Human T-lymphotropic virus 1: Wikis


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Human T-lymphotropic virus
Virus classification
Group: Group VI (ssRNA-RT)
Family: Retroviridae'
Subfamily: Orthoretrovirinae
Genus: Deltaretrovirus
Species: Simian T-lymphotropic virus

Human T-lymphotropic virus

HTLV-I is an abbreviation for the human T-cell lymphotropic virus type 1, also called the Adult T-cell lymphoma virus type 1, a virus that has been seriously implicated in several kinds of diseases including HTLV-I-associated myelopathy, Strongyloides stercoralis hyper-infection, and a virus cancer link for leukemia (see adult T-cell leukemia/lymphoma). Between one in twenty and one in twenty-five infected persons are thought to develop cancer as a result of the virus.

HTLV was discovered in 1977 in Japan. The virus was first isolated by Drs. Bernard Poiesz and Francis Ruscetti and their co-workers in the laboratory of Robert C. Gallo at the NCI.[1] It was the first identified human retrovirus.

Infection with HTLV-I, like infection with other retroviruses, probably occurs for life and can be inferred when antibody against HTLV-1 is detected in the serum.


Signs and Symptoms

Signs and symptoms of HLTV myelopathy

Signs and symptoms of HLTV myelopathy include:

  • Motor and sensory changes in the extremities
  • Spastic gait in combination with weakness ofthe lower limbs
  • Clonus
  • Bladder dysfunction

Other neurologic findings that may be found in HLTV include:

  • Mild cogntive deficits
  • Erectile dysfunction[2]


HTLV-I infection in the United States appears to be about half as prevalent as HIV infection among IV drug users and about one-tenth as prevalent in the population at large. Although little serologic data exist, prevalence of infection is thought to be highest among blacks living in the Southeast. 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.[3] It is possible that prevalence of infection is increasing in this risk group.

HTLV-I infection in Australia is very high among the Indigenous peoples of central and northern Australia, with a prevalence rate of 10-30%. It is also high among the Inuit of Northern Canada.Japan, in northeastern Iran,[4] in Peru, in the Pacific coast of Colombia and Ecuador, in the Caribbean, and in Africa.


Transmission of HTLV-I is believed to occur from mother to child via breastfeeding; by sexual contact; and through exposure to contaminated blood, either through blood transfusion or sharing of contaminated needles. The importance of the various routes of transmission is believed to vary geographically.

  • In Japan, the geographic clustering of infections suggest that the virus is more dependent on mother-to-child transmission.[5]
  • In the Caribbean, the geographic distribution of the virus is more uniform, and it is more common among those with many sexual partners, indicating that sexual transmission is more common.[6]


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.[7]

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.



HTLV-1, unlike the distantly related retrovirus HIV, has an immunostimulating effect, which, however, turns out to be 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 end 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).


In the central Australian Aboriginal population, HTLV-1 is thought to be related to their extremely high rate of death from sepsis.

It is 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-infection which may lead to death from polymicrobial sepsis.

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 DNA incorporated into host lymphocyte DNA, and chronic stimulation of the lymphocytes at the cytokine level may play a role in development of malignancy. The malignancy ranges from a very indolent and slowly progressive lymphoma to a very aggressive and nearly uniformaly lethal proliferative lymphoma.

HTLV-1 is also associated with a progressive demyelinating upper motor neurone disease known as HAM/TSP for HTLV-1 associated myelopathy/Tropical Spastic Paraparesis characterized by sensory and motor deficits, particularly of the lower extremities, incontinence and impotence.[8] Less than 2% of infected individuals develop HAM/TSP, but this will vary dramatically from one geographic location to another.[citation needed]


Treatment for opportunistic infections varies depending on the type of disease and varies from careful observation to aggressive chemotherapy and antiretroviral agents.[citation needed] Adult T cell lymphoma is a common complication of HLTV infection, and requires aggresive chemotherapy, typically R-CHOP. Other treatments for ATL in HLTV infected patients include interferon alpha, zidovudine with interferon alpha, and CHOP with arsenic trioxide. Treatments for HLTV myelopathy are even more limited, and focus mainly on symptomatic therapy. Therapies studied include corticosteroids,plasmapherisis,cyclophosphamide, and interferon, which may produce a temporary symptomatic improvement in myelopathy symptoms.Valporic acid has been studied to determine if it might slow the progression of HLTV 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 valporic acid combined with zidovudine showed a major decrease in the viral load of baboons infected with HLTV-1. It is important to monitor for opportunistic infections such as cytomegalovirus, histoplasmosis, scabies, pneumocystis pneumonia, and staphylococcal infections in HLTV patients. HIV testing should also be performed, as some patients may be co-infected with both viruses. [9]Allogenic bone marrow transplantation has been investigated in the treatment of HLTV-1 disease, with varied results. One case report describes a HLTV-1 infected woman who devoloped chronic refractory eczema, corneal injury, and adult T cell leukemia. She was subsequently treated with allogenic stem cell transplantion, and had complete resolution of symptoms. One year posttransplant, she has had no recurrence of any symptoms, and furthermore has had a decrease in her proviral load.[10]


  1. ^ Poiesz BJ, Ruscetti FW, Reitz MS, Kalyanaraman VS, Gallo RC (1981). "Isolation of a new type C retrovirus (HTLV) in primary uncultured cells of a patient with Sézary T-cell leukaemia". Nature 294 (5838): 268–71. PMID 6272125. 
  2. ^
  3. ^ Cantor KP, Weiss SH, Goedert JJ, Battjes RJ (1991). "HTLV-I/II seroprevalence and HIV/HTLV coinfection among U.S. intravenous drug users". J. Acquir. Immune Defic. Syndr. 4 (5): 460–7. PMID 2016683. 
  4. ^ Sabouri, AH. (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". J Gen Virol 86 (3): 773–81. doi:10.1099/vir.0.80509-0. PMID 15722539. 
  5. ^ Tajima, K. (1988). "The third nation-wide study on adult T-cell leukaemia/lymphoma (ATL) in Japan: characteristic patterns of HLA antigen and HTLV-I infection in ATL patients and their relatives. The T- and B-cell Malignancy Study Group". Int J Cancer 41 (4): 505–12. doi:10.1002/ijc.2910410406. PMID 2895748. 
  6. ^ Clark J, Saxinger C, Gibbs W, Lofters W, Lagranade L, Deceulaer K, Ensroth A, Robert-Guroff M, Gallo R, Blattner W (1985). "Seroepidemiologic studies of human T-cell leukemia/lymphoma virus type I in Jamaica". Int J Cancer 36 (1): 37–41. doi:10.1002/ijc.2910360107. PMID 2862109. 
  7. ^ 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): 449–59. PMID 14622599. 
  8. ^ Osame, M. (1986). "HTLV-I associated myelopathy, a new clinical entity". Lancet 3 (1): 1031–2. doi:10.1016/S0140-6736(86)91298-5. PMID 2871307. 
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