279
In most studies total crosslinks have been determined after acid hydrolysis of urine. More recently, simplified methods have been developed based on the consistent proportion of free crosslinks present in urine21,22 or on the assay of specific peptides derived from bone.23 Such simple, direct urinary immunoassays for measurement of bone resorption will have many clinical applications not only in the diagnosis and monitoring of therapy in metabolic bone diseases but also as part of screening programmes to assess the risks of osteoporotic fracture. 1. Delmas PD. Clinical use of biochemical markers of bone remodeling in osteoporosis. Bone 1992; 13: S17-S21. 2. Eyre DR. New markers of bone resorption. J Clin Endocrinol Metab 1992; 74: 470A-C. 3. Eyre DR, Koob TJ, Van Ness KP. Quantitation of hydroxypyridinium crosslinks in collagen by high-performance liquid chromatography. Anal Biochem 1984; 137: 380-88. 4. Black D, Duncan A, Robins SP. Quantitative analysis of the pyridinium crosslinks of collagen in urine using ion-paired reversed-phase high-performance liquid chromatography. Anal Biochem 1988; 169: 197-203. 5. Uebelhart D, Gineyts E, Chapuy M-C, Delmas PD. Urinary excretion of pyridinium crosslinks: a new marker of bone resorption in metabolic bone disease. Bone Min 1990; 8: 87-96. 6. Robins SP, Black D, Paterson CR, Reid DM, Duncan A, Seibel MJ. Evaluation of urinary hydroxypyridinium crosslink measurements as resorption markers in metabolic bone diseases. Eur J Clin Invest 1991; 21: 310-15. 7. McLaren AM, Hordon LD, Bird HA, Robins SP. Urinary excretion of
pyridinium crosslinks of collagen in patients with osteoporosis and the effects of bone fracture. Ann Rheum Dis 1992; 51: 648-51. 8. Seibel MJ, Gartenberg F, Silverberg SJ, Ratcliffe A, Robins SP, Bilezikian JP. Urinary hydroxypyridinium crosslinks of collagen as markers of bone resorption in primary hyperparathyroidism. J Clin Endocrinol Metab 1992; 74: 481-86. 9. Uebelhart D, Schlemmer A, Johansen JS, Gineyts E, Christiansen C, Delmas PD. Effect of menopause and hormone replacement therapy on the urinary excretion of pyridinium cross-links. J Clin Endocrinol Metab 1991; 72: 367-73. 10. Eastell R, Hampton L, Colwell A, et al. Urinary collagen crosslinks are highly correlated with radioisotopic measurements of bone resorption. In: Christiansen C, Overgaard K, eds. Osteoporosis 1990. Copenhagen: Osteopress ApS, 1990: 469-70. 11. Delmas PD, Schlemmer A, Gineyts E, Riis B, Christiansen C. Urinary excretion of pyridinoline crosslinks correlates with bone turnover measured on iliac crest biopsy in patients with vertebral osteoporosis. J Bone Min Res 1991; 6: 639-44. 12. Colwell A, Eastall R, Assiri AM A, Russell RGG. Effect of diet on deoxypyridinoline excretion. In: Christiansen C, Overgaard K, eds. Osteoporosis 1990. Copenhagen: Osteopress ApS, 1990: 590-91. 13. Seibel MJ, Duncan A, Robins SP. Urinary hydroxy-pyridinium crosslinks provide indices of cartilage and bone involvement in arthritic diseases. J Rheumatol 1989; 16: 964-70. 14. Harvey RD, McHardy KC, Paterson F, Bewsher PD, Duncan A, Robins SP. Measurement of bone collagen degradation in hyperthyroidism and during thyroxine replacement therapy using pyridinium crosslinks as specific urinary markers. J Clin Endocrinol Metab 1991; 72: 1188-94. 15. Paterson CR, Robins SP, Horobin JM, Preece PE, Cuschieri A. Pyridinium crosslinks as markers of bone resorption in patients with breast cancer. Br J Cancer 1991; 64: 884-86. 16. Body JJ, Delmas PD. Urinary pyridinium cross-links as markers of bone resorption in tumor-associated hyperglycemia. J Clin Endocrinol Metab 1992; 74: 471-75. 17. Fujimoto D, Suzuki M, Uchiyama A, Miyamoto S, Inoue T. Analysis of pyridinoline, a crosslinking compound of collagen fibers, in human urine. J Biochem 1983; 94: 1133-36. 18. Beardsworth LJ, Eyre DR, Dickson IR. Changes with age in the urinary excretion of lysyl- and hydroxylysylpyridinoline, two new markers of bone collagen turnover. J Bone Min Res 1990; 5: 671-76. 19. Schlemmer A, Hassager C, Jensen SB, Christiansen C. Marked diurnal variation in urinary excretion of pyridinium cross-links m premenopausal women. J Clin Endocrinol Metab 1992; 74: 476-80. 20. Eastell R, Calvo MS, Burritt MF, et al. Abnormalities in circadian patterns of bone resorption and renal calcium conservation in type I osteoporosis. J Clin Endocrinol Metab 1992; 74: 487-94.
SP, Duncan A, Riggs BL. Direct measurement of free hydroxy-pyridinium crosslinks of collagen in urine as new markers of bone resorption in osteoporosis. In: Christiansen C, Overgaard K, eds. Osteoporosis 1990. Copenhagen: Osteopress ApS, 1990: 465-68. 22. Robins SP, Duncan A, McLaren AM. Structural specificity of an ELISA for the collagen crosslink, pyridinoline: implications for the measurement of free pyridinium crosslinks as indices of bone resorption in metabolic bone diseases. J Bone Min Res 1991; 6 (suppl): 642a. 23. Hanson DA, Eyre DR. A specific immunoassay for bone resorption based on cross-linked collagen peptides in urine. J Bone Min Res 1991; 6 (suppl): 669a. 21. Robins
Cricket under stress Cricket, that summer anchor of the very identity of many a nation, is threatened by a new disease-spinal stress fractures in fast bowlers. Or so one might think from headlines in the lay press. What is the truth behind such stories? Although renewed interest in spinal stress fractures in fast bowlers gives the impression that a "new" condition has arrived and is about to cull the brightest bowling prospects, the vulnerability of sportsmen and sportswomen to stress fractures is well recognised. Such fractures characteristically occur in a normal bone that is subject to repeated cyclical loading, the load being less than that which causes acute fracture. Bowlers typically get a bilateral fracture of the pars interarticularis of one of their lower lumbar vertebrae (spondylolysis), which is believed to be related to the hyperextension that precedes delivery. A contributory factor is the force of the delivery (to which today’s armour-clad batsmen bear witness), since fast bowlers are most afflicted. Several fast bowlers have had their
interrupted by a spondylolysis. Anxiety about the impact of stress fractures will not have been lessened by a report by Hardcastle and colleagues,1 who conducted a detailed study, including computed tomography (CT) and magnetic resonance imaging (MRI), of 24 fast bowlers aged 16-18 years who had been selected for special training careers
in Western Australia. Pars interarticularis defects diagnosed in 54%, and 63% had disc degeneration. These alarming figures warrant further were
analysis. The reported frequency of isthmic spondylolysis in European populations is about 5-7%,zand this figure is higher in sportsmen and sportswomen. However, such figures are based on standard radiographic examinations and predate the use of MRI and CT. Moreover, in the Australian series 50% of the defects were unilateral; such defects are rarely identified by conventional
radiography
and
are
not
always
symptomatic. This condition has previously been described in detail in a fast bowler.3Whereas the bilateral lesion is thought to be the result of extension, the main cause for the unilateral lesion may well be rotation. Symptomless lesions on the opposite side at the same level can be a predisposing factor. The high figure for defects in the lumbar spine in the Australian series therefore of detection.
largely reflects sensitive new methods
280
What about disc degeneration? Figures for this condition are highly influenced by the method of definition; in the report by Hardcastle and colleagues, degeneration was probably determined by MRI, although this is not clearly stated. Such changes have been noted in 35% of young symptom-free subjects4,5 and might be expected to be higher in young athletes. In a control series of 13 batsmen described by Hardcastle et al, the frequency of disc degeneration was 54%. Thus fast bowling might contribute to disc degeneration in young men but is not the sole cause. Surveys with up-to-date sensitive techniques of investigation will always produce abnormal findings, which should be regarded cautiously, especially if they are not symptomatic. If they are, treatment must be considered. In most cases a stress fracture will heal with rest from the activity that initiated it. When it does not, selective surgery should be contemplated. Whether a stress fracture of the lumbar spine in a fast bowler constitutes an industrial or occupational disease has not been discussed. 1. Hardcastle
P, Annear DH, Foster DH, et al. Spinal abnormalities in young fast bowlers. J Bone Joint Surg 1992; 74B: 421-25. 2. Wynne-Davies R, Scott JHS. Inheritance and spondylolisthesis: a radiographic family survey. J Bone Joint Surg 1979; 61B: 301-05. 3. Weatherley CR, Mehdian H, Vanden Berghe L. Low back pain with fracture of the pedicle and contralateral spondylolysis. J Bone Joint Surg 1991; 73B: 990-93. 4. Evans W, Jobe W, Seibert C. Cross-sectional prevalence study of lumbar disc degeneration in a working population. Spine 1989; 14: 60-64. 5. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg 1990; 72A: 403-08.
AIDS minus HIV? Those attending the VIII International Conference AIDS in Amsterdam (July 19-24) were told of the dramatic discovery of a "new" virus not at a plenary session but in their hotel rooms on television. Peer-reviewed work presented in the scientific meetings was sidelined by an announcement to the press by Dr Sudhir Gupta in Irvine, California. Dr Gupta claims that the agent, human intracisternal virus (or MTV, media-transmitted virus, as delegates were quick to dub it) has caused an AIDS-like disease in a 66-year-old woman. The resultant stir forced an emergency session in Amsterdam, where Dr J. Laurence, Dr J. Curran, Dr A. Fauci, and others presented some of the privileged data from the Centers for Disease Control (CDC) and the National Institute of Alergy and Infectious Diseases concerning similar cases before publication of Laurence’s article in this issue of The Lancet on
tests were done for HIV-1 by enzymeimmunosorbent (ELISA) and assay immunoblotting, for HIV-2 by immunoblotting or by competition peptide ELISA, and for HTLV types I and II by immunoblotting. Cultures of peripheral blood mononuclear cells were assessed for p24 Gag antigen and by polymerase chain reaction amplification of DNA primers. Two of the patients were gay men, one was a woman who had received a blood transfusion, and two were heterosexual men. The patients were investigated for other causes of
serological linked
immunodeficiency, including malignant disease, but without success. Evidence of reverse transcriptase activity was found in two of them. At the meeting Dr Curran (head of the CDC HIV-AIDS programme) and Dr David Ho reported on other cases currently under investigation, and scientists at major HIV treatment centres in Europe and America described similar patients. In contrast to patients reported earlier, who presented with HIVnegative Kaposi’s sarcoma,l,2 the latest group had opportunistic infections typical of the clinical picture of HIV. Dr Curran ran into semantic difficulties as he attempted to distinguish these rare cases from the CDC surveillance case definition of AIDS; in fact the term "acquired immunedeficiency" describes them precisely, except for the absence of obvious HIV. This development raises a number of questions that must be addressed. Does a new virus causing a syndrome similar to HIV infection exist? Although numerous experts carefully stated that no such aetiological factor has been defined, it is possible that such an agent may yet be identified. These are case-reports rather than planned series, so there are several gaps in the information. For example, the CD4 lymphocyte depletion suggests an agent that is both lymphotropic and cytopathic. Was a cytopathic effect seen in the cultures? And what does the evidence of reverse transcriptase (RT) activity mean? RT activity can be seen with endogenous retroviruses or retroids, virus particles. As with HIV, it must be confirmed that patients, especially the cases described, have antibodies to the putative agent before a definite link can be established. Finally, why are all these cases, from disparate locations, suddenly appearing now? The media has created a panic with stories of a cover-up as well as public health concerns about blood supply and safety. The public does have a right to know-but know what? Further investigation is necessary to determine whether a new rare virus has indeed been identified or whether HIV is merely revealing to us another side of its tantalising face.
(p273). Laurence et al report five individuals from the New York City area who presented with clinical evidence of immunodeficiency and CD4 depletion but who had no evidence of human immunodeficiency virus (HIV) 1 or 2 infection. They have all been investigated by serological and molecular techniques; standard
1. Soriano V, Hewlett I, Friedman-Kien A, Tor J, Huang YI, Epstein J Definitive exclusion of HIV infection in a bisexual man with Kaposi’s sarcoma: suggestions of a pathogenic model of KS. VII International Conference on AIDS. Florence, Italy, June 16-21, 1991, Abstr TuB82. 2. Safai B, Peralata H, Menzies K, et al. Kaposi’s sarcoma among HIV seronegative high risk populations. VII International Conference on AIDS. Florence, Italy, June 16-21, 1991, Abstr TuB83.
In most studies total crosslinks have been determined after acid hydrolysis of urine. More recently, simplified methods have been developed based on the consistent proportion of free crosslinks present in urine21,22 or on the assay of specific peptides derived from bone.23 Such simple, direct urinary immunoassays for measurement of bone resorption will have many clinical applications not only in the diagnosis and monitoring of therapy in metabolic bone diseases but also as part of screening programmes to assess the risks of osteoporotic fracture. 1. Delmas PD. Clinical use of biochemical markers of bone remodeling in osteoporosis. Bone 1992; 13: S17-S21. 2. Eyre DR. New markers of bone resorption. J Clin Endocrinol Metab 1992; 74: 470A-C. 3. Eyre DR, Koob TJ, Van Ness KP. Quantitation of hydroxypyridinium crosslinks in collagen by high-performance liquid chromatography. Anal Biochem 1984; 137: 380-88. 4. Black D, Duncan A, Robins SP. Quantitative analysis of the pyridinium crosslinks of collagen in urine using ion-paired reversed-phase high-performance liquid chromatography. Anal Biochem 1988; 169: 197-203. 5. Uebelhart D, Gineyts E, Chapuy M-C, Delmas PD. Urinary excretion of pyridinium crosslinks: a new marker of bone resorption in metabolic bone disease. Bone Min 1990; 8: 87-96. 6. Robins SP, Black D, Paterson CR, Reid DM, Duncan A, Seibel MJ. Evaluation of urinary hydroxypyridinium crosslink measurements as resorption markers in metabolic bone diseases. Eur J Clin Invest 1991; 21: 310-15. 7. McLaren AM, Hordon LD, Bird HA, Robins SP. Urinary excretion of
pyridinium crosslinks of collagen in patients with osteoporosis and the effects of bone fracture. Ann Rheum Dis 1992; 51: 648-51. 8. Seibel MJ, Gartenberg F, Silverberg SJ, Ratcliffe A, Robins SP, Bilezikian JP. Urinary hydroxypyridinium crosslinks of collagen as markers of bone resorption in primary hyperparathyroidism. J Clin Endocrinol Metab 1992; 74: 481-86. 9. Uebelhart D, Schlemmer A, Johansen JS, Gineyts E, Christiansen C, Delmas PD. Effect of menopause and hormone replacement therapy on the urinary excretion of pyridinium cross-links. J Clin Endocrinol Metab 1991; 72: 367-73. 10. Eastell R, Hampton L, Colwell A, et al. Urinary collagen crosslinks are highly correlated with radioisotopic measurements of bone resorption. In: Christiansen C, Overgaard K, eds. Osteoporosis 1990. Copenhagen: Osteopress ApS, 1990: 469-70. 11. Delmas PD, Schlemmer A, Gineyts E, Riis B, Christiansen C. Urinary excretion of pyridinoline crosslinks correlates with bone turnover measured on iliac crest biopsy in patients with vertebral osteoporosis. J Bone Min Res 1991; 6: 639-44. 12. Colwell A, Eastall R, Assiri AM A, Russell RGG. Effect of diet on deoxypyridinoline excretion. In: Christiansen C, Overgaard K, eds. Osteoporosis 1990. Copenhagen: Osteopress ApS, 1990: 590-91. 13. Seibel MJ, Duncan A, Robins SP. Urinary hydroxy-pyridinium crosslinks provide indices of cartilage and bone involvement in arthritic diseases. J Rheumatol 1989; 16: 964-70. 14. Harvey RD, McHardy KC, Paterson F, Bewsher PD, Duncan A, Robins SP. Measurement of bone collagen degradation in hyperthyroidism and during thyroxine replacement therapy using pyridinium crosslinks as specific urinary markers. J Clin Endocrinol Metab 1991; 72: 1188-94. 15. Paterson CR, Robins SP, Horobin JM, Preece PE, Cuschieri A. Pyridinium crosslinks as markers of bone resorption in patients with breast cancer. Br J Cancer 1991; 64: 884-86. 16. Body JJ, Delmas PD. Urinary pyridinium cross-links as markers of bone resorption in tumor-associated hyperglycemia. J Clin Endocrinol Metab 1992; 74: 471-75. 17. Fujimoto D, Suzuki M, Uchiyama A, Miyamoto S, Inoue T. Analysis of pyridinoline, a crosslinking compound of collagen fibers, in human urine. J Biochem 1983; 94: 1133-36. 18. Beardsworth LJ, Eyre DR, Dickson IR. Changes with age in the urinary excretion of lysyl- and hydroxylysylpyridinoline, two new markers of bone collagen turnover. J Bone Min Res 1990; 5: 671-76. 19. Schlemmer A, Hassager C, Jensen SB, Christiansen C. Marked diurnal variation in urinary excretion of pyridinium cross-links m premenopausal women. J Clin Endocrinol Metab 1992; 74: 476-80. 20. Eastell R, Calvo MS, Burritt MF, et al. Abnormalities in circadian patterns of bone resorption and renal calcium conservation in type I osteoporosis. J Clin Endocrinol Metab 1992; 74: 487-94.
SP, Duncan A, Riggs BL. Direct measurement of free hydroxy-pyridinium crosslinks of collagen in urine as new markers of bone resorption in osteoporosis. In: Christiansen C, Overgaard K, eds. Osteoporosis 1990. Copenhagen: Osteopress ApS, 1990: 465-68. 22. Robins SP, Duncan A, McLaren AM. Structural specificity of an ELISA for the collagen crosslink, pyridinoline: implications for the measurement of free pyridinium crosslinks as indices of bone resorption in metabolic bone diseases. J Bone Min Res 1991; 6 (suppl): 642a. 23. Hanson DA, Eyre DR. A specific immunoassay for bone resorption based on cross-linked collagen peptides in urine. J Bone Min Res 1991; 6 (suppl): 669a. 21. Robins
Cricket under stress Cricket, that summer anchor of the very identity of many a nation, is threatened by a new disease-spinal stress fractures in fast bowlers. Or so one might think from headlines in the lay press. What is the truth behind such stories? Although renewed interest in spinal stress fractures in fast bowlers gives the impression that a "new" condition has arrived and is about to cull the brightest bowling prospects, the vulnerability of sportsmen and sportswomen to stress fractures is well recognised. Such fractures characteristically occur in a normal bone that is subject to repeated cyclical loading, the load being less than that which causes acute fracture. Bowlers typically get a bilateral fracture of the pars interarticularis of one of their lower lumbar vertebrae (spondylolysis), which is believed to be related to the hyperextension that precedes delivery. A contributory factor is the force of the delivery (to which today’s armour-clad batsmen bear witness), since fast bowlers are most afflicted. Several fast bowlers have had their
interrupted by a spondylolysis. Anxiety about the impact of stress fractures will not have been lessened by a report by Hardcastle and colleagues,1 who conducted a detailed study, including computed tomography (CT) and magnetic resonance imaging (MRI), of 24 fast bowlers aged 16-18 years who had been selected for special training careers
in Western Australia. Pars interarticularis defects diagnosed in 54%, and 63% had disc degeneration. These alarming figures warrant further were
analysis. The reported frequency of isthmic spondylolysis in European populations is about 5-7%,zand this figure is higher in sportsmen and sportswomen. However, such figures are based on standard radiographic examinations and predate the use of MRI and CT. Moreover, in the Australian series 50% of the defects were unilateral; such defects are rarely identified by conventional
radiography
and
are
not
always
symptomatic. This condition has previously been described in detail in a fast bowler.3Whereas the bilateral lesion is thought to be the result of extension, the main cause for the unilateral lesion may well be rotation. Symptomless lesions on the opposite side at the same level can be a predisposing factor. The high figure for defects in the lumbar spine in the Australian series therefore of detection.
largely reflects sensitive new methods
280
What about disc degeneration? Figures for this condition are highly influenced by the method of definition; in the report by Hardcastle and colleagues, degeneration was probably determined by MRI, although this is not clearly stated. Such changes have been noted in 35% of young symptom-free subjects4,5 and might be expected to be higher in young athletes. In a control series of 13 batsmen described by Hardcastle et al, the frequency of disc degeneration was 54%. Thus fast bowling might contribute to disc degeneration in young men but is not the sole cause. Surveys with up-to-date sensitive techniques of investigation will always produce abnormal findings, which should be regarded cautiously, especially if they are not symptomatic. If they are, treatment must be considered. In most cases a stress fracture will heal with rest from the activity that initiated it. When it does not, selective surgery should be contemplated. Whether a stress fracture of the lumbar spine in a fast bowler constitutes an industrial or occupational disease has not been discussed. 1. Hardcastle
P, Annear DH, Foster DH, et al. Spinal abnormalities in young fast bowlers. J Bone Joint Surg 1992; 74B: 421-25. 2. Wynne-Davies R, Scott JHS. Inheritance and spondylolisthesis: a radiographic family survey. J Bone Joint Surg 1979; 61B: 301-05. 3. Weatherley CR, Mehdian H, Vanden Berghe L. Low back pain with fracture of the pedicle and contralateral spondylolysis. J Bone Joint Surg 1991; 73B: 990-93. 4. Evans W, Jobe W, Seibert C. Cross-sectional prevalence study of lumbar disc degeneration in a working population. Spine 1989; 14: 60-64. 5. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg 1990; 72A: 403-08.
AIDS minus HIV? Those attending the VIII International Conference AIDS in Amsterdam (July 19-24) were told of the dramatic discovery of a "new" virus not at a plenary session but in their hotel rooms on television. Peer-reviewed work presented in the scientific meetings was sidelined by an announcement to the press by Dr Sudhir Gupta in Irvine, California. Dr Gupta claims that the agent, human intracisternal virus (or MTV, media-transmitted virus, as delegates were quick to dub it) has caused an AIDS-like disease in a 66-year-old woman. The resultant stir forced an emergency session in Amsterdam, where Dr J. Laurence, Dr J. Curran, Dr A. Fauci, and others presented some of the privileged data from the Centers for Disease Control (CDC) and the National Institute of Alergy and Infectious Diseases concerning similar cases before publication of Laurence’s article in this issue of The Lancet on
tests were done for HIV-1 by enzymeimmunosorbent (ELISA) and assay immunoblotting, for HIV-2 by immunoblotting or by competition peptide ELISA, and for HTLV types I and II by immunoblotting. Cultures of peripheral blood mononuclear cells were assessed for p24 Gag antigen and by polymerase chain reaction amplification of DNA primers. Two of the patients were gay men, one was a woman who had received a blood transfusion, and two were heterosexual men. The patients were investigated for other causes of
serological linked
immunodeficiency, including malignant disease, but without success. Evidence of reverse transcriptase activity was found in two of them. At the meeting Dr Curran (head of the CDC HIV-AIDS programme) and Dr David Ho reported on other cases currently under investigation, and scientists at major HIV treatment centres in Europe and America described similar patients. In contrast to patients reported earlier, who presented with HIVnegative Kaposi’s sarcoma,l,2 the latest group had opportunistic infections typical of the clinical picture of HIV. Dr Curran ran into semantic difficulties as he attempted to distinguish these rare cases from the CDC surveillance case definition of AIDS; in fact the term "acquired immunedeficiency" describes them precisely, except for the absence of obvious HIV. This development raises a number of questions that must be addressed. Does a new virus causing a syndrome similar to HIV infection exist? Although numerous experts carefully stated that no such aetiological factor has been defined, it is possible that such an agent may yet be identified. These are case-reports rather than planned series, so there are several gaps in the information. For example, the CD4 lymphocyte depletion suggests an agent that is both lymphotropic and cytopathic. Was a cytopathic effect seen in the cultures? And what does the evidence of reverse transcriptase (RT) activity mean? RT activity can be seen with endogenous retroviruses or retroids, virus particles. As with HIV, it must be confirmed that patients, especially the cases described, have antibodies to the putative agent before a definite link can be established. Finally, why are all these cases, from disparate locations, suddenly appearing now? The media has created a panic with stories of a cover-up as well as public health concerns about blood supply and safety. The public does have a right to know-but know what? Further investigation is necessary to determine whether a new rare virus has indeed been identified or whether HIV is merely revealing to us another side of its tantalising face.
(p273). Laurence et al report five individuals from the New York City area who presented with clinical evidence of immunodeficiency and CD4 depletion but who had no evidence of human immunodeficiency virus (HIV) 1 or 2 infection. They have all been investigated by serological and molecular techniques; standard
1. Soriano V, Hewlett I, Friedman-Kien A, Tor J, Huang YI, Epstein J Definitive exclusion of HIV infection in a bisexual man with Kaposi’s sarcoma: suggestions of a pathogenic model of KS. VII International Conference on AIDS. Florence, Italy, June 16-21, 1991, Abstr TuB82. 2. Safai B, Peralata H, Menzies K, et al. Kaposi’s sarcoma among HIV seronegative high risk populations. VII International Conference on AIDS. Florence, Italy, June 16-21, 1991, Abstr TuB83.
