Geographical Distribution

HTLV-1 has an ubiquitous distribution, with well-described endemic areas. An area is called endemic for HTLV-1 if 2–10 percent of the healthy adult population is infected. The islands of Kyushu and Okinawa, in southwestern Japan, are hyperendemic areas for HTLV-1, 15 percent of the healthy adult population carry the virus (Blattner, 1990). Moderate rates of infection have been reported in West Africa, Australia, and the Caribbean (Caribbean Epidemiology Center, 1990; Delaporte et al., 1989; Nerurkar et al., 1993). In South America, Brazil, Colombia, and Peru are HTLV-1 endemic areas (Zurita et al., 1997; Gabbai et al., 1993; Zaninovic et al., 1994); the virus is also present in Ecuador (Guderian et al., 1994), Paraguay (de Cabral et al., 1995), Chile (Cartier and Cartier, 1996) and Argentina (Bouzas et al., 1994). In Peru, the virus is highly prevalent in some population and ethnic groups. Sixteen percent of immigrants from Japan—particularly from Okinawa—are seropositive. However, in the first generation of these immigrants born in Peru, the virus is prevalent in 4 percent of the population, and is not present in the second generation (Gotuzzo et al., 1996). Similar trends were reported in Hawaii (Blattner et al., 1986) and Bolivia (Tsugane et al., 1988). A study of HTLV-1 infection in asymptomatic women in Peru found prevalence rates of 3.8 percent among Afro-American women in Chincha, a coastal town south of Lima, 1.3 percent among the Quechua population of the central highlands (Ayacucho) and 3.8 percent in the population of northern Lima (Sanchez-Palacios, 2003). In other regions in South America, in which there is a strong presence of African Americans, such as Tumaco (Colombia) and Bahia (Brazil), the prevalence of HTLV-1 ranges from 2–5 percent in the healthy adult population.

Transmission

HTLV-1 is transmitted through modes similar to those described for HIV, but there are also important differences that are explained by the requirement of infected lymphocytes for the transmission of HTLV-1.

Adult T-Cell Leukemia/Lymphoma (ATLL)

In the 1970s, an epidemic of ATLL was described in Japan (Takatsuki et al., 1977)—the striking observation being that this phenomenon occurred in Okinawa and Kyushu and not in northern Japan. In 1980, two groups determined the relationship between HTLV-1 and ATLL; the HTLV-1 provirus is integrated into the neoplastic cell DNA and the virus can be isolated from malignant cells (Seiki et al., 1983). The clinical presentation of ATLL involves fever, lymphadenopathy, hepatosplenomegaly, bone lesions with hypercalcemia, skin lesions, and a fatal course with poor response to chemotherapy. Chronic and smoldering types of leukemia, with more lymphoma-like characteristics, slower courses, and more extensive skin involvement have also been described. Males aged 50–60 years are the group most frequently affected. Studies conducted in the HTLV-1 hyperendemic areas of Japan have estimated a lifetime risk for ATLL of 2–4 percent (Tajima and Hinuma, 1992). In Jamaica, Murphy reported the lifetime risk of ATLL to be 4 percent for those infected with HTLV-1 before 20 years of age (Murphy et al., 1996). In South America, the association between HTLV-1 and ATLL has been recognized in Brazil, Colombia, and in Argentina. Three hundred new cases of non-Hodgkin's lymphoma are detected at the National Institute of Cancer in Lima, Peru, each year, and 10 percent (30) of these cases are associated with HTLV-1.

Tropical Spastic Paraparesis

The general term “tropical spastic paraparesis” (TSP) was introduced by Mani et al. in 1969 for a chronic progressive paraparesis of unknown cause observed in tropical areas; however, it was not until 1985 that the association between this syndrome and HTLV-1 infection was recognized (Gessain et al., 1985). The designation HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) was proposed in 1989.

It has been reported that TSP occurs in 1–4 percent of people infected with HTLV-1 (Kaplan et al., 1990).·TSP predominantly affects adult females, an observation that is also confirmed in WHO's guidelines for diagnosis of TSP. The risk of TSP appears to be higher in Latin America than in Japan and associations have been reported between TSP and certain HLA alleles (Jeffrey et al., 1999). Furthermore, the association between HTLV-1 and TSP varies between geographical regions; in Colombia, 87 percent of TSP cases were HTLV-1-seropositive and in Peru, 55–65 percent of TSP patients were carriers of HTLV-1. On the other hand, in a study in Mexico, less than 1 percent of TSP cases were found to carry HTLV-1 (unpublished data, J. Sotelo, Inst Nal Neurol, Mexico City). These observations suggest that genetic background can influence susceptibility to TSP, and that HTLV-1 and other cofactors, that remain unknown, are involved in the pathogenesis of this disease.

An autoimmune mechanism has been proposed to explain the pathogenesis of TSP. According to this hypothesis, cytokines, such as tumor necrosis factor-α, are released against viral proteins in the surface of infected lymphocytes thereby causing chronic inflammation and tissue damage within the thoracic middle portion of the spinal cord.

The clinical symptoms of TSP consist of a gradually appearing symmetrical paraparesis with signs of pyramidal tract involvement that usually progresses slowly and relentlessly. However, some patients present rapid progression of the neurological symptoms; in these patients, higher antibody titers to HTLV-1 have been found (Nakagawa et al., 1995). In a recent retrospective study in Peru, 22 percent of TSP patients presented rapid progression, defined as less than 2 years between onset of symptoms and confinement to a wheelchair. Some patients presented more rapid progression, with the time between onset of symptoms and the inability to walk unaided as short as 6 months. As noted in a previous report (Nakagawa et al., 1995), there was an association between age of onset and rapid progression of TSP; 67 percent of patients with rapid progression were at least 50 years of age at disease onset, compared with 38 percent among slow progressors, p < 0.01. With the exception of unintentional tremor, no differences were found in clinical symptoms (38 percent of patients with rapid progression reported tremor versus 9 percent among slow progressors, p < 0.001) (E. Gotuzzo, unpublished data).

Urinary symptoms are a frequent complaint of TSP patients. Initially, patients report difficulties to initiate voiding. Not uncommonly, patients mention the need to put external pressure on their lower abdomen in order to urinate. In severe cases, patients cannot maintain voiding without compressing the abdomen, sometimes leading to urinary retention. Recurrent urinary infections are common, probably reflecting disorders in bladder emptying. Dysfunction of the detrusor muscle has been implicated in the urinary tract involvement in TSP.

Manifestations of immune hyperactivity other than TSP—such as Sjögren's syndrome, uveitis, arthritis, Behçet's disease and thyroiditis—have been repeatedly observed among patients with TSP.

Currently, there is neither specific nor standardized treatment for HTLV-1 and TSP. Prolonged periods of systemic steroids appear to improve clinical symptoms of TSP and recently, antiretroviral drugs effective in treating HIV, such as lamivudine and zidovudine, have been used with relative success in treating patients with TSP (Sheremata et al., 1993). A combination of corticosteroids, antiretroviral drugs, and rehabilitation might considerably improve the quality of life of TSP patients—particularly if treatment is started early in the course of the disease in those cases with rapid progression (Araujo et al., 1995).

Association of HTLV-1 with Strongyloidiasis

Strongyloides stercoralis is a soil-transmitted intestinal nematode that has been estimated to infect at least 60 million people worldwide. Infection is often asymptomatic, but can cause nonspecific abdominal symptoms and mild diarrhea. While strongyloidiasis is generally a self-limited disease in immunocompetent hosts, S. stercoralis behaves as an opportunistic pathogen, producing disseminated and life-threatening infections (Neva, 1986) in immunocompromised hosts who are incapable of mounting an appropriate immune response. An association of disseminated S. stercoralis infection with malignant tumors, severe malnutrition, acquired immunodeficiency syndrome (AIDS), corticosteroid therapy, and renal transplantation has been well documented. Studies in Japan and Jamaica have shown a significant association between the presence of S. stercoralis infection and HTLV-1 (Nakada et al., 1984). In Sao Paulo, 12 percent of HTLV-1-positive blood donors carried strongyloidiasis, compared to 1.6 percent of the control group (Nakada et al., 1984). In our institute in Lima, Peru, 10 percent of strongyloidiasis patients are HTLV-1-positive. Another study conducted in Lima, Peru reveals a strong association between the phenomenon of hyperinfection with S. stercoralis and HTLV-1. Eighty-six percent (18 out of 21) of patients with S. stercoralis hyperinfection were infected with HTLV-1, but were not infected with other immunosuppressive diseases such as AIDS or cancer. The difference with the HTLV-1 prevalence in a carefully matched control group (5 percent, 1 out of 21) and in a group with intestinal strongyloidiasis (10 percent, 6 of 62) was statistically significant (p < 0.001) (Gotuzzo et al., 1999). A report of decreased therapeutic efficacy of thiabendazole exists among patients with concomitant S. stercoralis-HTLV-1 infection in Okinawa (Sato et al., 1994). Terashima showed that the failure of the standard treatment against intestinal strongyloidiasis with thiabendazole or ivermectin was an important marker for suspecting HTLV-1 infection. Some reports suggest that there is a relation between strongyloidiasis and ATLL in HTLV-1-positive patients. It is not clear whether Strongyloides acts as a trigger, shortening the incubation time of leukemia, or a marker of high proviral load.

Association of HTLV-1 with Crusted Scabies

Crusted scabies, a severe form of scabies with generalized itching and massive numbers of mites, has been described among patients undergoing chemotherapy and with various immunosuppressive conditions, such as Down's syndrome, cancer, and AIDS (Paterson et al., 1973). Several reports on the association between HTLV-1 and severe scabies have been published. In a study in 6 hospitals in Lima, Peru, 23 patients were diagnosed with Norwegian scabies over 19 months. Seventy percent of patients were serologically confirmed to have HTLV-1 infection; 9 percent were on long-term oral corticosteroid treatment; 1 patient had Down's syndrome; 2 patients were chronically malnourished; and 2 patients had no known risk factors for crusted scabies. A study conducted in Bahia, Brazil, found a similar association between HTLV-1 and severe scabies but also identified dual infection (HIV/HTLV-1) as a risk factor for even more severe forms of scabies. The crusted form of the disease was highly predictive of double retroviral infection and seemed to be associated with severe immunodeficiency, because HIV/HTLV-1 coinfected patients were more likely to die during the study period. These data suggest that coinfection by HIV-HTLV-1 is associated with a deeper degree of immunodeficiency, which increases the risk of developing severe forms of scabies (Brites et al., 2002).

Coinfection of HTLV-1 with HIV

In spite of the similarities between HTLV-1 and HIV with respect to transmission, both epidemics are still largely separated in Peru. Nevertheless, dual infections do occur. In 1989, 19 percent of HIV-infected Peruvian men and 5 percent of HIV-infected women were found to be HTLV-1 coinfected; and in men, dual infection was associated with a higher number of sexual partners compared with HIV-only infected patients (Phillips et al., 1991). Dual infection has also been reported in Trinidad (Bartholomew et al., 1987), Brazil (Cortes et al., 1989), and the United States (Pierik and Murphy, 1991). Several studies have suggested that patients with dual infection are at higher risk of developing AIDS (Bartholomew et al., 1987). In a prospective study of HIV-positive intravenous drug users, patients infected with both viruses were three times more likely to die from AIDS during follow-up than those infected with HIV-I alone (Page et al., 1990). In a Peruvian study, the mortality rate was 63 percent in HIV-infected patients and 80 percent in dually-infected patients. Of 50 patients who died without receiving any antiretroviral treatment, survival time was 5.02 ± 3.27 months in patients with dual infection, shorter than that of patients with HIV alone (10.07 ± 4.42 months) (Gotuzzo et al., 1992).

Association of HTLV-1 with Tuberculosis

It is well known that the incidence and clinical picture of tuberculosis (TB) is adversely affected by HIV infection. Similarly, in a Brazilian study, patients with TB and HTLV-1 exhibited a worse clinical course and a poorer prognosis than those without HTLV-1. In a study among 131 inpatients with TB in Lima, Peru, those patients infected with HIV-1 or with HTLV-1 were more likely to die during hospitalization than seronegative TB patients (RR = 2.6 for HIV [95 percent confidence interval = 1.05–6.30] and RR = 5.8 for HTLV-1 [95 percent confidence interval = 2.3–14.3]). The association was particularly strong among patients infected with both HIV-1 and HTLV-1 (RR = 6.61, 95 percent confidence interval = 2.5–17.2) (Henriquez et al., 2002).

Association of HTLV-1 with Chronic Infective Dermatitis

The term infective dermatitis was proposed by Sweet in 1966 for a relapsing eczematous condition in Jamaican children, usually associated with cutaneous infections by Staphylococcus aureus or β-hemolytic Streptococcus (Sweet, 1966). In 1990, LaGrenade described an association between chronic infective dermatitis and infection with HTLV-1 (LaGrenade et al., 1990). This syndrome has also been described in Colombia (Blank et al., 1995). Chronic infective dermatitis is commonly seen in children and is rare in adults. This disease presents with symmetric lesions on the scalp, face, armpits, and groin. These lesions improve markedly with antibiotics, but usually relapse when antibiotics are stopped.

REFERENCES

• Araujo AQ, Leite AC, Dultra SV, Andrada-Serpa MJ. Progression of neurological disability in HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Journal of the Neurological Sciences. 1995;129:147–151. [PubMed: 7608729]
• Bartholomew C, Blattner W, Cleghorn F. Progression to AIDS in homosexual men co-infected with HIV and HTLV-I in Trinidad. Lancet. 1987;2:1469. [PubMed: 2892033]
• Bartholomew C, Saxinger C, Clark JW, Gail M, Dudgeon A, Mahabir B, Hull-Drysdale B, Cleghorn F, Gallo RC, Blattner WA. Transmission of HTLV-1 and HIV among homosexual men in Trinidad. Journal of the American Medical Association. 1987;257:2604–2608. [PubMed: 2883330]
• Blank A, Herrera M, Lourido MA, Rueda R, Blank M. Infective dermatitis in Colombia. Lancet. 1995;346:710. [PubMed: 7658857]
• Blattner WA. Epidemiology of HTLV-1 and associated diseases. In: Blattner WA, editor. Human Retrovirology: HTLV-1. New York: Raven Press; 1990.
• Blattner WA, Nomura A, Clark JW, Ho GY, Nakao Y, Gallo R, Robert-Guroff M. Modes of transmission and evidence for viral latency from studies of human T-cell lymphotropic virus type I in Japanese migrant populations in Hawaii. Proceedings of the National Academies of Sciences USA. 1986;83:4895–4898. [PMC free article: PMC323850] [PubMed: 3014518]
• Bouzas MB, Zapiola I, Quiruelas S, Gorvein D, Panzita A, Rey J, Carnese FP, Corral R, Perez C, Zala C, et al. HTLV Type I and HTLV Type II infection among Indians and Natives from Argentina. AIDS Research and Human Retroviruses. 1994;10:1567–1571. [PubMed: 7888211]
• Brites C, Weyll M, Pedroso C, Badaro R. Severe and Norwegian scabies are strongly associated with retroviral (HIV/HTLV-1) infection in Bahia, Brazil. AIDS. 2002;16:1292–1293. [letter] [PubMed: 12045498]
• Caribbean Epidemiology Center. Public Health Implications of HTLV-1 in the Caribbean. Weekly Epidemiological Record. 1990;65:63–65. [PubMed: 2386723]
• Cartier L, Cartier E. HTLV-I/II in Chile. In: Zaninovic V, editor. HTLV, Truths and Questions. Cali, Colombia: Fundación MAR; 1996. pp. 150–158.
• Cortes E, Detels R, Aboulafia D, Li XL, Moudgil T, Alam M, Bonecker C, Gonzaga A, Oyafuso L, Tondo M. HIV-1, HIV-2 and HTLV-I infection in high risk groups in Brazil. New England Journal of Medicine. 1989;320:953–958. [PubMed: 2927478]
• de Cabral MB, Vera ME, Samudio M, Arias AR, Cabello A, Moreno R, Zapiola I, Bouzas MB, Muchinik G. HTLV-I/II antibodies among three different Indian groups from Paraguay. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology. 1995;19:548–549. [PubMed: 9859972]
• Delaporte E, Peeters M, Durand JP, Dupont A, Schrijvers D, Bedjabaga L, Honore C, Ossari S, Trebucq A, Josse R, et al. Seroepidemiological survey of HTLV-1 infection among randomized population of western central African countries. Journal of AIDS. 1989;2:410–413. [PubMed: 2754613]
• Gabbai AA, Bordin JO, Vieira-Filho JP, Kuroda A, Oliveira AS, Cruz MV, Ribeiro AA, Delaney SR, Henrard DR, Rosario J, et al. Selectivity of human T lymphotropic virus type I (HTLV-I) and HTLV-II infection among different populations in Brazil. American Journal of Tropical Medicine and Hygiene. 1993;49:664–671. [PubMed: 8279633]
• Gessain A, Barin F, Vernant JC, Gout O, Maurs L, Calender A, de The G. Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis. Lancet. 1985;2:407–410. [PubMed: 2863442]
• Gotuzzo E, Escamilla J, Phillips IA, Sanchez J, Wignall FS, Antigoni J. The impact of human T lymphotropic virus type I/II infection on the prognosis of sexually acquired cases of acquired immunodeficiency syndrome. Archives of Internal Medicine. 1992;152:1429–1432. [PubMed: 1352675]
• Gotuzzo E, Yamamoto V, Kanna M, et al. Human T lymphotropic virus type I infection among Japanese immigrants in Peru. International Journal of Infectious Diseases. 1996;1:75–77.
• Gotuzzo E, Terashima A, Alvarez H, Tello R, Infante R, Watts DM, Freedman DO. Strongyloides stercoralis hyperinfection associated with human T cell lymphotropic virus type-I infection in Peru. American Journal of Tropical Medicine and Hygiene. 1999;60:146–149. [PubMed: 9988339]
• Gradilone A, Zani M, Barillari G, Modesti M, Agliano AM, Maiorano G, Ortona L, Frati L, Manzari V. HTLV-1 and HIV infection in drug addicts in Italy. Lancet. 1986;2:753–754. [PubMed: 2876222]
• Guderian R, Guevara A, Cooper P, Rugeles MT, Arango C. HTLV-1 infection and tropical spastic paraparesis in Esmeraldas Province of Ecuador. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1994;88:399–400. [PubMed: 7570816]
• Henriquez C, Gotuzzo E, Cairampoma, et al. Impact of infection with HIV and/or HTLV-1 on the outcome of hospitalization for tuberculosis in a public hospital in Peru. Abstract at the 4^th World Congress on Tuberculosis; Washington, DC. June 3–5, 2002.
• Hinuma Y, Nagata K, Hanaoka M, Nakai M, Matsumoto T, Kinoshita KI, Shirakawa S, Miyoshi I. 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 USA. 1981;78:6476–6480. [PMC free article: PMC349062] [PubMed: 7031654]
• Jeffrey KJ, Usuku K, Hall SE, Matsumoto W, Taylor GP, Procter J, Bunce M, Ogg GS, Welsh KI, Weber JN, Lloyd AL, Nowak MA, Nagai M, Kodama D, Izumo S, Osame M, Bangham CR. HLA alleles determine human T-lymphotropic virus-I (HTLV-1) proviral load and the risk of HTLV-1-associated myelopathy. Proceedings of the National Academy of Sciences USA. 1999;96:3848–3853. [PMC free article: PMC22383] [PubMed: 10097126]
• Kaplan JE, Osame M, Kubota H, Igata A, Nishitani H, Maeda Y, Khabbaz RF, Janssen RS. The risk of development of HTLV-1 associated myelopathy/tropical spastic paraparesis among persons infected with HTLV-1. AIDS. 1990;3:1096–1101. [PubMed: 2213510]
• Katamine S. Milk-borne transmission of human T-cell lymphotropic virus Type 1 (HTLV-1) and its intervention in Nagasaki. Acta Medica Nagasakiensia. 1999;44:1–6.
• Khabbaz R, Darrow WW, Hartley TM, Witte J, Cohen JB, French J, Gill PS, Potterat J, Sikes RK, Reich R, et al. Seroprevalence and risk factors for HTLV-1 infection among female prostitutes in the United States. Journal of the American Medical Association. 1990;263:60–64. [PubMed: 2293689]
• LaGrenade L, Hanchard B, Fletcher V, Cranston B, Blattner W. Infective dermatitis of Jamaican children: a marker for HTLV-1 infection. Lancet. 1990;336:1345–1347. [PubMed: 1978165]
• Larson C, Taswell H. Human T-cell leukemia virus (HTLV-1) and blood transfusion. Mayo Clinic Proceedings. 1988;63:869–875. [PubMed: 2900915]
• Mani KS, Mani AJ, Montgomery RD. A spastic paraplegic syndrome in South India. Journal of the Neurological Sciences. 1969;9:179–199. [PubMed: 4185984]
• Murphy EL, Hanchard B, Figueroa JP, Gibbs WN, Lofters WS, Campbell M, Goedert JJ, Blattner WA. Modelling the risk of adult T cell leukemia/lymphoma in persons infected with human T lymphotropic virus type I. International Journal of Cancer. 1989;43:250–253. [PubMed: 2917802]
• Murphy EL, Wilks K, Hanchard B, Cranston B, Figueroa JP, Gibbs WN, Murphy J, Blattner WA. A case-control study of risk factors for seropositivity to HTLV-1 in Jamaica. International Journal of Epidemiology. 1996;25:1083–1089. [PubMed: 8921498]
• Nakada K, Kohakura M, Komoda H, Hinuma Y. High incidence of HTLV antibody in carriers of Strongyloides stercoralis. Lancet. 1984;1:633. [letter] [PubMed: 6142338]
• Nakagawa M, Izumo S, Ijichi S, Kubota H, Arimura K, Kawabata M, Osame M. HTLV-1-associated myelopathy: analysis of 213 patients based on clinical features and laboratory findings. Journal of Neurovirology. 1995;1:50–61. [PubMed: 9222342]
• Nerurkar VR, Song KJ, Saitou N, Melland RR, Yanagihara R. Interfamilial genomic diversity and molecular phylogeny of human T-cell lymphotrophic virus type I from Papua New Guinea and the Solomon Islands. Virology. 1993;196:506–513. [PubMed: 8372432]
• Neva FA. Biology and immunology of human strongyloidiasis. Journal of Infectious Diseases. 1986;153:397–406. [PubMed: 3081656]
• Okochi K, Sata H, Hinuma Y. A retrospective study on transmission of adult T-cell leukemia virus via blood transfusion: seroconversion in recipients. Vox Sanguinis. 1984;46:245–253. [PubMed: 6328765]
• Page JB, Lai SH, Chitwood DD, Klimas NG, Smith PC, Fletcher MA. HTLV-I/II seropositivity and death from AIDS among HIV-1 seropositive intravenous drug users. Lancet. 1990;335:1439–1441. [PubMed: 1972217]
• Paterson WD, Allen BR, Beveridge GW. Norwegian scabies during immunosuppressive therapy. British Medical Journal. 1973;4:211–212. [PMC free article: PMC1587312] [PubMed: 4758393]
• Phillips I, Hyams KC, Wignall FS, Moran AY, Gotuzzo E, Sanchez J, Roberts CR. HTLV-1 co-infection in a HIV-1 infected Peruvian population. Journal of Acquired Immune Deficiency Syndromes. 1991;4:301–302. [PubMed: 1992107]
• Pierik LT, Murphy EL. The clinical significance of HTLV-I and HTLV-II infection in the AIDS epidemic. In: Volberding P, Jacobson MA, editors. AIDS Clinical Review. New York: Marcel Dekker; 1991. pp. 41–57. [PubMed: 1868010]
• Poiesz BJ, Ruscetti FW, Gadzar AF, Bunn PA, Minna JD, Gallo RC. Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T cell lymphoma. Proceedings of the National Academy of Sciences USA. 1980;77:7415–7419. [PMC free article: PMC350514] [PubMed: 6261256]
• Sanchez-Palacios C, Gotuzzo E, Vandamme AM, Maldonado Y. Seroprevalence and risk factors for human T-cell lymphotropic virus (HTLV-1) infection among ethnically and geographically diverse Peruvian women. International Journal of Infectious Diseases. 2003;7:132–137. [PubMed: 12839715]
• Sato Y, Shiroma Y, Kiyuna S, Toma H, Kobayashi J. Reduced efficacy of chemotherapy might accumulate concurrent HTLV-1 infection among strongyloidiasis patients in Okinawa, Japan. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1994;88:59. [PubMed: 8154005]
• Seiki M, Hattori S, Hirayama Y, Yoshida M. Human adult T-cell leukemia virus: Completed nucleotide sequence of the provirus genoma integrated in leukemia cell DNA. Proceedings of the National Academy of Sciences USA. 1983;80:3618–3622. [PMC free article: PMC394101] [PubMed: 6304725]
• Sheremata WA, Benedict D, Squilacote DC, Sazant A, DeFreitas E. High-dose zidovudine induction in HTLV-1-associated myelopathy: safety and possible efficacy. Neurology. 1993;43:2125–2129. [PubMed: 8413977]
• Sweet RD. A pattern of eczema in Jamaica. British Journal of Dermatology. 1966;78:93–100. [PubMed: 5907441]
• Tajima K, Hinuma Y. Epidemiology of HTLV-I/II in Japan and the world. Gann Monograph on Cancer Research. 1992;39:129–149.
• Tajima K, Tominaga S, Suchi, Kawagoe T, Komoda H, Hinuma Y, Oda T, Fujita K. Epidemiological analysis of the distribution of antibody to adult T-cell leukemia-virus-associated antigen: possible horizontal transmission of adult T-cell leukemia virus. Gann. 1982;73:893–901. [PubMed: 6984401]
• Takatsuki K, Uchiyama J, Sagawa K, Yodoi J. Adult T-cell leukemia in Japan. In: Sano S, Takaku F, Irino S, editors. Topics in Hematology. Amsterdam: Excerpta Medica; 1977. pp. 73–77.
• Tsugane S, Watanabe S, Sugimura H, Otsu T, Tobinai K, Shimoyama M, Nanri S, Ishii H. Infectious status of human T lymphotropic virus type I and hepatitis B virus among Japanese immigrants in the Republic of Bolivia. American Journal of Epidemiology. 1988;128:1153–1161. [PubMed: 3189289]
• Wignall FS, Hyams KC, Phillips IA, Escamilla J, Tejada A, Li O, Lopez F, Chauca G, Sanchez S, Roberts CR. Sexual transmission of human T-cell lymphotropic virus type I in Peruvian prostitutes. Journal of Medical Virology. 1992;38:44–48. [PubMed: 1402830]
• Zaninovic V, Sanzón F, López F, Velandia G, Blank A, Blank M, Fujiyama C, Yashiki S, Matsumoto D, Katahira Y, et al. Geographic independence of HTLV-I and HTLV-II foci in the Andes Highland, the Atlantic Coast, and the Orinoco of Colombia. AIDS Research and Human Retroviruses. 1994;10:97–101. [PubMed: 8179968]
• Zurita S, Costa C, Watts D, Indacochea S, Campos P, Sanchez J, Gotuzzo E. Prevalence of human retroviral infection in Quillabamba and Cuzco, Peru: a new endemic area for human T-cell lymphotropic virus type 1. American Journal of Tropical Medicine and Hygiene. 1997;56:561–565. [PubMed: 9180608]