Gibbon-ape leukemia virus (GaLV) is an oncogenic, type C retrovirus that has been isolated from primate neoplasms, including the white-handed gibbon and woolly monkey.

These include cross-species transmission of the retrovirus present within a species of East Asian rodent or bat, and the inoculation or blood transfusion of a MbRV-related virus into captured gibbons populations housed at medical research institutions.

[5] Phylogenetic analysis have revealed 7 strains of GaLV; GaLV-SF, GaLV-SEATO, GaLV-BR, GALV-X, GaLV-Mar, GaLV-H and SSV, which have emerged as a result of selection pressures from the host immune system.

[4] The discovery of a contagious oncogenic gammaretrovirus in sub-human primates stimulated a great deal of research into the pathogenesis of GaLV and its origins including the virus' intermediate host, which is currently disputed.

[2] An alternative hypothesis is based on the high sequence similarity of GaLV-SEATO and the Melomys Burtoni retrovirus (MbRV), isolated from a species of rodent from Papua New Guinea.

[2] However, due to the lack of geographic overlap of grassland melomys in PNG and Thailand, MbRV was initially considered ill-suited as the intermediate host of GaLV.

which offered a valid hypothesis for the spread of MbRV from PNG to Thailand by divulging SEATO facility reports and reviewing geographical movement of gibbons during the 1960s and 1970's.

The GaLV replication cycle proceeds as follows: Research published within the Retroviruses and Insights into Cancer Journal, highlights the potential of viral resistance within gibbon-apes, due to the partial proviral transcription of an intact envelope gene.

[17] Pathology study published by Kawakami et al in 1980, identifies the development of chronic granulocytic leukemia within young GaLV infected gibbons after latency periods of 5–11 months.

[21] Pathology study of the endogenizing integration of KoRV-A into the host's genome is essential in developing a therapeutic vaccine which decreases the incidence rate of 3% per year.

[30] Contrarily, FeLV-B is derived via recombination of exogenous FeLV-A with endogenous sequences (enFeLV) whilst the limited research into the origins of FeLV-C leans towards recombination/ or mutation.

[33] However, diagnosis of PERV in vivo has not occurred within; recipients of pig nerve cells or skin grafts, patients with porcine-based liver or pancreatic xenografts, and butchers in contact with porcine tissue.

[34] The earliest retroviral vectors were based on the Moloney murine leukemia virus (MMLV) which when pseudotyped with GaLV envelope protein, enabled gene transfer to various host cells.

[35] Furthermore, the development of "hybrid murine amphotropic viral envelope with the extracellular domains of GALV also helps to increase the cell infection rate within the host during gene therapy.

Furthermore, Lam et al evidenced the 8 fold greater expression of GLVR-1 than GLVR-2, which demonstrates that human T lymphocyte gene transfer methods should utilise the GaLV envelope protein that binds to the GLVR-1 surface receptor.