Gibbon ape leukemia virus

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Gibbon-ape Leukaemia Virus
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Pararnavirae
Phylum: Artverviricota
Class: Revtraviricetes
Order: Ortervirales
Family: Retroviridae
Genus: Gammaretrovirus
Species:
Gibbon-ape Leukaemia Virus
Synonyms
  • Gibbon sarcoma and leukemia virus

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. [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 1970s. Epidemiological research into the origins of GaLV has developed two hypotheses for the virus' emergence. 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. [2] The virus was subsequently identified in captive gibbon populations in Thailand, the US and Bermuda. [3]

Contents

GaLV is transmitted horizontally by contact with excretory products of infected gibbons. [4] However, it is also hypothesised to be vertically transmitted via parent-progeny transmission. [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. [3] Recently, full genome sequences of these strains have been made available which broadens the possibilities for GaLV's utility as a viral vector in gene transfer. [6]

Epizootiology

History

Cases of malignant lymphomas and leukemias were not described in gibbons until the 1960s, 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. [7] In 1971, phylogenetic analysis of the Leukemia-inducing retrovirus, lead to the identification of GaLV-SEATO, published within De Paoli et al. (1971). [3] Following this discovery, five other strains of GaLV was identified from animals whose associated neoplastic syndromes were exclusively recorded in captive gibbon populations, which include:

GaLV Phylogenetic trees derived from genome sequences of GaLV strains; GaLV-SEATO, GaLV-Br, GaLV-H, GaLV-X and GaLV-SF. Gibbon-ape leukemia virus Phylogenetic tree.jpg
GaLV Phylogenetic trees derived from genome sequences of GaLV strains; GaLV-SEATO, GaLV-Br, GaLV-H, GaLV-X and GaLV-SF.

These strains exhibit high genetic similarity, demonstrated through DNA sequencing which reveals approx. 90% sequence identity and more than 93% amino acid genome identity between strains of GaLV. Differences between these strains occurs in the env gene, with divergence ranging from 85% to 99%. [4]

Origins

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] 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). Furthermore, this hypothesis was based on results derived from low resolution serological and DNA homology methods. [3] 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 rodent hosts which share a sufficiently high degree of sequence identity to GALV to confirm an intermediate rodent host as the precursor for GaLV. [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. Immunological analysis highlights that MbRV shares 93% sequence homology with GaLV-SEATO which is significantly higher than McERV and MDEV. [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. [11] However, in 2016 the Mammal Review published "Is gibbon ape leukaemia virus still a threat?" 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. [3] The SEATO facility report demonstrated that gibbons were frequently inoculated with biomaterial from humans, Southeast Asian rodents and other gibbons, for pathogenetic study of human diseases including malaria and dengue fever. It is therefore proposed that blood and tissue samples used at SEATO were contaminated with MbRV-related virus and later introduced into Gibbon test subjects via blood transfusion or inoculation, thereby resulting in the development of GaLV within two gibbons (S-76 and S-77). [3]

The last hypothesis is based on the sequence similarity of GaLV and retroviruses present within Southeast Asian bat species. [12] Mobile bat species are potential intermediate hosts of GALV as they can disperse rapidly over large geographical areas and have also been linked to several zoonotic diseases. [13]

Replication cycle

GaLV belongs to the retrovirus family which utilises an enzyme called reverse transcriptase in viral replication. Retroviruses have single stranded genomes (ssRNA) which undergoes reverse transcription to form double-stranded DNA (dsNDA) prior to proviral integration into the genome of the host cell. The GaLV replication cycle proceeds as follows:

  1. Binding: The first step of GaLV retroviral replication is the adsorption of adsorbate particles on the surface of human cells using receptor molecules SLC20A1 (GLVR-1, PIT-1) and SLC20A2 (GLVR-2, PIT-2). [14] Both molecules are cellular proteins (phosphate transporters).
  2. Entry into host cell: Then GaLV particles use these cell-surface proteins on the cell membrane, as specific receptors to enter their host cells. [15]
  3. Reverse transcription: The viral core then enters the cytoplasm of the target cell where the enzyme, reverse transcriptase, generates a complementary DNA strand from 3' to 5'. [15]
  4. Nuclear entry: The proviral integration of GaLV into the host genome requires entry into the nucleus of the target cell. However, GaLV is incapable of infecting non-dividing cells and therefore relies on the breakdown of the nuclear membrane during mitosis cell division for nuclear entry. [15]
  5. Replication: Once the proviral DNA enters the nucleus of the host cell, replication occurs via polypeptide synthesis and becomes integrated into the host genome. [15]

Viral resistance

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. The expression of the GaLV envelope gene was exhibited within an asymptomatic 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. [16] Furthermore, antibodies against the retrovirus was identified in gibbons without evidence of disease which suggests a natural immunological resistance to GaLV. [17]

Transmission

GaLV is an exogenous virus that is horizontally transmitted via contact with GaLV contaminated biomaterials such as urine and faces. [18] This is confirmed within hybrizidation assay which evidenced the lack of proviral genome within uninfected gibbons. Furthermore, experimental research conducted at the Comparative Oncology Laboratory demonstrates the "horizontal transmission of GaLV within a 14-month-old uninfected gibbon which contracted GaLV within six weeks of exposure to viremic individuals." Furthermore, GaLV is also transmitted prenatally via parent-progeny transmission in utero, of which offspring exhibit a large quantity of proviral DNA in opposed to postnatal transmission. [5]

Signs and symptoms

Conditions associated with GALV include neoplastic syndromes leading to susceptible secondary and often fatal diseases including; malignant lymphoma, lymphoblastic leukemia, osteoporosis and granulocytic leukemia. In cases of granulocytic leukemia, increased granulocytes in the peripheral blood infiltrated bone marrow and liver lymph nodes, causing a greenish hue (chlorosis) within these tissues. [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. Additionally, the introduction of GaLV into 14-month-old gibbons, demonstrated the production of neutralising antibodies which enabled individuals to remain asymptomatic and free of hematopoietic disease, thereby demonstrating the host's immune response to GaLV infection. [8]

Gammaretrovirus outbreaks

Koala retrovirus (KoRV)

KoRV belongs to the gammaretrovirus genus and is closely related to GaLV with an 80% nucleotide similarity. [19] The retrovirus is isolated from lymphomas and leukemias, present within infected captive and free-living koala populations in Australasia. [20] Accordingly, a study published within the journal of virology, Molecular Dynamics and Mode of Transmission of Koala Retrovirus as It Invades and Spreads through a Wild Queensland Koala Population, highlights that 80% of koalas that developed neoplasia was also KoRV-B positive, thereby linking the widespread infection of leukemia and lymphoma to KoRV. At present, KoRV is the only retroviral that induces germ-line infections and therefore presents the opportunity for scientists to understand the processes regulating retrovirus endogenization. [21]

9 subtypes of KoRV have been identified, with the primary strains being; KoRV-A, KoRV-B and KoRV-J, which induces immodulation resulting in neoplastic syndromes and chlamydiosis. Moreover, the study demonstrated the diseases associated with KoRV-B including; developed abdominal lymphoma, a nonspecified proliferative/bone marrow condition, osteochondroma and mesothelioma. [22] Nature by Tarlington and colleagues, provides epidemiological evidence that germline infections are present in populations found in Queensland, yet some individuals in Southern Australia lack the provirus, suggesting that retroviral endogenization began in Northern Australia between the last 100 to 200 years. [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. [23] [22]

Feline leukaemia virus (FeLV)

FeLV is an oncogenic gammaretrovirus belonging to the orthoretrovirinae subfamily and retroviridae family. [24] First discovered in 1964 within a cluster of cats with lymphosarcoma. FeLV is identified as the infectious agent causing immunomodulation within bone marrow and the immune system, which renders infected cats susceptible to a variety of secondary and opportunistic infections. [25] Associated diseases of FeLV include; lymphoma, non-regenerative anemias and thymic degenerative disease. [26] Currently, the prevalence of FeLV has decreased since the 1970s and 1980s, due to veterinary interventions, vaccination, biosecurity protocols and quarantine or euthanasia of infected animals. [27] Accurate blood testing procedures revolving around the detection of FeLV P27 enables diagnosis via two methods; enzyme-linked immunosorbent assay (ELISA), which detects the presence of free FeLV particles that are found in the bloodstream and indirect immunofluorescent antibody assay (IFA), which detects the presence of retroviral particles within white blood cells. [28]

FeLV is horizontally and vertically transmitted through biomaterials; saliva, blood, breast milk, urine and feces. Furthermore, transmission can also occur postnatally or prenatally within parent-progeny relationships. The potency of parasitic fleas as a viral vector for FeLV was identified in 2003, which confirmed horizontal transmission of FeLV without close contact with infected individuals. [29] Furthermore, the three strains of FeLV are A,B,C. FeLV-A is the least pathogenic strain that is transmittable in nature especially within unvaccinated animals. [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. [31]

Porcine endogenous retrovirus (PERV)

PERV was first described in 1970, belonging to the gammaretrovirus genus, Orthoretrovirinae subfamily and Retroviridae family,. [32] PERV is categorised into three replication competent subtypes: PERV-A, PERV-B and PERV-C. PERV-A and PERV-B are polytropic viruses which are capable of infecting humans and porcine cells, whereas PERV-C is an ecotropic virus which effects only porcine cells. [33] The cross-species transmission of PERV's in human cells have been demonstrated in vitro which raises concern regarding the xenotransplantation of porcine cells, tissues and organs. [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. [32]

In medicine

GaLV envelope protein

GaLV Envelope Protein has biomedical significance due to its utility as a viral vector in cancer gene therapy and gene transfer. [20] Retroviral vectors are used in ex vivo gene therapy, which involves the modification of cells in vitro, to replace genes that code for dysfunctional proteins. The inserted gene undergoes transcription and translation within the nucleus and ribosome of the host cell producing "normal" secretable proteins. [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." [36] [37]

Gene transfer is dependent on the relationship between receptor expression and transduction efficiency. Human T-lymphocytes have two surface receptors (GLVR-1 and GLVR-2) that detect the presence of GaLV. 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. [38] However, because gammaretroviruses are incapable of infecting non-dividing cells, the utility of GaLV envelope protein in gene transfer is being superseded by lentiviral vectors. [35]

Related Research Articles

<span class="mw-page-title-main">Retrovirus</span> Family of viruses

A retrovirus is a type of virus that inserts a DNA copy of its RNA genome into the DNA of a host cell that it invades, thus changing the genome of that cell. After invading a host cell's cytoplasm, the virus uses its own reverse transcriptase enzyme to produce DNA from its RNA genome, the reverse of the usual pattern, thus retro (backwards). The new DNA is then incorporated into the host cell genome by an integrase enzyme, at which point the retroviral DNA is referred to as a provirus. The host cell then treats the viral DNA as part of its own genome, transcribing and translating the viral genes along with the cell's own genes, producing the proteins required to assemble new copies of the virus. Many retroviruses cause serious diseases in humans, other mammals, and birds.

Mouse mammary tumor virus (MMTV) is a milk-transmitted retrovirus like the HTL viruses, HI viruses, and BLV. It belongs to the genus Betaretrovirus. MMTV was formerly known as Bittner virus, and previously the "milk factor", referring to the extra-chromosomal vertical transmission of murine breast cancer by adoptive nursing, demonstrated in 1936, by John Joseph Bittner while working at the Jackson Laboratory in Bar Harbor, Maine. Bittner established the theory that a cancerous agent, or "milk factor", could be transmitted by cancerous mothers to young mice from a virus in their mother's milk. The majority of mammary tumors in mice are caused by mouse mammary tumor virus.

<i>Feline leukemia virus</i> Species of virus

Feline leukemia virus (FeLV) is a retrovirus that infects cats. FeLV can be transmitted from infected cats when the transfer of saliva or nasal secretions is involved. If not defeated by the animal's immune system, the virus weakens the cat's immune system, which can lead to diseases which can be lethal. Because FeLV is cat-to-cat contagious, FeLV+ cats should only live with other FeLV+ cats.

<i>Gammaretrovirus</i> Genus of viruses

Gammaretrovirus is a genus in the Retroviridae family. Example species are the murine leukemia virus and the feline leukemia virus. They cause various sarcomas, leukemias and immune deficiencies in mammals, reptiles and birds.

<span class="mw-page-title-main">Endogenous retrovirus</span> Inherited retrovirus encoded in an organisms genome

Endogenous retroviruses (ERVs) are endogenous viral elements in the genome that closely resemble and can be derived from retroviruses. They are abundant in the genomes of jawed vertebrates, and they comprise up to 5–8% of the human genome.

Virus latency is the ability of a pathogenic virus to lie dormant within a cell, denoted as the lysogenic part of the viral life cycle. A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which, after initial infection, proliferation of virus particles ceases. However, the viral genome is not eradicated. The virus can reactivate and begin producing large amounts of viral progeny without the host becoming reinfected by new outside virus, and stays within the host indefinitely.

The Abelson murine leukemia virus is a retrovirus used to induce malignant transformation of murine lymphoid cells. As a retrovirus, it has a single-stranded, positive sense RNA genome which replicates via a DNA intermediate mediated by a reverse transcriptase. The Abelson murine leukemia virus is named for the American pediatrician Herbert T. Abelson, who together with Louise S Rabstein, first described and isolated it.

The murine leukemia viruses are retroviruses named for their ability to cause cancer in murine (mouse) hosts. Some MLVs may infect other vertebrates. MLVs include both exogenous and endogenous viruses. Replicating MLVs have a positive sense, single-stranded RNA (ssRNA) genome that replicates through a DNA intermediate via the process of reverse transcription.

Human foamy virus (HFV) is a retrovirus and specifically belongs to the genus Spumavirus. The spumaviruses are complex and significantly different from the other six genera of retroviruses in several ways. The foamy viruses derive their name from the characteristic ‘foamy’ appearance of the cytopathic effect (CPE) induced in the cells. Foamy virus in humans occurs only as a result of zoonotic infection.

Simian foamy virus (SFV) is a species of the genus Spumavirus that belongs to the family of Retroviridae. It has been identified in a wide variety of primates, including prosimians, New World and Old World monkeys, as well as apes, and each species has been shown to harbor a unique (species-specific) strain of SFV, including African green monkeys, baboons, macaques, and chimpanzees. As it is related to the more well-known retrovirus human immunodeficiency virus (HIV), its discovery in primates has led to some speculation that HIV may have been spread to the human species in Africa through contact with blood from apes, monkeys, and other primates, most likely through bushmeat-hunting practices.

The gag-onc fusion protein is a general term for a fusion protein formed from a group-specific antigen ('gag') gene and that of an oncogene ('onc'), a gene that plays a role in the development of a cancer. The name is also written as Gag-v-Onc, with "v" indicating that the Onc sequence resides in a viral genome. Onc is a generic placeholder for a given specific oncogene, such as C-jun..

Env is a viral gene that encodes the protein forming the viral envelope. The expression of the env gene enables retroviruses to target and attach to specific cell types, and to infiltrate the target cell membrane.

<span class="mw-page-title-main">ERV3</span> Protein-coding gene in the species Homo sapiens

HERV-R_7q21.2 provirus ancestral envelope (Env) polyprotein is a protein that in humans is encoded by the ERV3 gene.

<span class="mw-page-title-main">SLC20A1</span> Protein-coding gene in the species Homo sapiens

Sodium-dependent phosphate transporter 1 is a protein that in humans is encoded by the SLC20A1 gene.

Koala retrovirus (KoRV) is a retrovirus that is present in many populations of koalas. It has been implicated as the agent of koala immune deficiency syndrome (KIDS), an AIDS-like immunodeficiency that leaves infected koalas more susceptible to infectious disease and cancers. The virus is thought to be a recently introduced exogenous virus that is also integrating into the koala genome. Thus the virus can transmit both horizontally and vertically. The horizontal modes of transmission are not well defined but are thought to require close contact.

Bovine immunodeficiency virus (BIV) is a retrovirus belonging to the genus Lentivirus. It is similar to the human immunodeficiency virus (HIV) and infects cattle. The cells primarily infected are lymphocytes and monocytes/macrophages.

The walleye epidermal hyperplasia viruses are two species of retroviruses classified under Epsilonretrovirus, a genus in the family of Retroviridae. There are three genome sequenced and identified exogenous retroviruses of this genus which include two known types associated with walleye epidermal hyperplasia disease. Both viral types are confirmed to be the causative agents of the neoplastic condition in the freshwater fish species, the North American walleye (Sander vitreus). The specific association of retroviral infection with proliferative lesions in fish is based on the presence of retrovirus-like particles and reverse transcriptase activity from neoplastic tissue. Although both virus types have been observed in lesions of diseased fish, each cell of the infected tissue is host to a specific virus. Transmission studies have also shown that WEHV-2 has been the more proliferative agent of the condition as compared to WEHV-1.

Mason-Pfizer monkey virus (M-PMV), formerly Simian retrovirus (SRV), is a species of retroviruses that usually infect and cause a fatal immune deficiency in Asian macaques. The ssRNA virus appears sporadically in mammary carcinoma of captive macaques at breeding facilities which expected as the natural host, but the prevalence of this virus in feral macaques remains unknown. M-PMV was transmitted naturally by virus-containing body fluids, via biting, scratching, grooming, and fighting. Cross contaminated instruments or equipment (fomite) can also spread this virus among animals.

An endogenous viral element (EVE) is a DNA sequence derived from a virus, and present within the germline of a non-viral organism. EVEs may be entire viral genomes (proviruses), or fragments of viral genomes. They arise when a viral DNA sequence becomes integrated into the genome of a germ cell that goes on to produce a viable organism. The newly established EVE can be inherited from one generation to the next as an allele in the host species, and may even reach fixation.

Feline foamy virus or Feline syncytial virus is a retrovirus and belongs to the family Retroviridae and the subfamily Spumaretrovirinae. It shares the genus Felispumavirus with only Puma feline foamy virus. There has been controversy on whether FeFV is nonpathogenic as the virus is generally asymptomatic in affected cats and does not cause disease. However, some changes in kidney and lung tissue have been observed over time in cats affected with FeFV, which may or may not be directly affiliated. This virus is fairly common and infection rates gradually increase with a cat's age. Study results from antibody examinations and PCR analysis have shown that over 70% of felines over 9 years old were seropositive for Feline foamy virus. Viral infections are similar between male and female domesticated cats whereas in the wild, more feral females cats are affected with FeFV.

References

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