- Email: [email protected]
ISOLATION OF HTLV-I FROM CEREBROSPINAL FLUID OF A PATIENT WITH MYELOPATHY
397 VF, on the other hand, is associated with large complicated infarcts (frequently causing ventricular aneurysms), and it almost always recurs sooner or later, despite prophylaxis. In view of these clinical differences, it would be surprising if the best means of prophylaxis for early VF did not differ from that for late VF. The discussion of the ISIS paper does not consider these differences either in relation to the trial results or in the analysis of results from the smaller trials (table VIII). For instance our finding’* that only 2 of 364 patients treated with propranolol compared with 14 of 371 control patients had early VF (p 0-006) is blurred in the ISIS analysis by the addition of 5 treated patients (in whom the treatment had in any case been stopped) and 4 control patients who had late VF. Although VF occurring in the coronary-care unit may be an incident rather than a calamity, we still need a "first-aid" prophylactic regimen for prevention of VF for patients seen outside hospital who cannot be given immediate paramedical or coronarycare surveillance. As the authors concede, there are theoretical reasons why &bgr;2-blockade should be important for prevention of early VF. Moreover, there are important differences between our trial and ISIS, apart from the choice of &bgr;-blocker. It seems that we still need a large randomised trial of early intervention to settle these doubts about the prophylaxis of early VF. Although the most exciting therapeutic prospects may now be offered by reperfusion6 rather than by &bgr;-blockade, the question of the correct prophylaxis for early VF will remain a problem which is not answered by the results either of ISIS or of MIAMI.’ =
MT-2 cells.3 This was confirmed by western blot analysis with an MT-2 cell lysate. The serum formed specific bands with viral proteins, including p19, p24, and p28, while the CSF reacted with p24 only (fig 1). Serological tests for syphilis and HTLV-III were negative. The patient was born and raised in Kochi, a virusendemic area, and her son and sister were also seropositive for HTLV-I. For virus isolation, a 5 ml CSF sample was centrifuged and the sedimented cells were co-cultivated with 3 x 106 peripheral lymphocytes from a seronegative healthy man. The co-culture was maintained in 3 ml of RPMI 1640 medium supplemented with 10% human cord serum, 10% fetal calf serum, 10% crude T-cell growth factor, and antibiotics. After 3 weeks, the cells were adapted to grow without T-cell growth factor and 2 weeks later a continuous culture line of lymphoid cells was established. Chromosome analysis of this cell line showed a normal female karyotype. The cells were reactive with monoclonal antibodies to T-cells (Leu-1) and Ia antigens (OKIal). HTLV-I antigens were detected in the majority of the cells in an indirect immunofluorescence test using reference ATL patient’s serum and monoclonal antibodies to HTLV-I p19and p24. Electron microscopy revealed type C virus particles in these cells (fig 2). The source of the virus in the T-cell line was considered to be the CSF lymphocytes because the patient, but not the male donor, was seropositive for HTLV-1. This finding may be due solely to the
Coronary-Care Unit, Green Lane Hospital, Auckland, 3,
R. M. NORRIS
New Zealand 1. Lawrie
DM, Higgins MR, Godman MJ, Oliver MF, Julian DG, Donald KW. Ventricular fibrillation complicating acute myocardial infarction. Lancet 1968; ii: 523-28. 2. Nordrehaug JE, von der Lippe G. Hypokalaemia and ventricular fibrillation in acute myocardial infarction. Br Heart J 1983; 50: 525-29. 3. Adams P, et al. Plasma potassium and VF in acute myocardial infarction: a prospective study. Circulation 1984; 70 (suppl II): 311. 1984; 70 (suppl II): 311. 4. Schwartz PJ, Stone HL. Left stellectomy in the prevention of ventricular fibrillation caused by acute myocardial ischemia in conscious dogs with anterior myocardial infarction. Circulation 1980; 62: 1256-65. 5. Norris RM, Brown MA, Clarke ED, Barnaby PF, Geary GG, Logan RL, Sharpe DN. Prevention of ventricular fibrillation during acute myocardial infarction by intravenous propranolol. Lancet 1984; ii: 883-86. 6. GISSI. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; i: 397-402. 7. The MIAMI trial research group. Metoprolol in acute myocardial infarction (MIAMI). A randomised placebo-controlled international trial (with discussants. Eur Heart J 1985; 6: 199-226.
Fig 1-Western blot analysis of serum (lane 2) and CSF (lane 3) from a myelopathy patient with reference ATL patient’s serum (lane i B
ISOLATION OF HTLV-I FROM CEREBROSPINAL FLUID OF A PATIENT WITH MYELOPATHY
SIR,—The seropositive
rate
for human T-cell leukaemia virus
type I (HTLV-I) in patients with tropical spastic paraparesis (TSP) is high in Martinique1 and in Jamaica and Colombia.2 Recently, Osame et al (May 3, p 1031) described a TSP-like myelopathy in 6 Japanese patients in Kagoshima where HTLV-I and adult T-cell leukaemia (ATL) are more prevalent than in the Caribbean. They proposed the term HTLV-I-associated myelopathy (HAM) for this disorder. We report here the isolation of HTLV-I from the cerebrospinal fluid (CSF) of a Japanese patient with such a
myelopathy. A 45-year-old woman was admitted for a gait disturbance that had been slowly progressive for about 20 years. She also had occasional headaches but no sensory or sphincter impairment. Physical examination revealed hyperactive knee and ankle jerks with a positive Babinski sign and ankle clonus on both sides. A cranial computerised tomographic scan of the cranium and myelography were normal. A CSF sample contained protein 26 mg/dl, glucose 58 mg/dl, and 2 x 103/ml mononuclear cells (mostly normal-looking lymphocytes). Her leucocyte count was normal but there were 1-2%abnormal lymphocytes with bilobed nuclei. Serum and CSF antibodies to HTLV-I were positive at titres of 1/640 and 1/1, respectively, in an immunofluorescence assay against
Fig 2-Electron micrograph of HTLV-I isolated from CSF of myelopathy patient.
a
398 presence of HTLV-1 genome-positive lymphocytes in the CSF or may represent a possible pathogenic role of HTLV-I in TSP/ HAM. HTLV-I has not been previously isolated from the central nervous system. However, another lymphotropic retrovirus, the human immunodeficiency virus, has been isolated from the CSF
and neural tissues of patients with various
acquired immunodeficiency syndrome neurological manifestations such as encephalopathy, meningitis, or myelopathy.4,S
Kochi Medical School, Kochi 781-51, Japan
SHOZO HIROSE YOSHIKI UEMURA MASATOSHI FUJISHITA TAKAO KITAGAWA MAKOTO YAMASHITA JUN IMAMURA YUJI OHTSUKI HIROKINI TAGUCHI ISAO MIYOSHI
A, Barin F, Vernant JC, et al. Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis. Lancet 1985; ii. 407-09. 2. Rodgers-Johnson P, Gajdusek DC, Morgan OC, et al. HTLV-I and HTLV-III antibodies and tropical spastic paraparesis. Lancet 1985; ii: 1247-48 3. Miyoshi I, Kubonishi I, Yoshimoto S, et al. Type C virus particles in a cord T-cell line derived by co-cultivating normal human cord leukocytes and human leukaemic T 1. Gessain
cells. Nature 1981; 294: 770-71. DD, Rota TR, Schooley RT, et al Isolation of HTLV-III from cerebrospinal fluid and neural tissues of patients with neurologic syndrome related to the acquired immunodeficiency syndrome. N Engl J Med 1985; 313: 1493-97. 5. Levy JA, Shimabukuro J, Hollander H, Mills J, Kaminsky L. Isolation of AIDS-associated retroviruses from cerebrospinal fluid and brain of patients with neurological symptoms. Lancet 1985; ii. 586-88
4 Ho
HIV INFECTION IN RENAL ALLOGRAFT RECIPIENTS
SIR,—Patients on dialysis and renal allograft recipients receive frequent blood transfusions and are in a chronic state of immunosuppression. They are at high risk of hepatitis B infection and may be at risk of infection with the human immunodeficiency virus (HIV) also. We have investigated 115 patients given cadaveric renal transplants between August, 1981, and November, 1985. All but 1 patient had been transfused before transplantation (median 5 units), and during the operation and postoperatively the patients received up to 63 units of blood (median 6). Immunosuppressive therapy consisted of steroids and azathioprine (5 patients) or cyclosporin and low-dose steroids (110 patients). 34 patients had had at least one rejection episode treated with methylprednisolone pulses. At the time of investigation all patients had stable graft function. We used a screening ELISA (Abbott) for HIV antibody with confirmation by western blotting and immunofluorescence. We also measured urinary neopterin excretion.1 70 (of 114) patients had raised urinary neopterin levels, demonstrating that activation of T lymphocytes/macrophages can be seen even in allograft recipients under immunosuppressive treatment without evidence of rejection. 10 of 114 (8.7%) patients showed positive or questionable ELISA reactivity but only 1 was confirmed as positive. In this patient the kidney donor had a history of intravenous drug abuse and the recipient of the other kidney became HIV antibody positive too.2 Thus, none of 1018 blood units (donated before HIV antibody screening had been introduced) was the source of seroconversion. The ELISA false-positive rate was high (8°oin our transplant patients compared with only 0.44% in 27 668 blood donors). The seropositive patient, a 39-year-old woman, has been treated with cyclosporin plus steroids for 16 months and has no symptoms of AIDS-related disease. Her continuous immunosuppressive therapy may have reduced activation of CD4 cells, such T-cell activation being a co-factor in HIV infection.3-5 Since, as our urinary neopterin measurements show, activation of T-cells is present in some kidney transplant recipients it may be that administration of cyclosporin reduces replication of HIV. There is independent evidence from other HIV-infected renal transplant recipients that immunosuppressive therapy reduces and rejection episodes enhance virus propagation.2,6,7 Cyclosporin has been discontinued in only 1 of 4 recipients of HIV infected kidneys, and only this patient has had generalised lymphadenopathy.2The stored sera of
further patient with a renal allograft have been found to have been HIV seropositive at the time of starting dialysis 7 months before and 18 months after transplantation.7 This patient remained well until a rejection episode on day 14 post transplantation. From then on he had multiple opportunistic infections. Perhaps this ’ deterioration resulted from activation of the cellular immune system caused by a
rejection. A place
for cyclosporin in the control of HIV infection is However, in view of the effect of T-cell activation on the expression of HIV, it would seem sensible to avoid immunostimulatory measures and not to withdraw immunosuppressive therapy entirely in HIV-positive transplant recipients.
unproven.
Supported by Fonds project P 6036 M.
zur
Forderung der wissenschaftlichen Forschung,
Department of Surgery I, Institute for Medical Chemistry and Biochemistry, Institute for Hygiene, Central Laboratory for Blood Coagulation and Immunology, University of Innsbruck; Ludwig Boltzmann Institute for AIDS Research, Innsbruck A-6020 Innsbruck, Austria
R. MARGREITER D. FUCHS A. HAUSEN P. HENGSTER D. SCHÖNITZER M. SPIELBERGER M. P. DIERICH H. WACHTER
1. Fuchs
D, Hausen A, Reibnegger G, Wachter H. Automatized routine estimation of neopterin in human urine by HPLC on reversed phase. In: Wachter H, Curtius HCh, Pfleiderer W, eds. Biochemical and clinical aspects of pteridines Vol I. Berlin and New York: de Gruyter, 1982: 67-79. 2. L’Age-Stehr J, Schwarz A, Offermann G, et al. HTLV-III infection in kidney transplant recipients. Lancet 1985; ii: 1361-62. 3. Fuchs D, Hausen A, Reibnegger G, et al. Urinary neopterin evaluation in nsk groups for the acquired immunodeficiency syndrome (AIDS). In: Pfleiderer W, Wachter H, Curtius HCh, eds. Biochemical and clinical aspects of pteridines: Vol III. Berlin and New York: de Gruyter, 1984: 457-67. 4. Wachter H, Fuchs D, Hausen A, et al. Are conditions linked with T-cell stimulation necessary for progressive HTLV-III infection? Lancet 1986; i: 97. 5. Hausen A, Diench MP, Fuchs D, et al. Immunosuppressants in patients with AIDS Nature 1986; 320: 114. 6. Neumayer HH, Wagner K, Kreese S. HTLV-III antibodies in patients with kidney transplants or on haemodialysis. Lancet 1986; i: 497 7. Oliveira DBG, Winearls CH, Cohen J, Ind PW, Williams G. Severe immunosuppression in a renal transplant recipient with HTLV-III antibodies Transplantation 1986; 41: 260-61.
SHOULD LESBIANS GIVE BLOOD?
SIR,—The current panic about AIDS and the rapid spread of HIV (HTLV-III) infection amongst high-risk groups has led to many irrational and harmful situations such as those mentioned in letters by Dr Summerfield and Dr Henley in your July 12 issue (p 112). These illogical reactions are not limited to non-medical agencies. A Nottingham woman recently attempted to re-register as a blood donor after a lapse of several years. In response to a question about her sexual partners she stated that she had a monogamous relationship with a woman. Her donation was refused and she received a letter from the Sheffield Regional Transfusion Centre which stated: "Although it is accepted that lesbians are probably people least at risk of developing anti-HTLV III nevertheless the policy of the National Blood Transfusion Service is not to accept their blood for clinical transfusion purposes ... I therefore feel that you should not donate blood and you should give this advice to.your friends who are blood donors". It is clear from recent reviews on the subjectl-3 that lesbians as a group are at particularly low risk of being infected with HIV. There have been widespread and frequent requests by the National Blood Transfusion Service for more donors, to reduce its dependence on potentially HIV-contaminated blood products from North America. In view of this it seems odd that the NBTS should be refusing low-risk donors. Perhaps the NBTS should reconsider this policy, which I can only assume is based on homophobia rather than reason. Women in Medicine, 15 Lyons Fold, Sale, Cheshire M33 1LF
J. H. DOWNTON
M. The natural history of human T lymphotrophic virus-III infection the of AIDS Br Med J 1986; 292: 5-12. 2. Editorial. AIDS in the UK. Lancet 1985; ii: 1103-05. 3. Acheson ED AIDS. a challenge for the public health. Lancet 1986, i. 662-66 1.
Melbye
cause
MT-2 cells.3 This was confirmed by western blot analysis with an MT-2 cell lysate. The serum formed specific bands with viral proteins, including p19, p24, and p28, while the CSF reacted with p24 only (fig 1). Serological tests for syphilis and HTLV-III were negative. The patient was born and raised in Kochi, a virusendemic area, and her son and sister were also seropositive for HTLV-I. For virus isolation, a 5 ml CSF sample was centrifuged and the sedimented cells were co-cultivated with 3 x 106 peripheral lymphocytes from a seronegative healthy man. The co-culture was maintained in 3 ml of RPMI 1640 medium supplemented with 10% human cord serum, 10% fetal calf serum, 10% crude T-cell growth factor, and antibiotics. After 3 weeks, the cells were adapted to grow without T-cell growth factor and 2 weeks later a continuous culture line of lymphoid cells was established. Chromosome analysis of this cell line showed a normal female karyotype. The cells were reactive with monoclonal antibodies to T-cells (Leu-1) and Ia antigens (OKIal). HTLV-I antigens were detected in the majority of the cells in an indirect immunofluorescence test using reference ATL patient’s serum and monoclonal antibodies to HTLV-I p19and p24. Electron microscopy revealed type C virus particles in these cells (fig 2). The source of the virus in the T-cell line was considered to be the CSF lymphocytes because the patient, but not the male donor, was seropositive for HTLV-1. This finding may be due solely to the
Coronary-Care Unit, Green Lane Hospital, Auckland, 3,
R. M. NORRIS
New Zealand 1. Lawrie
DM, Higgins MR, Godman MJ, Oliver MF, Julian DG, Donald KW. Ventricular fibrillation complicating acute myocardial infarction. Lancet 1968; ii: 523-28. 2. Nordrehaug JE, von der Lippe G. Hypokalaemia and ventricular fibrillation in acute myocardial infarction. Br Heart J 1983; 50: 525-29. 3. Adams P, et al. Plasma potassium and VF in acute myocardial infarction: a prospective study. Circulation 1984; 70 (suppl II): 311. 1984; 70 (suppl II): 311. 4. Schwartz PJ, Stone HL. Left stellectomy in the prevention of ventricular fibrillation caused by acute myocardial ischemia in conscious dogs with anterior myocardial infarction. Circulation 1980; 62: 1256-65. 5. Norris RM, Brown MA, Clarke ED, Barnaby PF, Geary GG, Logan RL, Sharpe DN. Prevention of ventricular fibrillation during acute myocardial infarction by intravenous propranolol. Lancet 1984; ii: 883-86. 6. GISSI. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; i: 397-402. 7. The MIAMI trial research group. Metoprolol in acute myocardial infarction (MIAMI). A randomised placebo-controlled international trial (with discussants. Eur Heart J 1985; 6: 199-226.
Fig 1-Western blot analysis of serum (lane 2) and CSF (lane 3) from a myelopathy patient with reference ATL patient’s serum (lane i B
ISOLATION OF HTLV-I FROM CEREBROSPINAL FLUID OF A PATIENT WITH MYELOPATHY
SIR,—The seropositive
rate
for human T-cell leukaemia virus
type I (HTLV-I) in patients with tropical spastic paraparesis (TSP) is high in Martinique1 and in Jamaica and Colombia.2 Recently, Osame et al (May 3, p 1031) described a TSP-like myelopathy in 6 Japanese patients in Kagoshima where HTLV-I and adult T-cell leukaemia (ATL) are more prevalent than in the Caribbean. They proposed the term HTLV-I-associated myelopathy (HAM) for this disorder. We report here the isolation of HTLV-I from the cerebrospinal fluid (CSF) of a Japanese patient with such a
myelopathy. A 45-year-old woman was admitted for a gait disturbance that had been slowly progressive for about 20 years. She also had occasional headaches but no sensory or sphincter impairment. Physical examination revealed hyperactive knee and ankle jerks with a positive Babinski sign and ankle clonus on both sides. A cranial computerised tomographic scan of the cranium and myelography were normal. A CSF sample contained protein 26 mg/dl, glucose 58 mg/dl, and 2 x 103/ml mononuclear cells (mostly normal-looking lymphocytes). Her leucocyte count was normal but there were 1-2%abnormal lymphocytes with bilobed nuclei. Serum and CSF antibodies to HTLV-I were positive at titres of 1/640 and 1/1, respectively, in an immunofluorescence assay against
Fig 2-Electron micrograph of HTLV-I isolated from CSF of myelopathy patient.
a
398 presence of HTLV-1 genome-positive lymphocytes in the CSF or may represent a possible pathogenic role of HTLV-I in TSP/ HAM. HTLV-I has not been previously isolated from the central nervous system. However, another lymphotropic retrovirus, the human immunodeficiency virus, has been isolated from the CSF
and neural tissues of patients with various
acquired immunodeficiency syndrome neurological manifestations such as encephalopathy, meningitis, or myelopathy.4,S
Kochi Medical School, Kochi 781-51, Japan
SHOZO HIROSE YOSHIKI UEMURA MASATOSHI FUJISHITA TAKAO KITAGAWA MAKOTO YAMASHITA JUN IMAMURA YUJI OHTSUKI HIROKINI TAGUCHI ISAO MIYOSHI
A, Barin F, Vernant JC, et al. Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis. Lancet 1985; ii. 407-09. 2. Rodgers-Johnson P, Gajdusek DC, Morgan OC, et al. HTLV-I and HTLV-III antibodies and tropical spastic paraparesis. Lancet 1985; ii: 1247-48 3. Miyoshi I, Kubonishi I, Yoshimoto S, et al. Type C virus particles in a cord T-cell line derived by co-cultivating normal human cord leukocytes and human leukaemic T 1. Gessain
cells. Nature 1981; 294: 770-71. DD, Rota TR, Schooley RT, et al Isolation of HTLV-III from cerebrospinal fluid and neural tissues of patients with neurologic syndrome related to the acquired immunodeficiency syndrome. N Engl J Med 1985; 313: 1493-97. 5. Levy JA, Shimabukuro J, Hollander H, Mills J, Kaminsky L. Isolation of AIDS-associated retroviruses from cerebrospinal fluid and brain of patients with neurological symptoms. Lancet 1985; ii. 586-88
4 Ho
HIV INFECTION IN RENAL ALLOGRAFT RECIPIENTS
SIR,—Patients on dialysis and renal allograft recipients receive frequent blood transfusions and are in a chronic state of immunosuppression. They are at high risk of hepatitis B infection and may be at risk of infection with the human immunodeficiency virus (HIV) also. We have investigated 115 patients given cadaveric renal transplants between August, 1981, and November, 1985. All but 1 patient had been transfused before transplantation (median 5 units), and during the operation and postoperatively the patients received up to 63 units of blood (median 6). Immunosuppressive therapy consisted of steroids and azathioprine (5 patients) or cyclosporin and low-dose steroids (110 patients). 34 patients had had at least one rejection episode treated with methylprednisolone pulses. At the time of investigation all patients had stable graft function. We used a screening ELISA (Abbott) for HIV antibody with confirmation by western blotting and immunofluorescence. We also measured urinary neopterin excretion.1 70 (of 114) patients had raised urinary neopterin levels, demonstrating that activation of T lymphocytes/macrophages can be seen even in allograft recipients under immunosuppressive treatment without evidence of rejection. 10 of 114 (8.7%) patients showed positive or questionable ELISA reactivity but only 1 was confirmed as positive. In this patient the kidney donor had a history of intravenous drug abuse and the recipient of the other kidney became HIV antibody positive too.2 Thus, none of 1018 blood units (donated before HIV antibody screening had been introduced) was the source of seroconversion. The ELISA false-positive rate was high (8°oin our transplant patients compared with only 0.44% in 27 668 blood donors). The seropositive patient, a 39-year-old woman, has been treated with cyclosporin plus steroids for 16 months and has no symptoms of AIDS-related disease. Her continuous immunosuppressive therapy may have reduced activation of CD4 cells, such T-cell activation being a co-factor in HIV infection.3-5 Since, as our urinary neopterin measurements show, activation of T-cells is present in some kidney transplant recipients it may be that administration of cyclosporin reduces replication of HIV. There is independent evidence from other HIV-infected renal transplant recipients that immunosuppressive therapy reduces and rejection episodes enhance virus propagation.2,6,7 Cyclosporin has been discontinued in only 1 of 4 recipients of HIV infected kidneys, and only this patient has had generalised lymphadenopathy.2The stored sera of
further patient with a renal allograft have been found to have been HIV seropositive at the time of starting dialysis 7 months before and 18 months after transplantation.7 This patient remained well until a rejection episode on day 14 post transplantation. From then on he had multiple opportunistic infections. Perhaps this ’ deterioration resulted from activation of the cellular immune system caused by a
rejection. A place
for cyclosporin in the control of HIV infection is However, in view of the effect of T-cell activation on the expression of HIV, it would seem sensible to avoid immunostimulatory measures and not to withdraw immunosuppressive therapy entirely in HIV-positive transplant recipients.
unproven.
Supported by Fonds project P 6036 M.
zur
Forderung der wissenschaftlichen Forschung,
Department of Surgery I, Institute for Medical Chemistry and Biochemistry, Institute for Hygiene, Central Laboratory for Blood Coagulation and Immunology, University of Innsbruck; Ludwig Boltzmann Institute for AIDS Research, Innsbruck A-6020 Innsbruck, Austria
R. MARGREITER D. FUCHS A. HAUSEN P. HENGSTER D. SCHÖNITZER M. SPIELBERGER M. P. DIERICH H. WACHTER
1. Fuchs
D, Hausen A, Reibnegger G, Wachter H. Automatized routine estimation of neopterin in human urine by HPLC on reversed phase. In: Wachter H, Curtius HCh, Pfleiderer W, eds. Biochemical and clinical aspects of pteridines Vol I. Berlin and New York: de Gruyter, 1982: 67-79. 2. L’Age-Stehr J, Schwarz A, Offermann G, et al. HTLV-III infection in kidney transplant recipients. Lancet 1985; ii: 1361-62. 3. Fuchs D, Hausen A, Reibnegger G, et al. Urinary neopterin evaluation in nsk groups for the acquired immunodeficiency syndrome (AIDS). In: Pfleiderer W, Wachter H, Curtius HCh, eds. Biochemical and clinical aspects of pteridines: Vol III. Berlin and New York: de Gruyter, 1984: 457-67. 4. Wachter H, Fuchs D, Hausen A, et al. Are conditions linked with T-cell stimulation necessary for progressive HTLV-III infection? Lancet 1986; i: 97. 5. Hausen A, Diench MP, Fuchs D, et al. Immunosuppressants in patients with AIDS Nature 1986; 320: 114. 6. Neumayer HH, Wagner K, Kreese S. HTLV-III antibodies in patients with kidney transplants or on haemodialysis. Lancet 1986; i: 497 7. Oliveira DBG, Winearls CH, Cohen J, Ind PW, Williams G. Severe immunosuppression in a renal transplant recipient with HTLV-III antibodies Transplantation 1986; 41: 260-61.
SHOULD LESBIANS GIVE BLOOD?
SIR,—The current panic about AIDS and the rapid spread of HIV (HTLV-III) infection amongst high-risk groups has led to many irrational and harmful situations such as those mentioned in letters by Dr Summerfield and Dr Henley in your July 12 issue (p 112). These illogical reactions are not limited to non-medical agencies. A Nottingham woman recently attempted to re-register as a blood donor after a lapse of several years. In response to a question about her sexual partners she stated that she had a monogamous relationship with a woman. Her donation was refused and she received a letter from the Sheffield Regional Transfusion Centre which stated: "Although it is accepted that lesbians are probably people least at risk of developing anti-HTLV III nevertheless the policy of the National Blood Transfusion Service is not to accept their blood for clinical transfusion purposes ... I therefore feel that you should not donate blood and you should give this advice to.your friends who are blood donors". It is clear from recent reviews on the subjectl-3 that lesbians as a group are at particularly low risk of being infected with HIV. There have been widespread and frequent requests by the National Blood Transfusion Service for more donors, to reduce its dependence on potentially HIV-contaminated blood products from North America. In view of this it seems odd that the NBTS should be refusing low-risk donors. Perhaps the NBTS should reconsider this policy, which I can only assume is based on homophobia rather than reason. Women in Medicine, 15 Lyons Fold, Sale, Cheshire M33 1LF
J. H. DOWNTON
M. The natural history of human T lymphotrophic virus-III infection the of AIDS Br Med J 1986; 292: 5-12. 2. Editorial. AIDS in the UK. Lancet 1985; ii: 1103-05. 3. Acheson ED AIDS. a challenge for the public health. Lancet 1986, i. 662-66 1.
Melbye
cause