Abstract
This Chapter is concerned with the spread and survival of avian leukosis virus (ALV) in populations of domestic fowl, and the various factors which influence infection rate and incidence of disease. The term ALV as used here denotes the common “wild-type” exogenous avian retrovirus which causes mainly lymphoid leukosis (LL). Elsewhere it has also been termed LL virus. The avian retroviruses are remarkable for the strategies they have envolved for their survival. Some, those belonging to the endogenous virus group, are transmitted from generation to generation as viral genes in the genome of the host germ cells, where they may be regarded as forms of parasitic DNA, the eucaryotic equivalents of plasmids in procaryotes. Others comprise the exogenous virus group, being transmitted as infectious virions which invade cells, individuals and populations from their environment. These viruses are transmitted vertically, maintaining the infection from generation to generation, and also horizontally, spreading between contemporaries. The exogenous viruses fall into four subgroups, A, B, C and D, on the basis of viral envelope properties, whereas the endogenous viruses belong to subgroup E. The exogenous ALVs are usually fully expressed, while endogenous viral (ev) genes encode some of the structural proteins. However, some of the ev genes encode infectious virions which behave as exogenous viruses (see Chapter 5). Viruses of subgroups A, B, C and D differ genetically from those of subgroup E in several ways, and the relationship between them is not clear. Temin (1) believes that the endogenous subgroup E viruses represent an evolutionary stage between normal moveable genetic cellular elements termed transposons, and more virulent genetic entities capable of extracellular existence which we know as the exogenous viruses. Knowledge is being gained that genetic recombination can occur between endogenous and exogenous viruses and that they can interact in the host in other ways (2). The avian retroviruses are remarkably successful parasites: those of subgroup E have little if any detrimental effect on the host, while those of the other subgroups usually cause serious disease in only a small minority of the fowl they infect. For the commonly occurring wild-type exogenous ALV induction of neoplasms is an uncommon accident of infection and forms no essential part of the life cycle of the virus.
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Payne, L.N. (1986). Epizootiology of Avian Leukosis Virus Infections. In: De Boer, G.F. (eds) Avian Leukosis. Developments in Veterinary Virology, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2059-3_3
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