Avian Leukosis: Will We Be Able to Get Rid of It?

Simple Summary Historically avian leukosis has produced severe economic losses, due to decreased productivity, higher mortality from immunosuppression-associated infections, and tumor development. It is virtually eradicated in commercial poultry of the western world, but infection by avian leukosis virus (ALV) still remains in hobby, fancy, backyard and native and indigenous chickens from which it may jump to commercial birds. In addition, relics of ancient infections by ALV remain in the genome of birds, with which ALV may recombine and generate new viruses. In this review we analyze the virus, its infection in the cell, and how the immune system of the bird reacts against it to better understand the strategies which are being explored to avoid the reemergence of this disease. Scientific research focuses on manipulating the genome of birds, in order to obtain animals that the virus cannot infect, due to the absence of a compatible receptor in the cells, or modify their immune response to make it stronger. In addition, hens and chickens are analyzed to eliminate those which might be infected. But, more studies are needed to better understand this complex disease. Avian leukosis viruses (ALVs) have been virtually eradicated from commercial poultry. However, some niches remain as pockets from which this group of viruses may reemerge and induce economic losses. Such is the case of fancy, hobby, backyard chickens and indigenous or native breeds, which are not as strictly inspected as commercial poultry and which have been found to harbor ALVs. In addition, the genome of both poultry and of several gamebird species contain endogenous retroviral sequences. Circumstances that support keeping up surveillance include the detection of several ALV natural recombinants between exogenous and endogenous ALV-related sequences which, combined with the well-known ability of retroviruses to mutate, facilitate the emergence of escape mutants. The subgroup most prevalent nowadays, ALV-J, has emerged as a multi-recombinant which uses a different receptor from the previously known subgroups, greatly increasing its cell tropism and pathogenicity and making it more transmissible. In this review we describe the ALVs, their different subgroups and which receptor they use to infect the cell, their routes of transmission and their presence in different bird collectivities, and the immune response against them. We analyze the different systems to control them, from vaccination to the progress made editing the bird genome to generate mutated ALV receptors or selecting certain haplotypes.