945
associated with diagnostic PCR work, especially when plasmids containing the target sequence are the positive controls.3This can be achieved by testing fresh samples and by screening the available specimens for plasmid contamination by amplifying plasmidspecific sequences.s We also suggest that additional evidence be sought by looking for HTLV-II-specific antibodies using typespecific peptide serological assays6 and by virus isolation from cell cultures. Did the patients thought to have HTLV-11infection have risk factors for HTLV-I I, such as intravenous drug use or a sexual partnership with drug users as noted with most instances of HTLV-II infection in North America and Europe ?7,8 Retrovirus Diseases Branch, Centers for Disease Control, Atlanta, Georgia 30333, USA
WALID HENEINE RIMA F. KHABBAZ JONATHAN E. KAPLAN
A, Blattner WA. The epidemiology of the human T-cell lymphotropic virus type I and type II. etiologic role in human disease. Transfusion 1991; 31: 67-75. 2. Hjelle B. Human T-cell leukemia/lymphoma viruses. Arch Pathol Lab Med 1991; 115: 440-50. 3. Persing DH. Polymerase chain reaction: trenches to benches J Clin Microbiol 1991; 29: 1281-85 4. Kwok S, Higuchi R. Avoiding false positives with PCR. Nature 1989; 339: 237-38. 5. Nerenberg MI, Minor T. Detection of plasmid contamination in PCR samples. Biotechnics 1991; 11: 332-35. 6. Lal RB, Heneine W, Rudolf DL, et al. Synthetic peptide based immunoassays for distinguishing between HTLV-I and HTLV-II infection in seropositive individuals. J Clin Microbiol 1991; 29: 2253-58. 7. Lee HH, Swanson P, Rosenblatt JD, et al. Relative prevalence and risk factors of HTLV-I and HTLV-II infection in US blood donors. Lancet 1991; 337: 1435-39. 8. Zella D, Mon L, Sala M, et al HTLV-II infection m Italian drug abusers Lancet 1990; 336: 575-76
were increased. She had no enlarged lymph nodes, skin lesions, or organomegaly. Her serum and cerebrospinal fluid were HTLV-I antibody positive by (’Eitest-ATL’). She thus fitted
reflexes
World Health Organisation criteria for HAM/TSP. Genomic DNA purified from peripheral blood mononuclear cells was examined by PCR with HTLV-I and HTLV-II specific primer pairs SK54/SK55 and SK58/59, respectively. PCR (figure) confirmed co-infection with HTLV-1 and HTLV-11 in both cases. These results do not suggest a very close correlation between co-infection and HAM/TSP. KAZUAKI ISHIBASHI NOBUHITO OHNO KIMIHARU UOZUMI SHUICHI HANADA TERUKATSU ARIMA
Second Department of Internal Medicine, Faculty of Medicine,
Kagoshima University, Kagoshima 890, Japan
1. Manns
SIR,-We have reported (Aug 31, p 572) that development of T-cell leukaemia (ATL) and HTLV-1-associated myelopathy or tropical spastic paraparesis (HAM/TSP) in HTLV-I carriers was not controlled by HLA-linked genes alone. Dr Kira and colleagues report that co-infection with HTLV-1 and HTLV-II might be important for the development of myelopathy in patients with HAM/TSP; Dr Kiyokawa and co-workers disagree (Aug 17, p 451). We describe here a 60-year-old man and his adult
daughter with ATL and HAM/TSP, respectively, in whom HTLV-I and HTLV-II infection were studied with the polymerase chain reaction (PCR). The father had lymphadenopathy diagnosed as malignant lymphoma, diffuse large cell type. Morphology and phenotyping of peripheral blood lymphocytes, HTLV-1 antibody testing, and evidence for monoclonal integration of HTLV-1 proviral DNA into peripheral blood cells confirmed the disease as ATL. No neurological abnormalities were present before chemotherapy was started. His 34-year-old daughter could not walk without shuffling when she visited our hospital. Symptoms of HAM/TSP had developed at age 31, and she had a 1-year history of urinary incontinence. She had paraparesis of her legs and the deep tendon
Use of inactivated
or
oral
poliovirus vaccine
in India SIR,-Mrs Kaul (Sept 14, p 702) comments on the use of either poliovirus vaccine (OPV) or inactivated poliovirus vaccine (IPV) in India. She points out that OPV confers a herd immunity that is better than IPV. OPV confers better gut immunity than does IPV, but how IPV confers herd immunity is not known.1 oral
Additionally, IPV
has one very important advantage: there is no chance of the virus reverting to neurovirulence. Patients have been reported in whom reversion to neurovirulence (with OPV) has occurred with mainly poliovirus types 2 or 3 causing paralysis, with an incidence of 1 in 500 000 first doses given to infants.2 At the molecular level, all three vaccine strains show some tendency to revert to neurovirulence. In type 2 and 3 strains back mutation at nucleotide 472 occurs within a few days of vaccine administration.3 The immunity induced by IPV also seems better than that by OPV. Various studies have demonstrated detectable antibody titres in 76-91 % of individuals vaccinated with OPV.’ All individuals vaccinated with IPV had detectable antibodies 4 The cost of IPV is certainly higher than that of OPV, but technological advances might reduce the cost. In addition, as Kaul points out, the cost-effectiveness of the two vaccines needs serious study before future vaccine policy in India is formulated. At present evidence favours the use of IPV instead of OPV, or of an increased number of doses of OPV,S which would substantially increase the cost and reduce compliance. Department of Parasitology, Postgraduate Institute of Medical Education and Research,
R. SEHGAL
Chandigarh 160012, India
1 Schaap GJ, Bijkerk H, Coutinho RA, et al. The spread of wild polio virus m the well vaccinated Netherlands in connection with the 1978 epidemic. Prog Med Virol 1984; 29: 124-40. 2. Nkowane BM, Wassilak SCF, Orenstein WA, et al. Vaccine associated paralytic poliomyelitis in United States: 1973 through 1984. JAMA 1987; 257: 1335-40. 3. Minor PD, Dunn G. The effect of sequences in the 5’ non coding region on the replication of polio viruses in the human gut. JGen Virol 1988; 69: 1091-96. 4. Salk FE, Drucker J. Non infectious polio vaccine. In: Plotkin SA, Mortimer EA, eds. Vaccines. Philadelphia: WB Saunders, 1988: 158-81. 5. Beale AJ. Polio vaccines: time for a change in immunisation policy? Lancet 1990; 335: 839-42.
Transsexualism SiR,—Your Sept 7 editorial notes the lack of convincing evidence for a biological cause of this disorder. However, a recent study has demonstrated abnormalities in the interstitial nuclei of the anterior hypothalamus in the brains of 19 homosexual men, and a biological difference was thus suggested as the root of sexual orientation.1 Other workers have noted very large suprachiasmatic nucleus in 2 male-to-female transsexuals2 and in 10 homosexual men.3 These reports, providing the first evidence for a possible association between organic brain changes and sexual orientation, have prompted us to report transsexual monozygotic male twins (confirmed by HLA typing) who underwent sex reassignment
associated with diagnostic PCR work, especially when plasmids containing the target sequence are the positive controls.3This can be achieved by testing fresh samples and by screening the available specimens for plasmid contamination by amplifying plasmidspecific sequences.s We also suggest that additional evidence be sought by looking for HTLV-II-specific antibodies using typespecific peptide serological assays6 and by virus isolation from cell cultures. Did the patients thought to have HTLV-11infection have risk factors for HTLV-I I, such as intravenous drug use or a sexual partnership with drug users as noted with most instances of HTLV-II infection in North America and Europe ?7,8 Retrovirus Diseases Branch, Centers for Disease Control, Atlanta, Georgia 30333, USA
WALID HENEINE RIMA F. KHABBAZ JONATHAN E. KAPLAN
A, Blattner WA. The epidemiology of the human T-cell lymphotropic virus type I and type II. etiologic role in human disease. Transfusion 1991; 31: 67-75. 2. Hjelle B. Human T-cell leukemia/lymphoma viruses. Arch Pathol Lab Med 1991; 115: 440-50. 3. Persing DH. Polymerase chain reaction: trenches to benches J Clin Microbiol 1991; 29: 1281-85 4. Kwok S, Higuchi R. Avoiding false positives with PCR. Nature 1989; 339: 237-38. 5. Nerenberg MI, Minor T. Detection of plasmid contamination in PCR samples. Biotechnics 1991; 11: 332-35. 6. Lal RB, Heneine W, Rudolf DL, et al. Synthetic peptide based immunoassays for distinguishing between HTLV-I and HTLV-II infection in seropositive individuals. J Clin Microbiol 1991; 29: 2253-58. 7. Lee HH, Swanson P, Rosenblatt JD, et al. Relative prevalence and risk factors of HTLV-I and HTLV-II infection in US blood donors. Lancet 1991; 337: 1435-39. 8. Zella D, Mon L, Sala M, et al HTLV-II infection m Italian drug abusers Lancet 1990; 336: 575-76
were increased. She had no enlarged lymph nodes, skin lesions, or organomegaly. Her serum and cerebrospinal fluid were HTLV-I antibody positive by (’Eitest-ATL’). She thus fitted
reflexes
World Health Organisation criteria for HAM/TSP. Genomic DNA purified from peripheral blood mononuclear cells was examined by PCR with HTLV-I and HTLV-II specific primer pairs SK54/SK55 and SK58/59, respectively. PCR (figure) confirmed co-infection with HTLV-1 and HTLV-11 in both cases. These results do not suggest a very close correlation between co-infection and HAM/TSP. KAZUAKI ISHIBASHI NOBUHITO OHNO KIMIHARU UOZUMI SHUICHI HANADA TERUKATSU ARIMA
Second Department of Internal Medicine, Faculty of Medicine,
Kagoshima University, Kagoshima 890, Japan
1. Manns
SIR,-We have reported (Aug 31, p 572) that development of T-cell leukaemia (ATL) and HTLV-1-associated myelopathy or tropical spastic paraparesis (HAM/TSP) in HTLV-I carriers was not controlled by HLA-linked genes alone. Dr Kira and colleagues report that co-infection with HTLV-1 and HTLV-II might be important for the development of myelopathy in patients with HAM/TSP; Dr Kiyokawa and co-workers disagree (Aug 17, p 451). We describe here a 60-year-old man and his adult
daughter with ATL and HAM/TSP, respectively, in whom HTLV-I and HTLV-II infection were studied with the polymerase chain reaction (PCR). The father had lymphadenopathy diagnosed as malignant lymphoma, diffuse large cell type. Morphology and phenotyping of peripheral blood lymphocytes, HTLV-1 antibody testing, and evidence for monoclonal integration of HTLV-1 proviral DNA into peripheral blood cells confirmed the disease as ATL. No neurological abnormalities were present before chemotherapy was started. His 34-year-old daughter could not walk without shuffling when she visited our hospital. Symptoms of HAM/TSP had developed at age 31, and she had a 1-year history of urinary incontinence. She had paraparesis of her legs and the deep tendon
Use of inactivated
or
oral
poliovirus vaccine
in India SIR,-Mrs Kaul (Sept 14, p 702) comments on the use of either poliovirus vaccine (OPV) or inactivated poliovirus vaccine (IPV) in India. She points out that OPV confers a herd immunity that is better than IPV. OPV confers better gut immunity than does IPV, but how IPV confers herd immunity is not known.1 oral
Additionally, IPV
has one very important advantage: there is no chance of the virus reverting to neurovirulence. Patients have been reported in whom reversion to neurovirulence (with OPV) has occurred with mainly poliovirus types 2 or 3 causing paralysis, with an incidence of 1 in 500 000 first doses given to infants.2 At the molecular level, all three vaccine strains show some tendency to revert to neurovirulence. In type 2 and 3 strains back mutation at nucleotide 472 occurs within a few days of vaccine administration.3 The immunity induced by IPV also seems better than that by OPV. Various studies have demonstrated detectable antibody titres in 76-91 % of individuals vaccinated with OPV.’ All individuals vaccinated with IPV had detectable antibodies 4 The cost of IPV is certainly higher than that of OPV, but technological advances might reduce the cost. In addition, as Kaul points out, the cost-effectiveness of the two vaccines needs serious study before future vaccine policy in India is formulated. At present evidence favours the use of IPV instead of OPV, or of an increased number of doses of OPV,S which would substantially increase the cost and reduce compliance. Department of Parasitology, Postgraduate Institute of Medical Education and Research,
R. SEHGAL
Chandigarh 160012, India
1 Schaap GJ, Bijkerk H, Coutinho RA, et al. The spread of wild polio virus m the well vaccinated Netherlands in connection with the 1978 epidemic. Prog Med Virol 1984; 29: 124-40. 2. Nkowane BM, Wassilak SCF, Orenstein WA, et al. Vaccine associated paralytic poliomyelitis in United States: 1973 through 1984. JAMA 1987; 257: 1335-40. 3. Minor PD, Dunn G. The effect of sequences in the 5’ non coding region on the replication of polio viruses in the human gut. JGen Virol 1988; 69: 1091-96. 4. Salk FE, Drucker J. Non infectious polio vaccine. In: Plotkin SA, Mortimer EA, eds. Vaccines. Philadelphia: WB Saunders, 1988: 158-81. 5. Beale AJ. Polio vaccines: time for a change in immunisation policy? Lancet 1990; 335: 839-42.
Transsexualism SiR,—Your Sept 7 editorial notes the lack of convincing evidence for a biological cause of this disorder. However, a recent study has demonstrated abnormalities in the interstitial nuclei of the anterior hypothalamus in the brains of 19 homosexual men, and a biological difference was thus suggested as the root of sexual orientation.1 Other workers have noted very large suprachiasmatic nucleus in 2 male-to-female transsexuals2 and in 10 homosexual men.3 These reports, providing the first evidence for a possible association between organic brain changes and sexual orientation, have prompted us to report transsexual monozygotic male twins (confirmed by HLA typing) who underwent sex reassignment
