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Recommendations for Counseling Persons Infected with Human T-Lymphotrophic Virus, Types I and II *

Summary

The human T-lymphotropic viruses, type I (HTLV-I) and type II (HTLV-II), are closely related but distinct retroviruses that can infect humans. They are different from the human immunodeficiency viruses that cause acquired immunodeficiency syndrome. Screening of the U.S. blood supply for HTLV-I/II, which began in 1988, identifies HTLV-I- and HTLV-II-infected persons who should be counseled regarding their infections. This document summarizes current information about HTLV, types I and II, and presents recommendations developed by CDC and a U.S. Public Health Service working group for counseling HTLV-I- and HTLV-II-infected persons.

INTRODUCTION

Human T-lymphotropic viruses, type I (HTLV-I) and type II (HTLV-II), were the first human retroviruses discovered (1,2). Both belong to the oncovirus subfamily of retroviruses and can transform human lymphocytes so that they are self-sustaining in vitro. They are only distantly related to the human immunodeficiency viruses (HIV-1 and HIV-2), which belong to the lentivirus subfamily of retroviruses and which cause acquired immunodeficiency syndrome (AIDS). Infections with HTLV-I and HTLV-II are most easily detected serologically. The presence of antibodies to HTLV-I or HTLV-II indicates that a person is infected with the virus.

In November 1988, the Food and Drug Administration (FDA) recommended that blood donation centers screen the U.S. blood supply for HTLV-I (3). Since then, all donations of whole blood and blood components in the United States have been screened for antibodies to HTLV-I. The screening tests that were licensed, as well as the investigational supplementary tests used to confirm seroreactivity (Western immunoblot and radioimmunoprecipitation assay), do not reliably differentiate between antibodies to HTLV-I and the closely related HTLV-II. In addition, the licensed screening tests, which use HTLV-I antigens, vary in their sensitivity to detect antibodies to HTLV-II (4,5).

Approximately 2,000 HTLV-I/II-infected volunteer blood donors were identified in the first year of screening in the United States; testing, after amplification by polymerase chain reaction, indicated that approximately half were infected with HTLV-I and half with HTLV-II (6). Such donors are counseled and permanently deferred from donating blood. Because the polymerase chain-reaction test is not routinely available, many donors and other persons positive by serologic assays have been told that they are infected with HTLV-I/II. The uncertainty regarding the identity of the infecting virus and the differing epidemiologic and clinical correlates of HTLV-I and HTLV-II infections have complicated counseling of HTLV-I/II-infected persons.

Until recently, the only reliable way to differentiate HTLV-I from HTLV-II infection was by polymerase chain reaction (7). Within the past 2 years, investigational peptide- and recombinant protein-based serologic assays that can more easily differentiate the antibodies to HTLV-I and HTLV-II have been developed (8,9). Preliminary data suggest that these investigational tests are potentially useful for typing serum samples (8,9).

The recommendations for counseling HTLV-I-, HTLV-II-, and HTLV-I/II-infected persons included in this document are intended for use by health-care workers and public health officials in the United States. They may not be applicable in developing countries, where the need for breast-feeding may outweigh concerns about transmission of these viruses.

HTLV-I

Prevalence

HTLV-I infection is endemic in southwestern Japan (10), the Caribbean basin (11), Melanesia (12), and in parts of Africa (13-15). In some areas where HTLV-I infection is endemic, prevalence rates as high as 15% have been reported in the general population. Seroprevalence increases with age; in older age groups, rates are usually higher among women than men.

In the United States, HTLV-I/II seroprevalence rates among volunteer blood donors average 0.016% (6). Approximately half of HTLV-I/II-seropositive blood donors nationwide are infected with HTLV-I. HTLV-I-infected donors most often report a history of birth in HTLV-I-endemic countries or sexual contact with persons from the Caribbean or Japan. Smaller percentages report a history of either injecting drug use or blood transfusion. Clusters of HTLV-I infections have also been reported in blacks from the southeastern United States (16) and in immigrants from HTLV-I-endemic areas residing in Brooklyn, New York (17).

Transmission

Transmission of HTLV-I occurs from mother to child (18), by sexual contact (19), by blood transfusion (20), and by sharing contaminated needles. Mother-to-child transmission occurs primarily through breast-feeding (21); in HTLV-I-endemic areas, approximately 25% of breast-fed infants born to HTLV-I-seropositive mothers acquire infection. Recent studies suggest that transmission of HTLV-I by breast-feeding may be associated with the presence of maternal antibodies to the HTLV-I transactivating protein, tax (22), or with elevated maternal titers of total antibodies to HTLV-I (23). However, the clinical usefulness of these markers has not been established. Intrauterine or perinatal transmission of HTLV-I does occur, but it appears to be less frequent than transmission by breast-feeding; approximately 5% of children born to infected mothers but not breast-fed acquire infection (24).

Sexual transmission of HTLV-I appears to be more efficient from males to females than from females to males. In one study of married couples in Japan, the efficiency of sexual transmission from males to females was estimated to be 60.8% over a 10-year period, compared with less than 1% from females to males (25). In another study, the presence of antibody to tax in the male partner was associated with sexual transmission to the female partner (26). In one study in Jamaica, genital ulcer disease in the male was identified as a risk for female-to-male sexual transmission (27). In the United States, approximately 25%-30% of sex partners of HTLV-I/II-seropositive blood donors are also seropositive (28,29).

Transmission of HTLV-I by blood transfusion occurs with transfusion of cellular blood products (whole blood, red blood cells, and platelets) but not with the plasma fraction or plasma derivatives from HTLV-I-infected blood. Seroconversion rates of 44% to 63% have been reported in recipients of HTLV-I-infected cellular components in HTLV-I endemic areas (20,30). Lower rates (approximately 20%) have been reported in recipients of contaminated cellular components in the United States (31). The probability of transmission by whole blood or packed red blood cells appears to diminish with greater duration of product storage; this finding has been ascribed to depletion of infected cells, presumably T-lymphocytes (30,32). Sharing blood-contaminated needles is the likely mode of transmission among injecting drug users.

HTLV-I is not transmitted by casual contact. Health-care workers caring for HTLV-I-infected persons need only be concerned about percutaneous exposure to HTLV-I-contaminated blood. One health-care worker who unintentionally inoculated himself with blood from an adult T-cell leukemia/lymphoma patient in Japan is reported to have seroconverted (33). However, no seroconversions occurred among 31 other laboratory and health-care workers exposed to HTLV-I via puncture wounds (34 ). Universal precautions, recommended for contact with all patients, are adequate to guard against HTLV-I transmission to health-care workers (35).

Diseases

Two diseases have been definitively associated with HTLV-I: adult T-cell leukemia/lymphoma (ATL) and a chronic degenerative neurologic disease, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

ATL is a malignancy of HTLV-I-infected CD4+ T-lymphocytes. The HTLV-I provirus is monoclonally integrated in the abnormal cell population. A spectrum of clinical and pathologic features has been described, including acute, chronic, lymphomatous, and smoldering forms (36,37). The acute form of ATL is characterized by infiltration of lymph nodes, viscera, and skin with malignant cells, resulting in a constellation of clinical features (Table 1). Circulating abnormal lymphocytes, called flower cells, are generally seen. Hypercalcemia, abnormal liver function values, and lytic bone lesions are common. Median survival is 11 months from diagnosis. Conventional chemotherapy is not curative, and relapses often occur quickly, although prolonged survival has been reported. ATL has been estimated to occur in 2%-4% of persons infected with HTLV-I in regions where HTLV-I is endemic and where early childhood infection is common (38,39). ATL occurs most frequently among persons 40-60 years of age, suggesting that a latent period as long as a few decades may be required for the disease to develop. One case of ATL in an immunocompromised patient has been reported in which the infection appears to have been transfusion acquired (40).

HAM/TSP is characterized by progressive, permanent lower-extremity weakness, spasticity, hyperreflexia, sensory disturbances, and urinary incontinence (Table 2). In patients with HAM/TSP, unlike those with multiple sclerosis, the signs and symptoms do not wax and wane, cranial nerves are not involved, and cognitive function is not affected. Antibodies to HTLV-I are characteristically found in the cerebrospinal fluid (41 ). Treatment with corticosteroids has been reported to be useful in some cases (42 ). Danazol, a synthetic androgen, reportedly improves symptoms, including bladder dysfunction (43,44). HAM/TSP develops in less than 1% of HTLV-I-infected persons (45), is believed to be immunologically mediated, and affects women more frequently than men. The latency period for HAM/TSP is shorter than that for ATL; cases of HAM/TSP have been associated with blood transfusion, with a median interval of 3.3 years between transfusion and development of HAM/TSP (46).

Recently, infective dermatitis, a chronic eczema associated with Staphylococcus aureus and beta-hemolytic streptococcus, has been reported in Jamaican children infected with HTLV-I (47).

The full spectrum of HTLV-I-associated diseases may include other disorders. Cases of polymyositis (48), chronic arthropathy (49), panbronchiolitis (50), and uveitis (51) have been reported in HTLV-I-infected patients.

HTLV-II

Prevalence

Until recently, partly because of the lack of serologic tests to differentiate HTLV-II from HTLV-I, no information was available regarding the seroepidemiology or modes of transmission of HTLV-II. HTLV-II is prevalent among injecting drug users in the United States and in Europe (52,53); more than 80% of HTLV-I/II seropositivity in drug users in the United States is due to HTLV-II infection (54). HTLV-II also appears to be endemic in American Indian populations, including the Guaymi Indians in Panama (55 ) and North American Indians in Florida (56) and New Mexico (57). Approximately half of U.S. volunteer blood donors seropositive for HTLV-I/II are infected with HTLV-II. HTLV-II-infected blood donors most often report either a history of injecting drug use or a history of sexual contact with an injecting drug user (6,58). A smaller percentage report a history of blood transfusion.

Transmission

HTLV-II is presumed to be transmitted similarly to HTLV-I, but much less is known about the specific modes and efficiency of transmission of HTLV-II. One study of 20 non-breast-fed children born to HTLV-II-infected women in New York City failed to show evidence of transmission to the newborns (59). The HTLV-II provirus has been detected in breast milk from HTLV-II-infected mothers (60), but no data are available regarding transmission to breast-fed infants.

HTLV-II can be transmitted sexually (61); the most commonly reported risk factor among HTLV-II-infected female U.S. blood donors is sexual contact with an injecting drug user (6,58).

HTLV-II can be transmitted by transfusion of cellular blood products (whole blood, red blood cells, and platelets) (31,32). The probability of transmission from red blood cells appears to diminish with greater duration of product storage (31).

The high prevalence of HTLV-II among injecting drug users is likely due to sharing blood-contaminated needles or other injection paraphernalia (62).

Diseases

HTLV-II infection has not been clearly associated with any diseases. The virus was first isolated from two patients with hairy-cell leukemia (2,63), but no evidence of HTLV-II infection was found in 21 additional patients with hairy-cell leukemia (64). In one study, rates of lymphoproliferative illnesses were not found to be increased in New Mexico, where HTLV-II is present in American Indians (65). Rare cases of HAM/TSP-like neurologic illnesses (66) and of mycosis fungoides (67) and large granular lymphocyte leukemia (68) have been reported in HTLV-II-infected persons. Cases of erythrodermatitis and bacterial skin infections have been reported in HIV-1- and HTLV-II-coinfected persons (69).

SEROLOGIC TESTS FOR HTLV-I AND HTLV-II

Serum specimens are screened for antibody to HTLV-I by using licensed enzyme immunoassays prepared from HTLV-I whole-virus lysate antigens. These assays vary in their sensitivity to detect antibodies to HTLV-II (4,5). Initially reactive specimens are retested in duplicate to minimize the chance that reactivity is due to technical error. Specimens that are reactive in either of the duplicate tests are considered repeatably reactive. Specimens that do not react in either of the duplicate repeat tests are considered nonreactive (3).

Additional tests, such as the Western immunoblot and the radioimmunoprecipitation assay, are needed to correctly interpret repeatably reactive specimens. Such supplementary tests must be inherently capable of identifying antibodies to the core (gag) and the envelope (env) proteins of HTLV-I/II. Indirect fluorescent antibody testing for HTLV-I/II has been used in some laboratories, but it does not distinguish antibodies to specific HTLV gene products. None of the supplementary tests have been licensed by the Food and Drug Administration, but they are available in research institutions, blood banks, some public health laboratories, and industrial laboratories, and as in-house tests in some diagnostic laboratories.

The following criteria for HTLV-I/II seropositivity were adopted by a U.S. Public Health Service (USPHS) working group in 1988 (3): a specimen that is repeatably reactive by enzyme immunoassay must demonstrate immunoreactivity to both the gag gene product p24 and to an env gene product (gp46 and/or gp61/68) to be considered seropositive for HTLV-I/II. Reactive serum specimens that do not satisfy these criteria but do show immunoreactivity to at least one suspected HTLV gene product are designated "indeterminate." Both Western immunoblot and radioimmunoprecipitation may be required to determine whether a specimen is positive or indeterminate. Serum specimens with no immunoreactivity to any HTLV gene product in additional, more specific tests are considered false positive. Several studies involving provirus amplification have supported the accuracy of these diagnostic criteria; persons whose specimens satisfy the criteria for positivity are virtually always infected with HTLV-I or HTLV-II (7,70). In contrast, persons whose specimens are "indeterminate" are rarely infected with either virus; for those who are found to be infected, repeat serologic testing frequently demonstrates seropositivity (70,71). In rare instances, persons with reactivity to p19 and to an env gene product (gp46 and/or gp61/68) but without reactivity to p24 have been found to be infected with HTLV-I/II (72).

An important advance in HTLV serologic testing has been the development of a recombinant env protein, p21e. Reactivity to p21e (in either enzyme immunoassay or "spiked" Western immunoblot) has been found to be highly sensitive for HTLV-I/II infection, being observed in virtually 100% of infected persons (73). However, the specificity of the p21e reactivity has been questioned (74,75). For purposes of notification and counseling, the positivity of samples showing p21e serologically should be confirmed by tests that detect env reactivity, such as radioimmunoprecipitation or recombinant protein-based assays (76), or by polymerase chain reaction until further information is available concerning this test.

The supplementary serologic tests discussed thus far are incapable of differentiating antibodies to HTLV-I and HTLV-II. The relative intensity of the reactivity to the gag proteins p19 and p24 on the "spiked" Western immunoblot has been used to differentiate HTLV-I from HTLV-II (77), but such differentiation may be unreliable (78). Recently, several synthetic peptides and recombinant proteins have been developed for this purpose (8,9,79). As with the previously discussed supplementary tests, all these tests are available for research only. Preliminary data indicate that such assays can be highly specific in differentiating antibodies to HTLV-I and HTLV-II (8,9,79). Not all HTLV-I/II-positive serum specimens, however, can be typed as HTLV-I or HTLV-II by using these tests. In these cases, more sophisticated methods, such as provirus amplification or virus isolation, may be needed to differentiate HTLV-I from HTLV-II infection.

NOTIFICATION AND DEFERRAL OF BLOOD DONORS

In the United States, blood donors whose serum specimens are repeatably reactive by the HTLV-I enzyme immunoassay and confirmed as seropositive for HTLV-I/II by the additional specific tests discussed above are notified and permanently deferred from donating blood. This deferral policy includes donors confirmed positive with antibodies to HTLV-I, HTLV-II, or HTLV-I/II (if differentiation between the infections is not attempted or is unsuccessful). Blood donors with serum specimens repeatably reactive on screening but not confirmed as seropositive for HTLV-I/II (a category that includes false-positive specimens and those indeterminate for HTLV) should also be notified and deferred if the same result is obtained on two separate donations. In some blood centers, such donors are deferred after the first such donation. Persons who are repeatably reactive on screening but not confirmed as seropositive for HTLV-I/II should not be told that they are infected with HTLV-I or HTLV-II. The above policies for donor deferral are based on FDA recommendations. In addition, FDA recommendations regarding the use of blood components should be followed.


RECOMMENDATIONS FOR COUNSELING

In consideration of the information presented above, the following recommendations for counseling HTLV-seropositive persons have been issued. In instances in which viral typing is possible, counseling should be virus specific. As noted above, HTLV-I and HTLV-II are two different retroviruses with differing epidemiologies and disease associations. The specific recommendations for persons infected with HTLV-I or HTLV-II should therefore take these differences into account.

HTLV-I

Persons found to be seropositive for HTLV-I/II according to the USPHS criteria and positive for HTLV-I by additional testing should be informed that they are infected with HTLV-I. They should be told that HTLV-I is not the AIDS virus, that it does not cause AIDS, and that AIDS is caused by a different virus called HIV. They should be told that HTLV-I is a lifelong infection. They should be given information regarding modes and efficiency of transmission, disease associations, and the probability of developing disease.

In particular, persons infected with HTLV-I should be advised to:

  • Share the information with their physician

  • Refrain from donating blood, semen, body organs, or other

    tissues

  • Refrain from sharing needles or syringes with anyone

  • Refrain from breast-feeding infants

  • Consider the use of latex condoms to prevent sexual

    transmission If the HTLV-I-positive person is in a mutually monogamous

sexual relationship, testing of the sex partner should be recommended to help formulate specific counseling advice. If the sex partner is also positive, no further recommendations are indicated. If the sex partner is negative, the couple should be advised that the use of latex condoms can help prevent transmission of HTLV-I to the negative partner, male or female. Male-infected, female-non-infected couples desiring pregnancy should be made aware of the finite risk of sexual transmission of HTLV-I during attempts at pregnancy and of the small risk for vertical transmission from mother to infant unrelated to breast-feeding. Such couples might be advised to use latex condoms at all times except during the fertile period while they are attempting pregnancy. The use of latex condoms is strongly recommended for HTLV-I-positive persons with multiple sex partners or otherwise engaging in non-mutually monogamous sexual relationships. These persons should be reminded of the risk of acquiring other sexually transmitted infections, including HIV.

HTLV-II

Persons found to be seropositive for HTLV-I/II according to the USPHS criteria and positive for HTLV-II by additional testing should be informed that they are infected with HTLV-II. They should be told that HTLV-II is not the AIDS virus, that it does not cause AIDS, and that AIDS is caused by a different virus called HIV. They should be told that HTLV-II is a lifelong infection. They should be given information regarding possible modes of transmission and the lack of firm disease associations.

  • In particular, they should be advised to:

  • Share the information with their physician

  • Refrain from donating blood, semen, body organs, or other

    tissues

  • Refrain from sharing drug needles or syringes with anyone

  • Refrain from breast-feeding infants Although the risks of transmission of HTLV-II by

breast-feeding and of disease from HTLV-II are unknown, the theoretical risk of transmission and disease, as for HTLV-I, makes it prudent to recommend that HTLV-II-infected mothers refrain from breast-feeding when and where safe nutritional alternatives exist.

Consider the use of barrier precautions to prevent sexual transmission

HTLV-II can be sexually transmitted, but the risks of disease are unknown. If the HTLV-II-positive person is in a mutually monogamous sexual relationship, testing of the sex partner should be recommended to help formulate specific counseling advice. If the sex partner is also positive, no further recommendations are indicated. If the sex partner is negative, the couple should be advised that the use of latex condoms can help prevent transmission of HTLV-II to the negative partner, male or female. The use of latex condoms is strongly recommended for HTLV-II-positive persons with multiple sex partners or otherwise engaging in non-mutually monogamous sexual relationships. These persons should be reminded of the risk of acquiring other sexually transmitted infections, including HIV.

HTLV-I/II

Persons found to be seropositive for HTLV-I/II according to the USPHS criteria but without differentiation of their infection should be informed they are positive for HTLV-I/II and that they are likely infected with either HTLV-I or HTLV-II. Because of the differences in the epidemiologic and clinical correlates of HTLV-I and HTLV-II, an effort to type the infection should be made. If such efforts are unsuccessful, these HTLV-I/II seropositive persons should be given information regarding possible modes and efficiency of transmission of HTLV-I and HTLV-II, disease associations of HTLV-I, and the probability of developing disease. Specific counseling advice should be the same as for HTLV-I-infected persons (refer to HTLV-I section).

HTLV Indeterminate

Blood donors with serum specimens that are HTLV-indeterminate on two occasions at least 3 months apart should be advised that their specimens were reactive in a screening test for HTLV-I but that the results could not be confirmed by a second, more specific test. They should be reassured that "indeterminate" test results are only rarely caused by HTLV-I or HTLV-II infection. Persons testing "indeterminate" for HTLV-I/II on one occasion should be offered retesting to make sure they are not recently infected with HTLV-I or HTLV-II and in the process of seroconverting. If subsequent test results are the same, they should be reassured that they are unlikely to be infected with HTLV-I or HTLV-II.

HTLV False Positive

Blood donors with serum specimens that are repeatably reactive by HTLV-I enzyme immunoassay but negative by Western immunoblot on two occasions should be advised that their HTLV-I screening test is falsely positive and that it could not be confirmed by a second, more specific test. They should be reassured that they are not infected with HTLV-I or HTLV-II.

Medical Follow-up

A periodic medical evaluation of HTLV-I- or HTLV-I/II-infected persons by a physician knowlegeable about these viruses is recommended. This evaluation might include a physical examination, including a neurologic examination, and a complete blood count with peripheral smear examination. Medical evaluation of HTLV-II-infected persons should be considered optional.

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  42. Osame M, Igata A, Matsumoto M, et al. HTLV-I associated myelopathy (HAM): treatment trials, retrospective survey and clinical and laboratory findings. Hematol Rev 1990; 3:271-4.
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  44. Bartholomew C, Edwards J, Maharaj M. A trial of danazol in TSP patients in Trinidad. Proceedings of the Fifth International Conference on Human Retrovirology; HTLV. Kumamoto, Japan, May 11- 13, 1992. {abstract #W-14B}.
  45. Kaplan JE, Osame M, Kubota H, et al. The risk of development of HTLV-I-associated myelopathy/tropical spastic paraparesis among persons infected with HTLV-I. J Acquir Immun Defic Syndr 1990;3:1096-1101.
  46. Osame M, Janssen R, Kubota H, et al. Nationwide survey of HTLV-I-associated myelopathy in Japan: association with blood transfusion. Ann Neurol 1990;28:50-6.
  47. LaGrenade L, Hanchard B, Fletcher V, Cranston B, Blattner W. Infective dermatitis of Jamaican children: a marker for HTLV-I infection. Lancet 1990;336:1345-7.
  48. Morgan OStC, Mora C, Rogers-Johnson P, Char G. HTLV-I and polymyositis in Jamaica. Lancet 1989;2:1184-7.
  49. Nishioka K, Maruyama I, Sato K, Kitajima I, Nakajima Y, Osame M. Chronic inflammatory arthropathy associated with HTLV-I. Lancet 1989;1:441.
  50. Sugimoto M, Nakashima H, Kawano O, Ando M, Araki S. Bronchoalveolar T-lymphocytosis in HTLV-I-associated myelopathy. Chest 1989;95:708. (letter)
  51. Shirao M, Yoshimura K, Mochizuki M, Araki S, Miyata N, Yamaguchi K. A seroepidemiologic study of HTLV-I uveitis. Proceedings of the Fifth International Conference on Human Retrovirology; HTLV. Kumamoto, Japan, May 11-13, 1992. {abstract #P-24}.
  52. Lee HH, Weiss SH, Brown LS, et al. Patterns of HIV-1 and HTLV-I/II in intravenous drug abusers from the middle Atlantic and central regions of the USA. J Infect Dis 1990;162:347-52.
  53. Zella D, Mori L. Sala M, et al. HTLV-II infection in Italian drug abusers. Lancet 1990;336:575-6. (letter)
  54. Khabbaz RF, Onorato IM, Cannon RO, et al. Seroprevalence of HTLV-I and HTLV-II among intravenous drug users and persons in clinics for sexually transmitted diseases. N Engl J Med 1992;326:375-80.
  55. Heneine W, Kaplan JE, Gracia F, et al. HTLV-II endemicity among Guaymi Indians in Panama. N Engl J Med 1991;324:565 (letter)
  56. Levine PH, Jacobson S, Elliott R, et al. HTLV-II infection in Florida Indians. AIDS Res Hum Retroviruses 1993;9:123-7.
  57. Hjelle B, Scalf R, Swenson S. High frequency of human T-cell leukemia-lymphoma virus type II infection in New Mexico blood donors: determination by sequence-specific oligonucleotide hybridization. Blood 1990;76:450-4.
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  63. Rosenblatt JD, Golde DW, Wachsman W, et al. A second isolate of HTLV-II associated with atypical hairy-cell leukemia. N Engl J Med 1986;315:372-7.

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  65. Hjelle B, Mills R, Swenson S, Mertz G, Key C, Allen S. Incidence of hairy cell leukemia, mycosis fungoides, and chronic lymphocytic leukemia in first known HTLV-II-endemic population. J Infect Dis 1991;163:435-40.

  66. Hjelle B, Appenzeller O, Mills R, et al. Chronic neurodegenerative disease associated with HTLV-II infection. Lancet 1992;339:645-6.

  67. Zucker-Franklin D, Hooper WC, Evatt BL. Human lymphotropic retroviruses associated with mycosis fungoides: evidence that human T-cell lymphotropic virus type II (HTLV-II) as well as HTLV-I may play a role in the disease. Blood 1992;80:1537-45.

  68. Loughran TP Jr, Coyle T, Sherman MP, et al. Detection of human T-cell leukemia/lymphoma virus, type II, in a patient with large granular lymphocyte leukemia. Blood 1992;80:1116-9.

  69. Kaplan MH, Hall WW, Susin M, et al. Syndrome of severe skin disease, eosinophilia, and dermatopathic lymphadenopathy in patients with HTLV-II complicating human immunodeficiency virus infection. Am J Med 1991;91:300-9.

  70. Khabbaz RF, Heneine W, Grindon A, Hartley TM, Shulman G, Kaplan J. Indeterminate HTLV serologic results in U.S. blood donors: are they due to HTLV-I or HTLV-II? J Acquir Immun Defic Syndr 1992;5:400-4.

  71. Kwok S, Lipka JJ, McKinney N, et al. Low incidence of HTLV infections in random blood donors with indeterminate Western blot patterns. Transfusion 1990;30:491-4.

  72. Donegan E, Pell P, Lee H, Shaw GM, Moseley JW, Transfusion Safety Study Group. Transmission of human T-lymphotropic virus type I by blood components from a donor lacking anti-p24: a case report. Transfusion 1992;32:68-71.

  73. Lillehoj EP, Alexander SS, Dubrule CJ, et al. Development and evaluation of a human T-cell leukemia virus type I serologic confirmatory assay incorporating a recombinant envelope polypeptide. J Clin Microbiol 1990;28:2653-8.

  74. Hartley TM, Malone GE, Khabbaz RF, Lal RB, Kaplan JE. Evaluation of a recombinant human T-cell lymphotropic virus type I (HTLV-I) p21E antibody detection enzyme immunoassay as a supplementary test in HTLV-I/II antibody testing algorithms. J Clin Microbiol 1991;29:1125-7.

  75. Lal RB, Brodine S, Kuzura J, et al. Sensitivity and specificity of a recombinant transmembrane glycoprotein (rgp21)-spiked Western immunoblot for serologic confirmation of human T-cell lymphotropic virus type I and type II infection. J Clin Microbiol 1992;30:296-9.

  76. Roberts BD, Foung SKH, Lipka JJ, et al. Evaluation of an immunoblot assay for serologic confirmation and differentiation of human T-cell lymphotropic virus types I and II. J Clin Microbiol 1993;31:260-4.

  77. Wiktor SZ, Alexander SS, Shaw GM, et al. Distinguishing between HTLV-I and HTLV-II by Western blot. Lancet 1990;335:153-34. (letter).

  78. Lal RB, Brodine SK, Coligan JE, Roberts CR. Differential antibody responsiveness to p19 gag results in serological discrimination between human T-lymphotropic virus type I and type II. J Med Virol 1991;35:232-6.

  79. Chen, Y-MA, Lee T-H, Wiktor SZ, et al. Type-specific antigens for serological discrimination of HTLV-I and HTLV-II infection. Lancet 1990;336:1153-5.

  • This report was previously published in Annals of Internal Medicine (Vol. 118, No. 6, March 15, 1993) and is printed here as a service to the MMWR readership.

SUGGESTED CITATION: Centers for Disease Control and Prevention. Recommendations for counseling persons infected with human T-lymphotropic virus, types I and II. Recommendations on prophylaxis and therapy for disseminated Mycobacterium avium complex for adults and adolescents infected with human immunodeficiency virus. MMWR 1993;(No. RR- 9):{inclusive page numbers}.

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