Human T-lymphotropic virus 1

Last updated
Human T-lymphotropic virus 1
HTLV-1 and HIV-1 EM 8241 lores.jpg
a micrograph showing both Human T-lymphotropic virus 1 and HIV
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Pararnavirae
Phylum: Artverviricota
Class: Revtraviricetes
Order: Ortervirales
Family: Retroviridae
Genus: Deltaretrovirus
Species:
Primate T-lymphotropic virus 1

Human T-cell lymphotropic virus type 1 or human T-lymphotropic virus (HTLV-I), also called the adult T-cell lymphoma virus type 1, is a retrovirus of the human T-lymphotropic virus (HTLV) family.

Contents

Most people with HTLV-1 infection do not appear to develop health conditions that can be directly linked to the infection. However, there is a subgroup of people who experience severe complications. The most well characterized are adult T-cell lymphoma (ATL) and HTLV-I-associated myelopathy/Tropical spastic paraparesis (HAM/TSP), both of which are only diagnosed in individuals testing positive to HTLV-1 infection. The estimated lifetime risk of ATL among people with HTLV-1 infection is approximately 5%, while that of HAM/TSP is approximately 2%. [1] [2] [3]

In 1977, Adult T-cell lymphoma (ATL) was first described in a case series of individuals from Japan. [4] The symptoms of ATL were different from other lymphomas known at the time. The common birthplace shared amongst most of the ATL patients was suggestive of an infectious cause, referred to as ATLV. [5] Strikingly, ATLV had the transforming activity in vitro. [6] These studies established that HTLV-1 was the causitive agent of ATL. The retrovirus is now generally called HTLV-I because later studies proved that ATLV is the same as the firstly identified human retrovirus called HTLV discovered by Bernard Poiesz and Francis Ruscetti and their co-workers in the laboratory of Robert C. Gallo at the National Cancer Institute. [7] Persistent lifelong infection is established when HTLV-1 integrates into the host genome as a provirus. A patient infected with HTLV-1 can be diagnosed when antibodies against HTLV-1 are detected in the serum. [8]

Virology

HTLV-1 is a retrovirus belonging to the family retroviridae and the genus deltaretrovirus. It has a positive-sense RNA genome that is reverse transcribed into DNA and then integrated into the cellular DNA. Once integrated, HTLV-1 continues to exist only as a provirus which can spread from cell to cell through a viral synapse. Few, if any, free virions are produced and there is usually no detectable virus in the blood plasma though the virus is present in genital secretions. Like HIV, HTLV-1 predominantly infects CD4+ T cells. [8]

The viral RNA is packed into the icosahedral capsid which is contained inside the protein inner envelope. The lipid outer envelope is of host cell origin but contains viral transmembrane and surface proteins. The virion is spherical in shape with a diameter of about 100 nm. [8]

HTLV-1 is genetically classified into seven subtypes, each defined by a unique geographic distribution influenced by population migration. The most globally widespread is the cosmopolitan subtype A, which further branches into several subgroups: transcontinental, Japanese, West African, North African, Senegalese, and Afro-Peruvian. [9] While subtypes B, D, E, F, and G are localized to distinct regions in Africa, subtype C is predominant in Australia and Oceania. [10]

HTLV-1 is believed to have originated from the simian T-lymphotropic virus type 1 (STLV-1), a retrovirus prevalent among numerous nonhuman primates in intertropical Africa. This theory is supported by the significant genetic diversity of HTLV-1 subtypes in Africa, potentially arising from repeated zoonotic transmissions during human interactions with STLV-1 endemic nonhuman primates. This correlation is further reinforced by the observation that individuals bitten by nonhuman primates exhibit HTLV-1 strains with sequences remarkably homologous to the STLV-1 found in local primate species. [11]

Epidemiology

The global distribution of HTLV-I is highly heterogeneous, with focal occurrence in diverse regions. Within areas where HTLV-I is found, its occurrence varies considerably, with endemic clusters often situated near populations with lower prevalence. This pattern might be influenced by the founder effect, suggesting prolonged viral transmission within isolated groups, but this theory warrants further investigation. Consistent findings reveal that HTLV-1 prevalence increases with age and is usually higher in adult females than males. Areas broadly regarded as having endemic regions include Japan, Iran, the Americas, the Caribbean, Melanesia, Central and West Africa, and Australia. Globally, there remains a lack of robust data from populous countries like India and Nigeria and most of North and East Africa. As such, current global prevalence estimates, which are based on known endemic regions, likely underestimate the true global prevalence. [1]

In Australia, HTLV-I has notably high prevalence among Aboriginal communities in Central Australia. Community-based cross-sectional studies from Central Australia report HTLV-1 prevalences exceeding 30%, representing the highest reported prevalence for any population worldwide. [12] In Taiwan, in Iran, and in Fujian (a Chinese province near Taiwan) the prevalence is 0.1–1%. The infection rate is about 1% in Papua New Guinea, the Solomon Islands, and Vanuatu, where the genotype C predominates. In Europe HTLV-1 is uncommon, although it is present in some populations, generally people who have migrated from known endemic regions. In the Americas HTLV-1 is found in some Indigenous populations and descendants of African ancestry from where it is thought to have originated. Prevalence ranges from 0.1 to 1%. In Africa the prevalence is not well known, but it is about 1% in some countries. [8]

HTLV-I infection in the United States appears to be about half as prevalent among IV drug users and about one-tenth as prevalent in the population at large as HIV infection.[ citation needed ] Although little serologic data exist, the prevalence of infection is thought to be highest among blacks living in the Southeast.[ citation needed ] A prevalence rate of 30% has been found among black intravenous drug users in New Jersey, and a rate of 49% has been found in a similar group in New Orleans. [13] [14] [ citation needed ]

It is also high among the Inuit of Northern Canada, in Japan, northeastern Iran, [15] Peru, the Pacific coast of Colombia and Ecuador, and the Caribbean.[ citation needed ]

Transmission

HTLV-1 has three main routes of transmission. Vertical transmission is most common, through which an infected mother transmits the virus to her child.[ citation needed ] The risk to a fetus while inside the womb is minimal, given the virtual absence of viral particles in human plasma. Most vertical infection occurs through breastfeeding. About 25% of infants who are breastfed by infected mothers are infected, while less than 5% of children born to but not breastfed by infected mothers are infected. Sexual transmission is second-most common, whereby an individual infects another through exchange of bodily fluids. Some evidence has suggested that male-to-female transmission is more efficient than female-to-male transmission. For example, one study in Japan found a 61% transmission rate for males to females vs. a less than 1% rate for females to males. Least common is parenteral transmission through blood transfusion, with an infection rate of 44-63% estimated in one study, and needle sharing among intravenous drug users. With proper prophylaxis (e.g. breastfeeding counseling for mothers, condom use, and donor blood screening), rates of transmission can be effectively reduced. [16] The importance of the various routes of transmission is believed to vary geographically. The research in discordant couples showed that probability of sexual transmission is about 0.9 per 100 person-years. [8]

Tropism

The term viral tropism refers to which cell types HTLV-I infects. Although HTLV-1 is primarily found in CD4+ T cells, other cell types in the peripheral blood of infected individuals have been found to contain HTLV-1, including CD8+ T cells, dendritic cells and B cells. HTLV-I entry is mediated through interaction of the surface unit of the virion envelope glycoprotein (SU) with its cellular receptor GLUT1, a glucose transporter, on target cells. [19]

Associated diseases

Malignancies

Adult T cell leukemia/lymphoma

HTLV-1 is also associated with adult T-cell leukemia/lymphoma and has been quite well studied in Japan. The time between infection and onset of cancer also varies geographically. It is believed to be about sixty years in Japan and less than forty years in the Caribbean. The cancer is thought to be due to the pro-oncogenic effect of viral RNA incorporated into host lymphocyte DNA. Chronic stimulation of the lymphocytes at the cytokine level may play a role in the development of the malignancy. The lymphoma ranges from a very indolent and slowly progressive type to a very aggressive and nearly uniformly lethal proliferative type.[ citation needed ]

Cutaneous T-cell lymphoma

There is some evidence that HTLV-1 is a causative agent of cutaneous T-cell lymphoma. [8]

Inflammatory diseases

HTLV myelopathy/tropical spastic paraparesis

HTLV-1 is also associated with a progressive demyelinating upper motor neuron disease known as HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), characterized by sensory and motor deficits, particularly of the lower extremities, incontinence and impotence. [20] Only 0.3 to 4% of infected individuals develop HAM/TSP, but this will vary from one geographic location to another. [8]

Signs and symptoms of HTLV myelopathy include:

  • Motor and sensory changes in the extremities
  • Spastic gait in combination with weakness of the lower limbs
  • Clonus
  • Bladder dysfunction (neurogenic bladder) and bladder cancer

Other neurologic findings that may be found in HTLV include:

Arthropathy

HTLV-1 is associated with a rheumatoid-like arthropathy, although the evidence is contradictory. In these cases patients have a negative rheumatoid factor. [8]

Uveitis

Studies from Japan demonstrated that HTLV-1 infection may be associated with an intermediate uveitis. At onset the patients present with blurred vision and floaters. The prognosis is favorable—the condition usually resolves within weeks. [8]

Opportunistic infections

Individuals infected with HTLV-1 are at risk for opportunistic infections—diseases not caused by the virus itself, but by alterations in the host's immune functions. [8]

HTLV-1, unlike the distantly related retrovirus HIV, has an immunostimulating effect which actually becomes immunosuppressive. The virus activates a subset of T-helper cells called Th1 cells. The result is a proliferation of Th1 cells and overproduction of Th1 related cytokines (mainly IFN-γ and TNF-α). Feedback mechanisms of these cytokines cause a suppression of the Th2 lymphocytes and a reduction of Th2 cytokine production (mainly IL-4, IL-5, IL-10 and IL-13). The result is a reduction in the ability of the infected host to mount an adequate immune response to invading organisms that require a predominantly Th2 dependent response (these include parasitic infections and production of mucosal and humoral antibodies).[ citation needed ]

In the central Australian Aboriginal population, HTLV-1 is thought to be related to their extremely high rate of death from sepsis. It is also particularly associated with bronchiectasis, a chronic lung condition predisposing to recurrent pneumonia. It is also associated with chronic infected dermatitis, often superinfected with Staphylococcus aureus and a severe form of Strongyloides stercoralis infection called hyper-infestation which may lead to death from polymicrobial sepsis. HTLV-1 infection has also been associated with Tuberculosis. [8]

Treatment

Treatment of opportunistic infections varies depending on the type of disease and ranges from careful observation to aggressive chemotherapy and antiretroviral agents.[ citation needed ] Adult T cell lymphoma is a common complication of HTLV infection and requires aggressive chemotherapy, typically R-CHOP. Other treatments for ATL in HTLV infected patients include interferon alpha, zidovudine with interferon alpha and CHOP with arsenic trioxide. Treatments for HTLV myelopathy are even more limited and focus mainly on symptomatic therapy. Therapies studied include corticosteroids, plasmapheresis, cyclophosphamide, and interferon, which may produce a temporary symptomatic improvement in myelopathy symptoms. [21]

Valproic acid has been studied to determine if it might slow the progression of HTLV disease by reducing viral load. Although in one human study it was effective in reducing viral load, there did not appear to be a clinical benefit. Recently however, a study of valproic acid combined with zidovudine showed a major decrease in the viral load of baboons infected with HTLV-1. It is important to monitor HTLV patients for opportunistic infections such as cytomegalovirus, histoplasmosis, scabies, pneumocystis pneumonia, and staphylococcal infections. HIV testing should also be performed, as some patients may be co-infected with both viruses.[ citation needed ]

Allogenic bone marrow transplantation has been investigated in the treatment of HTLV-1 disease with varied results. One case report describes an HTLV-1 infected woman who developed chronic refractory eczema, corneal injury and adult T cell leukemia. She was subsequently treated with allogenic stem cell transplantation and had complete resolution of symptoms. One year post-transplant, she has had no recurrence of any symptoms, and furthermore has had a decrease in her proviral load.[ citation needed ]

Related Research Articles

<span class="mw-page-title-main">HIV</span> Human retrovirus, cause of AIDS

The human immunodeficiency viruses (HIV) are two species of Lentivirus that infect humans. Over time, they cause acquired immunodeficiency syndrome (AIDS), a condition in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

<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 (backward). 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.

<i>Simian immunodeficiency virus</i> Species of retrovirus

Simian immunodeficiency virus (SIV) is a species of retrovirus that cause persistent infections in at least 45 species of non-human primates. Based on analysis of strains found in four species of monkeys from Bioko Island, which was isolated from the mainland by rising sea levels about 11,000 years ago, it has been concluded that SIV has been present in monkeys and apes for at least 32,000 years, and probably much longer.

<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.

<span class="mw-page-title-main">Adult T-cell leukemia/lymphoma</span> Human disease

Adult T-cell leukemia/lymphoma is a rare cancer of the immune system's T-cells caused by human T cell leukemia/lymphotropic virus type 1 (HTLV-1). All ATL cells contain integrated HTLV-1 provirus further supporting that causal role of the virus in the cause of the neoplasm. A small amount of HTLV-1 individuals progress to develop ATL with a long latency period between infection and ATL development. ATL is categorized into 4 subtypes: acute, smoldering, lymphoma-type, chronic. Acute and Lymphoma-type are known to particularly be aggressive with poorer prognosis.

This is a list of AIDS-related topics, many of which were originally taken from the public domain U.S. Department of Health Glossary of HIV/AIDS-Related Terms, 4th Edition.

<span class="mw-page-title-main">Oncovirus</span> Viruses that can cause cancer

An oncovirus or oncogenic virus is a virus that can cause cancer. This term originated from studies of acutely transforming retroviruses in the 1950–60s, when the term oncornaviruses was used to denote their RNA virus origin. With the letters RNA removed, it now refers to any virus with a DNA or RNA genome causing cancer and is synonymous with tumor virus or cancer virus. The vast majority of human and animal viruses do not cause cancer, probably because of longstanding co-evolution between the virus and its host. Oncoviruses have been important not only in epidemiology, but also in investigations of cell cycle control mechanisms such as the retinoblastoma protein.

<span class="mw-page-title-main">Cutaneous T-cell lymphoma</span> Type of immune system cancer

Cutaneous T-cell lymphoma (CTCL) is a class of non-Hodgkin lymphoma, which is a type of cancer of the immune system. Unlike most non-Hodgkin lymphomas, CTCL is caused by a mutation of T cells. The cancerous T cells in the body initially migrate to the skin, causing various lesions to appear. These lesions change shape as the disease progresses, typically beginning as what appears to be a rash which can be very itchy and eventually forming plaques and tumors before spreading to other parts of the body.

<span class="mw-page-title-main">T-cell lymphoma</span> Cancerous overproduction of T cells

T cell lymphoma is a rare form of cancerous lymphoma affecting T cells. Lymphoma arises mainly from the uncontrolled proliferation of T cells and can become cancerous.

A Tax Gene Product (Tax) is a nuclear protein that has a molecular weight of about 37,000 to 40,000 daltons.

Bovine leukemia virus (BLV) is a retrovirus which causes enzootic bovine leukosis in cattle. It is closely related to the human T‑lymphotropic virus type 1 (HTLV-I). BLV may integrate into the genomic DNA of B‑lymphocytes as a DNA intermediate, or exist as unintegrated circular or linear forms. Besides structural and enzymatic genes required for virion production, BLV expresses the Tax protein and microRNAs involved in cell proliferation and oncogenesis. In cattle, most infected animals are asymptomatic; leukemia is rare, but lymphoproliferation is more frequent (30%).

<span class="mw-page-title-main">Robert Gallo</span> American biomedical researcher

Robert Charles Gallo is an American biomedical researcher. He is best known for his role in establishing the human immunodeficiency virus (HIV) as the infectious agent responsible for acquired immune deficiency syndrome (AIDS) and in the development of the HIV blood test, and he has been a major contributor to subsequent HIV research.

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.

<span class="mw-page-title-main">Primate T-lymphotropic virus</span> Informal grouping of virus species

The primate T-lymphotropic viruses (PTLVs) are a group of retroviruses that infect primates, using their lymphocytes to reproduce. The ones that infect humans are known as human T-lymphotropic virus (HTLV), and the ones that infect Old World monkeys are called simian T-lymphotropic viruses (STLVs). PTLVs are named for their ability to cause adult T-cell leukemia/lymphoma, but in the case of HTLV-1 it can also cause a demyelinating disease called tropical spastic paraparesis. On the other hand, newer PTLVs are simply placed into the group by similarity and their connection to human disease remains unclear.

<span class="mw-page-title-main">Human T-lymphotropic virus 2</span> Species of virus

A virus closely related to HTLV-I, human T-lymphotropic virus 2 (HTLV-II) shares approximately 70% genomic homology with HTLV-I. It was discovered by Robert Gallo and colleagues.

Lennert lymphoma, also termed lymphoepithelioid lymphoma, lymphoepithelioid variant of peripheral T-cell lymphoma, and epithelioid cellular lymphogranulomatosis, is a rare subtype of the T cell lymphomas. It was first characterized by Karl Lennert in 1952 as a variant of Hodgkin lymphoma based on the presence of cells resembling the Reed–Sternberg cells that typify Hodgkin lymphoma. However, later studies concluded that these cells are not Reed-Sternberg cells and that Lennert lymphoma is not a variant of Hodgkin lymphoma.

<span class="mw-page-title-main">Infectious causes of cancer</span> Pathogens as a cause of cancer

Estimates place the worldwide risk of cancers from infectious causes at 16.1%. Viral infections are risk factors for cervical cancer, 80% of liver cancers, and 15–20% of the other cancers. This proportion varies in different regions of the world from a high of 32.7% in Sub-Saharan Africa to 3.3% in Australia and New Zealand.

Alexander F. Voevodin is a Russian-born biomedical scientist and educator. He is considered one of the leading early pioneers of HIV/AIDS research.

Viral synapse is a molecularly organized cellular junction that is similar in some aspects to immunological synapses. Many viruses including herpes simplex virus (HSV), human immunodeficiency virus (HIV) and human T-lymphotropic virus (HTLV) have been shown to instigate the formation of these junctions between the infected ("donor") and uninfected ("target") cell to allow cell-to-cell transmission. As viral synapses allow the virus to spread directly from cell to cell, they also provide a means by which the virus can escape neutralising antibody.

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. 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. The virus was subsequently identified in captive gibbon populations in Thailand, the US and Bermuda.

References

  1. 1 2 Legrand N, McGregor S, Bull R, Bajis S, Valencia BM, Ronnachit A, et al. (April 2022). "Clinical and Public Health Implications of Human T-Lymphotropic Virus Type 1 Infection". Clinical Microbiology Reviews. 35 (2): e0007821. doi:10.1128/cmr.00078-21. PMC   8941934 . PMID   35195446.
  2. ↑ Schierhout G, McGregor S, Gessain A, Einsiedel L, Martinello M, Kaldor J (January 2020). "Association between HTLV-1 infection and adverse health outcomes: a systematic review and meta-analysis of epidemiological studies". The Lancet. Infectious Diseases. 20 (1): 133–143. doi:10.1016/S1473-3099(19)30402-5. PMID   31648940. S2CID   204883551.
  3. ↑ "Human T-lymphotropic virus type 1: technical report". www.who.int. Retrieved 2023-10-27.
  4. ↑ Uchiyama T, Yodoi J, Sagawa K, Takatsuki K, Uchino H (September 1977). "Adult T-cell leukemia: clinical and hematologic features of 16 cases". Blood. 50 (3): 481–492. doi: 10.1182/blood.V50.3.481.481 . PMID   301762.
  5. ↑ Hinuma Y, Nagata K, Hanaoka M, Nakai M, Matsumoto T, Kinoshita KI, et al. (October 1981). "Adult T-cell leukemia: antigen in an ATL cell line and detection of antibodies to the antigen in human sera". Proceedings of the National Academy of Sciences of the United States of America. 78 (10): 6476–6480. Bibcode:1981PNAS...78.6476H. doi: 10.1073/pnas.78.10.6476 . JSTOR   11091. PMC   349062 . PMID   7031654.
  6. ↑ Miyoshi I, Kubonishi I, Yoshimoto S, Akagi T, Ohtsuki Y, Shiraishi Y, et al. (December 1981). "Type C virus particles in a cord T-cell line derived by co-cultivating normal human cord leukocytes and human leukaemic T cells". Nature. 294 (5843): 770–771. Bibcode:1981Natur.294..770M. doi:10.1038/294770a0. PMID   6275274. S2CID   4361348.
  7. ↑ Poiesz BJ, Ruscetti FW, Reitz MS, Kalyanaraman VS, Gallo RC (November 1981). "Isolation of a new type C retrovirus (HTLV) in primary uncultured cells of a patient with Sézary T-cell leukaemia". Nature. 294 (5838): 268–271. Bibcode:1981Natur.294..268P. doi:10.1038/294268a0. PMID   6272125. S2CID   262992.
  8. 1 2 3 4 5 6 7 8 9 10 11 Verdonck K, González E, Van Dooren S, Vandamme AM, Vanham G, Gotuzzo E (April 2007). "Human T-lymphotropic virus 1: recent knowledge about an ancient infection". The Lancet. Infectious Diseases. 7 (4): 266–281. doi:10.1016/S1473-3099(07)70081-6. PMID   17376384.
  9. ↑ Gessain A, Cassar O (2012). "Epidemiological Aspects and World Distribution of HTLV-1 Infection". Frontiers in Microbiology. 3: 388. doi: 10.3389/fmicb.2012.00388 . PMC   3498738 . PMID   23162541.
  10. ↑ Cassar O, Einsiedel L, Afonso PV, Gessain A (2013-09-26). Bausch DG (ed.). "Human T-cell lymphotropic virus type 1 subtype C molecular variants among indigenous australians: new insights into the molecular epidemiology of HTLV-1 in Australo-Melanesia". PLOS Neglected Tropical Diseases. 7 (9): e2418. doi: 10.1371/journal.pntd.0002418 . PMC   3784485 . PMID   24086779.
  11. ↑ Filippone C, Betsem E, Tortevoye P, Cassar O, Bassot S, Froment A, et al. (June 2015). "A Severe Bite From a Nonhuman Primate Is a Major Risk Factor for HTLV-1 Infection in Hunters From Central Africa". Clinical Infectious Diseases. 60 (11): 1667–1676. doi: 10.1093/cid/civ145 . PMID   25722199.
  12. ↑ Einsiedel L, Pham H, Talukder MR, Taylor K, Wilson K, Kaldor J, et al. (December 2021). "Very high prevalence of infection with the human T cell leukaemia virus type 1c in remote Australian Aboriginal communities: Results of a large cross-sectional community survey". PLOS Neglected Tropical Diseases. 15 (12): e0009915. doi: 10.1371/journal.pntd.0009915 . PMC   8654171 . PMID   34879069.
  13. ↑ Cantor KP, Weiss SH, Goedert JJ, Battjes RJ (1991). "HTLV-I/II seroprevalence and HIV/HTLV coinfection among U.S. intravenous drug users". Journal of Acquired Immune Deficiency Syndromes. 4 (5): 460–467. PMID   2016683.
  14. ↑ Chihara, D; Ito, H; Katanoda, K; Shibata, A; Matsuda, T; Tajima, K; Sobue, T; Matsuo, K (2012). "Increase in incidence of adult T-cell leukemia/lymphoma in non-endemic areas of Japan and the United States". Cancer Science. 103 (10): 1857–1860. doi:10.1111/j.1349-7006.2012.02373.x. ISSN   1349-7006. PMC   7659271 . PMID   22738276.
  15. ↑ Sabouri AH, Saito M, Usuku K, Bajestan SN, Mahmoudi M, Forughipour M, et al. (March 2005). "Differences in viral and host genetic risk factors for development of human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis between Iranian and Japanese HTLV-1-infected individuals". The Journal of General Virology. 86 (Pt 3): 773–781. doi: 10.1099/vir.0.80509-0 . PMID   15722539.
  16. ↑ Verdonck K, González E, Van Dooren S, Vandamme AM, Vanham G, Gotuzzo E (April 2007). "Human T-lymphotropic virus 1: recent knowledge about an ancient infection". The Lancet. Infectious Diseases. 7 (4): 266–281. doi:10.1016/S1473-3099(07)70081-6. PMID   17376384.
  17. ↑ Tajima K, et al. (The T- and B-cell Malignancy Study Group) (April 1988). "The third nation-wide study on adult T-cell leukemia/lymphoma (ATL) in Japan: characteristic patterns of HLA antigen and HTLV-I infection in ATL patients and their relatives". International Journal of Cancer. 41 (4): 505–512. doi:10.1002/ijc.2910410406. PMID   2895748. S2CID   24275659.
  18. ↑ Clark J, Saxinger C, Gibbs WN, Lofters W, Lagranade L, Deceulaer K, et al. (July 1985). "Seroepidemiologic studies of human T-cell leukemia/lymphoma virus type I in Jamaica". International Journal of Cancer. 36 (1): 37–41. doi:10.1002/ijc.2910360107. PMID   2862109. S2CID   9790144.
  19. ↑ Manel N, Kim FJ, Kinet S, Taylor N, Sitbon M, Battini JL (November 2003). "The ubiquitous glucose transporter GLUT-1 is a receptor for HTLV". Cell. 115 (4): 449–459. doi: 10.1016/S0092-8674(03)00881-X . PMID   14622599. S2CID   14399680.
  20. ↑ Osame M, Usuku K, Izumo S, Ijichi N, Amitani H, Igata A, et al. (May 1986). "HTLV-I associated myelopathy, a new clinical entity". Lancet. 1 (8488): 1031–1032. doi:10.1016/S0140-6736(86)91298-5. PMID   2871307. S2CID   5095354.
  21. ↑ Gonçalves DU, Proietti FA, Ribas JG, Araújo MG, Pinheiro SR, Guedes AC, Carneiro-Proietti AB (July 2010). "Epidemiology, treatment, and prevention of human T-cell leukemia virus type 1-associated diseases". Clinical Microbiology Reviews. 23 (3): 577–589. doi:10.1128/CMR.00063-09. PMC   2901658 . PMID   20610824.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.