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Gibbon-ape Leukaemia Virus
Virus classification Edit this classification
(unranked): Virus
Realm: Riboviria
Kingdom: Pararnavirae
Phylum: Artverviricota
Class: Revtraviricetes
Order: Ortervirales
Family: Retroviridae
Genus: Gammaretrovirus
Species:
Gibbon-ape Leukaemia Virus

Gibbon-ape leukaemia virus (GaLV) is an oncogenic, type C retrovirus that has been isolated from primate neoplasms, including the White-handed Gibbon and Woolly Monkey. [1]The virus was identified as the etiological agent of hematopoietic neoplasms, leukemias, and immune deficiencies within gibbons in 1971, during the epidemic of the late 1960s and early 1970's. Epidemiological research into the origins of GaLV has developed two hypothesises for the virus' emergence. These include; cross-species transmission through close contact with the retrovirus present within a species of East Asian rodents or the unwitting introduction of a MbRV-related virus into captured gibbons populations in Bangkok, Thailand.[2] The virus was subsequently identified in captive gibbon populations in Thailand, the USA and Bermuda.[3]

GaLV is shed in urine and faeces and may be transmitted horizontally by contact with these biomaterials and is also suspected to be transmitted sexually.[4] GaLV exists in 5 strains; GaLV-SF, GaLV-SEATO, GaLV-BR, GALV-X, GaLV-Mar and GaLV-H, due to selection pressures from the host immune system. [3] Recently, full genome sequences of these strains have been made available (Alfano et al. 2016), which broadens possibility's for GaLV's utility as a viral vector.[5]

Epizootiology

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History

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Cases of malignant lymphomas and leukemias were not described in gibbons until the 1960's, when several cases of haematopoietic neoplasia were reported in a single colony of white-handed gibbons housed at the SEATO research facility in Bangkok, Thailand.[6] In 1971, phylogenetic analysis of the Leukemia-inducing retrovirus, lead to the identification of GaLV-SEATO, published within De Paoli et al. (1971).[7] Following this discovery, five other strains of GaLV was identified from animals animals whose associated neoplastic syndromes were only recorded in specific cohorts from captive research institutes, which include:

  • GaLV-SF: which was identified from a gibbon lymphosarcomas in San Francisco and within captured gibbons populations at the University of California San Francisco Medical Center and the University of California. (Kawakami et al. and Snyder et al., 1973)
  • GALV‐X: detected in cell culture from a human T-cell line infected with HIV-1 in Louvain, Belgium and at the National Cancer Institute in Maryland, USA.[8]
  • GALV‐H: identified from a gibbon with lymphocytic leukemias from a colony of free-ranging gibbons at the Hall's Island, Bermuda.
  • GALV‐Br: Identified in frozen brain samples of non-leukemics gibbons at the Gulf South Research Institute in Louisiana. (Gallo et al., 1978)[8]
  • GaLV-Mar: detected in cell culture (in vitro) derived from Marmoset cells.[9]
  • Simian sarcoma (SSV): a defective GALV recombinant, derived from a single isolate of fibrosarcoma in a Woolly Monkey that was exposed to a GALV-infected captive gibbon.[10] For viral replication to occur within the host simian sarcoma-associated virus (SSAV) must also be present.[11]

The strains share more than 90% nucleotide sequence identity and more than 93% amino acid sequence identity (Alfano et al. 2016). GALV strains are extremely similar to each other genetically, and the divergence of the env gene between strains of GALV ranges from 85% to 99%.[3] Diversifying selection on the pathogenic strains of GALV is thought to be a response to pressures from the host immune system (Alfano et al. 2016).

Origins of GaLV

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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.[10] Virologist initially suggested that GaLV was related to murine leukaemia virus (MLV) detected in Southeast Asian rodents. The endogenous retroviruses with similar homology are; McERV detected within Mus Caroli, and Mus dunni endogenous virus (MDEV) isolated from the earth-coloured mouse (Lieber et al. 1975, Callahan et al. 1979). However, immunological assays demonstrated McERV had different host ranges and a plasmolipin receptor which indicates it's unlikelihood of being the precursor for GaLV. Furthermore, this hypothesis was based on results derived from low resolution serological and DNA homology methods. Thus, present phylogenetic analysis of proviral sequences of GALV‐SEATO and MLV shows a 68–69% similarity for pol and 55% similarity for env, thus indicating the limited sequence similarity.[3] Therefore, there are no published proviral sequences from any of these rodent hosts which share a sufficiently high degree of identity to GALV to support this hypothesis.[10]

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. Immunological assay highlights that MbRV shares 93% sequence homology with GaLV-SEATO which is significantly higher than McERV and MDEV.[10] However, due to the lack of geographic overlap of grassland melomys in PNG and Thailand, MbRV was initially considered ill-suited as the precursor of GaLV.[12] Yet, in 2016 the Mammal Review published Is gibbon ape leukaemia virus still a threat, in which offered a valid hypothesis of the trans species transmission of MbRV from PNG to Thailand through review of SEATO facility reports and transportation of gibbons during the 1960s and 1970s.[3] The SEATO facility report demonstrated that gibbons were frequently inoculated with blood and tissue from humans, Asian rodents and other gibbons as models for human disease such as malaria and dengue fever. It is therefore proposed that biomaterial from these rodents were contaminated with MbRV and later involved in blood transfusion which resulted in the development of GaLV within two gibbons (S-76 and S-77).

The last hypothesis is based off the sequence similarity of GaLV and retroviruses present within Southeast Asian bat species. [13] Mobile species such as bats are proposed as potential intermediate hosts of GALV as they can can fly and disperse rapidly and have additionally been linked to several zoonotic diseases. [14]

Viral resistance

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Research published within the Retroviruses and Insights into Cancer Journal, demonstrates the potential for the development of viral resistance within gibbon-apes, due to the partial proviral transcription with an intact envelope gene. The expression of the GaLV envelope gene was exhibited within a symptomless gibbon despite long term exposure to another highly viremic gibbon. Therefore, the expression of the GaLV envelope in the absence of replication-competent GaLV may have rendered the animal resistant to GaLV infection.[15] Furthermore, antibodies against the retrovirus was identified in gibbons without evidence of disease which suggests a natural immunological resistance to the retrovirus.[16]

Transmission

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GaLV is shed in urine and faces and may be transmitted horizontally by contract with these biomaterials and is also suspected to be transmitted horizontally.[17] GaLV can also be transmitted from viremic parents to their offspring either prenatally or postnatally, however prenatal infections obtain large quantities of proviral DNA.[18] Seroepidemiology established that GaLV-H was horizontally transmitted among gibbons within the colony.

Signs and Symptoms

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Conditions associated with GALV infection include malignant lymphoma, lymphoblastic leukemia, myelogenous (granulocytic) leukemia and “osteopetrosis” of long bones. In cases of granulocytic leukemia there is marked circulating granulocytosis with infiltration of bone marrow, liver, lymph nodes, and spleen. Infiltrated tissues often have a greenish hue (chlorosis)[19]

The infection of young gibbons with GALV resulted in the development of chronic granulocytic leukemia within multifocal bone lesions and metastases after latency periods of 5-11 months (Kawakamiet al., 1980). Gibbons infected at the age of 14 months developed persisting neutralising antibodies to the virus and remained free of hematopoietic disease. Infection of human blood cells with GALV led to enhanced induction of growth of B lymphoblasts.[8]


Gammaretrovirus Outbreaks

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KoRV

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The introduction of the KoRV precursor into koalas was first dated approximately 200 years ago. Meanwhile a widespread distribution of KoRV in the late 1800s was described. Transspecies Transmission of Gammaretroviruses and the Origin of the Gibbon Ape Leukaemia Virus (GaLV) and the Koala Retrovirus (KoRV)

GaLV in Gene Therapy

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The GaLV Envelope Fusogenic Membrane Glycoprotein (GaLV FMG) is the protein responsible for

External References

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References

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  1. ^ S, Delassus; P, Sonigo; S, Wain-Hobson (1989-11). "Genetic Organization of Gibbon Ape Leukemia Virus". Virology. PMID 2683360. Retrieved 2020-02-02. {{cite web}}: Check date values in: |date= (help)
  2. ^ J, McKee; N, Clark; F, Shapter; G, Simmons (2017-04). "A New Look at the Origins of Gibbon Ape Leukemia Virus". Virus genes. PMID 28220345. Retrieved 2020-02-02. {{cite web}}: Check date values in: |date= (help)
  3. ^ a b c d e Brown, Katherine (4/12/2016). "Is gibbon ape leukaemia virus still a treat". Mammal Review – via Wiley Online Library. {{cite journal}}: Check date values in: |date= (help)
  4. ^ Murphy, Hayley Weston; Switzer, William M. (2008-01-01), Fowler, Murray E.; Miller, R. Eric (eds.), "Chapter 31 - Occupational Exposure to Zoonotic Simian Retroviruses: Health and Safety Implications for Persons Working with Nonhuman Primates", Zoo and Wild Animal Medicine (Sixth Edition), W.B. Saunders, pp. 251–264, ISBN 978-1-4160-4047-7, retrieved 2020-02-02
  5. ^ "Complete genome of all strains of the gibbon ape leukemia virus sequenced". ScienceDaily. Retrieved 2020-02-09.
  6. ^ "Virologists unravel mystery of late 20th century gibbon leukaemia outbreak". ScienceDaily. Retrieved 2020-02-06.
  7. ^ "Is gibbon ape leukaemia virus still a threat?". Mammal Review.
  8. ^ a b c Hausen, Harald zur (2007-09-24). Infections Causing Human Cancer. John Wiley & Sons. ISBN 978-3-527-60929-1.
  9. ^ Burke, Mark; Ptito, Maurice (2018-05-30). Primates. BoD – Books on Demand. ISBN 978-1-78923-216-5.
  10. ^ a b c d McKee, J.; Clark, N.; Shapter, F.; Simmons, G. (2017-04). "A new look at the origins of gibbon ape leukemia virus". Virus Genes. 53 (2): 165–172. doi:10.1007/s11262-017-1436-0. ISSN 0920-8569. {{cite journal}}: Check date values in: |date= (help)
  11. ^ Murphy, Hayley Weston; Switzer, William M. (2008-01-01), Fowler, Murray E.; Miller, R. Eric (eds.), "Chapter 31 - Occupational Exposure to Zoonotic Simian Retroviruses: Health and Safety Implications for Persons Working with Nonhuman Primates", Zoo and Wild Animal Medicine (Sixth Edition), W.B. Saunders, pp. 251–264, ISBN 978-1-4160-4047-7, retrieved 2020-02-09
  12. ^ Simmons, Greg; Clarke, Daniel; McKee, Jeff; Young, Paul; Meers, Joanne (2014-09-24). Roca, Alfred L. (ed.). "Discovery of a Novel Retrovirus Sequence in an Australian Native Rodent (Melomys burtoni): A Putative Link between Gibbon Ape Leukemia Virus and Koala Retrovirus". PLoS ONE. 9 (9): e106954. doi:10.1371/journal.pone.0106954. ISSN 1932-6203. PMC 4175076. PMID 25251014.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  13. ^ J, Denner (2016-12-20). "Transspecies Transmission of Gammaretroviruses and the Origin of the Gibbon Ape Leukaemia Virus (GaLV) and the Koala Retrovirus (KoRV)". Viruses. PMID 27999419. Retrieved 2020-02-07.
  14. ^ Alfano, Niccolò; Michaux, Johan; Morand, Serge; Aplin, Ken; Tsangaras, Kyriakos; Löber, Ulrike; Fabre, Pierre-Henri; Fitriana, Yuli; Semiadi, Gono; Ishida, Yasuko; Helgen, Kristofer M. (2016-08-26). "Endogenous Gibbon Ape Leukemia Virus Identified in a Rodent (Melomys burtoni subsp.) from Wallacea (Indonesia)". Journal of Virology. 90 (18): 8169–8180. doi:10.1128/JVI.00723-16. ISSN 0022-538X. PMC 5008096. PMID 27384662.
  15. ^ Dudley, Jaquelin (2010-10-22). Retroviruses and Insights into Cancer. Springer Science & Business Media. ISBN 978-0-387-09581-3.
  16. ^ Lowenstine, Linda J.; McManamon, Rita; Terio, Karen A. (2018-01-01), Terio, Karen A.; McAloose, Denise; Leger, Judy St. (eds.), "Chapter 15 - Apes", Pathology of Wildlife and Zoo Animals, Academic Press, pp. 375–412, ISBN 978-0-12-805306-5, retrieved 2020-02-09
  17. ^ Murphy, Hayley Weston; Switzer, William M. (2008-01-01), Fowler, Murray E.; Miller, R. Eric (eds.), "Chapter 31 - Occupational Exposure to Zoonotic Simian Retroviruses: Health and Safety Implications for Persons Working with Nonhuman Primates", Zoo and Wild Animal Medicine (Sixth Edition), W.B. Saunders, pp. 251–264, ISBN 978-1-4160-4047-7, retrieved 2020-02-09
  18. ^ Journal of the National Cancer Institute. U.S. Public Health Service, National Institute of Health. 1978.
  19. ^ Terio, Karen A.; McAloose, Denise; Leger, Judy St (2018-10-08). Pathology of Wildlife and Zoo Animals. Academic Press. ISBN 978-0-12-809219-4.
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