becomes linearly integrated into the host
by genetic defects elsewhere in the viral genome. Non-defective genome. Subsequently, the proviral genes are transcribed into
Rous sarcoma virus (RSV) has the genome organization struc- viral RNAs, which are translated to produce precursor and mature
ture gag/pro-pol-env-src. The additional gene, src, responsible proteins that constitute the virion. Great effort has been made
for sarcomatous transformation, was acquired originally from a since the 1970s to elucidate these events, details of which have
normal cellular oncogene, cellular src. The gene cellular src is an been reviewed extensively (Luciw and Leung, 1992; Telesnitsky
example of a number of host cell genes, termed proto-oncogenes and Goff, 1997). Only an outline of the main events is provided
or onc genes, concerned with acute transformation (Enrietto and here.
Hayman, 1987; Wang and Hanafusa, 1988). Viral and cellular ver-
sions of onc genes distinguished by the prefixes v- and c- prefixes Penetration of the host cell
(e.g. v-myc genes, with c-myc), with the latter present in acutely Detailed reviews describing the recent understanding of the early
transforming viruses (Kung and Liu, 1997; Maeda et al., 2008). ALV interactions with the host cells are available (Barnard and
Young, 2003; Barnard et al., 2006). Although adsorption of the
virion to the cell membrane is non-specific, occurring even in
Viral proteins cells resistant to infection, penetration of cells is dependent on
The nature, location, and synthesis of proteins that constitute the presence, in the cell membrane, of host gene-encoded recep-
avian retroviruses have been extensively studied (Swanstrom tors specific for particular virus envelope subgroups and on fusion
and Wills, 1997). The virion core contains five non-glycosylated of viral and cell membranes. Virions taken into the cell in vacuoles
proteins encoded by the gag/pro gene: MA (matrix, p19); p10; and viral RNA in the nucleus within 120 minutes of attachment
CA (capsid, p27), which is the major gs antigen (Gag) in the core (Dales and Hanafusa, 1972). In recent years, considerable pro-
shell; NC (nucleocapsid, p12), involved in RNA processing and gress has been made in understanding the nature of the receptors
packaging; and PR (protease, p15), involved in cleavage of pro- used by the different ALV subgroups (Barnard et al., 2006). The
tein precursors. Other minor polypeptides have been reported. receptor for subgroup A ALV, designated TVA, is related to the
The pol gene encodes the enzyme reverse transcriptase (RT) human low-density lipoprotein receptor (Bates et al., 1993;
present in the core. It is a complex consisting of the b subunit Young et al., 1993; Gray et al., 2011). Binding of the virus to the
(95 kDa) and the a subunit (68 kDa) derived from it and has receptor for subgroup A ALV triggers a conformational change in
RNA- and DNA-dependent polymerase and DNA:RNA hybrid- the viral envelope glycoprotein that allows viral fusion with the
specific ribonuclease H activities. The b subunit also contains the cell membrane and viral entry (Gilbert et al., 1995). Decreased
IN domain (integrase, p32), the enzyme necessary for integra- susceptibility subgroup A ASLV in vitro and in vivo from intronic
tion of viral DNA into the host genome. Structural studies on deletions in close-bred line of domestic chickens resulting in inef-
the catalytic core domain of the ALSV integrase suggested that ficient splicing of the tva mRNA has been reported (Reinišová et
it can dimerize in more than one state allowing the flexibility for al., 2012). The receptors for ALV subgroups B, D, and E, desig-
s1
s3
multifunctionality during different steps of the viral life cycle nated TVB and TVB , resemble a receptor for cytokines of the
(Ballandras et al., 2011). tumour necrosis factor family (Adkins et al., 1997, 2000, 2001;
The virion envelope contains two glycoproteins encoded Klucking and Young, 2004; Reinišová et al., 2008) and the resist-
by the env gene: SU (surface, gp85), the viral surface knob-like ance to these viruses are due to a premature stop codon within
structures that determine viral envelope subgroup specificity of this allele (Klucking et al., 2002) and molecular tests to evaluate
the ALSV; and TM (transmembrane, gp37), representing the TVB haplotypes have been developed (Zhang et al., 2005). The
transmembrane structure that attaches the knobs to the envelope. TVB receptors are functional death receptors capable of induc-
These two envelope (Env) proteins are linked to form a dimer, ing death-signalling pathways leading to apoptosis (Brojatsch et
termed virion glycoprotein. Enzymes and other proteins are al., 2000; Klucking et al., 2005). The receptor for the subgroup C
found in virions and are considered to be cellular components avian sarcoma and leukosis viruses, TVC, is related to mamma-
incorporated during virus maturation (Swanstrom and Wills, lian butyrophilins, members of the immunoglobulin superfamily
1997). Of practical value is the presence in AMV obtained (Elleder et al., 2005; Munguia and Federspiel, 2008). The host
from blood of infected chickens, or from myeloblast cultures, cell receptor used by the ALV subgroup J, which has a distinct
of adenosine triphosphatase derived from the cell membrane envelope with limited homology to those of other subgroups,
and incorporated into the virus particle during maturation. This has been identified as the chicken Na(+)/H(+) exchanger type