- Email: [email protected]
HIV ANTIGEN TESTING
565 in these departments. The National Blood Transfusion Service (which in most instances does not provide a hospital blood bank service), is provided by twenty transfusion centres and is the responsibility of the consultants in these centres. As you state "In Britain, blood transfusion is closely allied to haematology and few can doubt the considerable advantages that this brings". Why disturb this arrangement which has worked well since the 1940s and seek to create a separate discipline, as you suggest? If training in blood transfusion does require to be widened, let this be considered within our current review of all training and examinations in pathology.
haematologists
Royal College of Pathologists, 2 Carlton House Terrace,
BARBARA E. CLAYTON,
London SW1Y 5AF
President
SIR,—In the UK blood transfusion is part of the specialty of haematology, and training programmes are approved and monitored by the JCHMT on whose Specialist Advisory Commitee (SAC) sit representatives of the Royal Colleges of Physicians, the Royal College of Pathologists, and the British Society for Haematology. The SAC has always included a regional blood transfusion director. A successful applicant for a consultant post will, after two to three years’ general medical training, normally have completed a JCHMT approved higher specialist training programme lasting at least three years which will include at least six months in a blood transfusion centre or, exceptionally, three months in a transfusion centre and
three months in an approved hospital transfusion service. Completion of this training will normally be marked by success in the final MRC Path examination in haematology. This examination includes a compulsory question on blood transfusion in the written paper, at least half a day spent solving practical blood transfusion problems, a clinical examination involving patients, and a searching oral examination. The criticism, from a Council of Europe working party, of lack of coordination, fragmentation, and inadequate clinical monitoring is not merited in the UK. There is no room for complacency but a new specialty "with a distinct training programme" hardly seems necessary. The clinical aspects of blood transfusion are essentially hospital based and are the responsibility of consultant haematologists. Regional transfusion centres and hospital blood transfusion services already work closely together and consultants in regional centres frequently have sessions in neighbouring hospitals and regularly advise on transfusion matters. Your suggestion that the certificate of transfusion medicine of the Royal College of Physicians of Edinburgh is an important step in the development of transfusion medicine as a recognised clinical specialty is hardly supported by the modest entry requirement of two years’ postgraduate medical experience plus at least twelve months’ experience of hospital blood banking or other experience approved by the examination board. Haematology requires a basic knowledge that extends into immunology, virology, obstetrics, therapeutics, chemical
and good manufacturing practice. Haematologists heavily involved in areas such as plasmapheresis, cardiac surgery, and paediatrics. The training is exacting and not likely to be improved significantly by the creation of a new specialty manned by holders of a certificate of transfusion medicine. Apart from this particular recommendation the general tenor of your proposals for the practice and development of blood transfusion are consistent with current UK practice and training in haematology and blood transfusion.
planned not only to satisfy the technical requirements but also to ensure a living environment that would contribute to the wellbeing of both patients and staff. Corridors, rooms, and operating theatres got colour schemes that made them works of art in themselves; the sculptural aspects were integrated with the architecture, and even the uniforms of the staff were planned as part of the overall scheme. The enthusiasm of all concerned was terrific-all, that is, except the bureaucrats. There would be some extra costs. I still remember my brother’s rage and grief when the first model rooms and corridors were enveloped in "hospital grey" from floor to ceiling. Paintings, lithographs, and sculptures are fine, but it takes more than that to make traditional hospital architecture worth living in. 43 avenue du Lignon, 1219 Le Lignon, Switzerland
EILIF LIISBERG
HIV ANTIGEN TESTING
SIR,—Following infection with human immunodeficiency virus type 1 (HIV-1) the viral antigen p24 can be detected in serum before antibody develops’ and also later in the infection especially if the individual becomes ill.2 We have assessed the prevalence of HIV antigen (HIV Ag) and antibodies in sera from patients in high-risk groups (mostly homosexual/bisexual men) and in low-risk controls.
We used an antigen capture ELISA (Abbott Laboratories) and sought antibodies to the p24 (core) and gp41 (envelope) proteins by competitive ELISA (Abbott) with recombinant antigens.’ Table I shows the HIV Ag/HIV Ab patterns found in patients with AIDS, persistent generalised lymphadenopathy, and AIDSrelated complex; in high-risk symptomless individuals who were positive or negative in a competitive ELISA for anti-HIV (Wellcome Diagnostics); and in patients (controls) with diseases such as rheumatoid arthritis, systemic lupus erythematosus, and hepatitis B or other viral infections. Specificity was checked by a neutralisation test with prior treatment of serum by a human polyclonal antibody to HIV-1. This abolished the reactivity in the antigen test in all individuals who had other serological evidence of HIV infection. 3 of the 68 controls (2 rheumatoid arthritis, 1 hepatitis B) had a positive reaction for HIV Ag on initial and repeat testing but this was unaffected by pretreatment with specific antibody. This neutralisation test is important to confirm the specificity of the antigen test. TABLE I-HIV ANTIGEN AND ANTIBODY* TEST RESULTS
°
engineering, bacteriology, are
also
department of Haematology, Manchester Royal Infirmary,
J. E. MACIVER,
Manchester M13 9WL
President, British Society for Haematology
HOSPITAL DESIGN
SIR,-Dr Baron’s article on art in hospitals (Dec 20/27, p 1438) reminded me of my late brother’s fight in 1953 with bureaucracy when trying-for the first time in history-to plan and build a hospital in close collaboration with patients, artists, and hospital staff. Painters, sculptors, and colour psychologists worked closely with the architect (my brother), who believed, with all the vision of a 25-year-old, that hospitals were meant to be more than square metres of rooms and high technology. The total environment was
*E=ann-gp41 (envelope), C=anti p24 (core); += antibody positive, —=antibody negative. t3 were antigen positive, not confirmable by neutralisation. tAIDS =acquired immunodeficiency syndrome (Centers for Disease Control group IV, subgroups Cl or D); PGL=persistent generalised lymphadenopathy (group Ii1); ARC = AIDS-related complex (group IV, subgroups A or C2).
Of the 32 patients with ARC (table I) 26 were a cohort recruited February and November, 1985, and all have so far been followed up for 13-23 months. There appeared to be a significant association between HIV Ag positivity and/or p24 antibody negativity in patients with ARC and progression to AIDS in this cohort (table 11). This supports the possible predictive value of HIV Ag testing2 and correlates with the reduction in p24 antibody levels demonstrated in HIV-infected patients in whom clinical manifestations developed.3 This new test may be used to select patients for clinical trials of drugs active against retroviruses and may also provide a more direct between
566 TABLE II-ARC PATIENTS: OUTCOME AFTER
13-23 MONTHS OF
FOLLOW UP
approach than reverse transcriptase assay as a method of assessing viral culture. However, the presence or absence of HIV antigen or p24 antibody does not yet have any certain predictive value: individuals may remain antigen positive for a long time without progressing to AIDS while those with p24 antibody may progress to AIDS without becoming antigen positive. We thank Dr A. J. Pinching, Dr J. R. W. Harris and the staff of St Mary’s Hospital for their cooperation, Abbott Laboratories for the use of kits and equipment, and Ms D. Patel for clerical assistance.
C. KENNY
J. PARKIN Departments of Virology and Immunology, St Mary’s Hospital Medical School, London W2 1PG; and Praed Street Clinic, St Mary’s Hospital
G. UNDERHILL
HIV antigenaemia has been detected before HIV antibody appearance4.5 but not temporally linked to acute disease. The HIV antigen test is useful for an early definitive diagnosis of acute HIV disease. Particularly in acute encephalopathy,6 an early aetiological diagnosis may obviate the need for unnecessary procedures and therapy. As HIV infection spreads beyond the currently recognised high-risk groups, detection of HIV antigenaemia will become increasingly useful in many clinical and laboratory situations. Departments of Microbiology and Infectious Diseases, Northwick Park Hospital and Clinical Research Centre, Harrow HA1 3UJ
R. A. WALL D. W. DENNING A. AMOS
Cooper DA, Gold J, Maclean P, et al. Acute AIDS retrovirus infection. Definition ofa clinical illness associated with seroconversion. Lancet 1985; i: 537-40. 2. Denning DW, Anderson J, Rudge P, Smith H Acute myelopathy associated with primary infection with human immunodeficiency virus. Br Med J 1987; 294: 1.
143-44.
(GACRIA) for anti HTLV LAV and its use as a Virol 1986; 14: 387-97. 4. Allain JP, Laurian Y, Paul DA, Senn D. Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs Lancet 1986; ii: 1233-36. 5. Goudsmit J, de Wolf F, Paul D, et al. Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic infection. Lancet 1986; ii: 177-80. 6. Carne CA, Tedder RS, Smith A, et al. Acute encephalopathy coincident with seroconversion for anti-HTLV-III. Lancet 1985; ii 1206-08. 3.
Parry JV. An IgG capture
assay
confirmatory test. J Med
N. SHAH B. BURNELL
E. OSBORNE D.
J. JEFFRIES
Allain JP, Laurian Y, Paul DA, Senn D. Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs. Lancet 1986; ii: 1233-36. 2. Lange JMA, Paul DA, Huisman HG, et al. Persistent HIV antigenaemia and decline 1.
of HIV core antibodies associated with transition to AIDS. Br Med J 1986; 293: 1459-62. 3. Weber JN, Clapham PR, Weiss RA, et al. Human immunodeficiency virus infection in two cohorts of homosexual men: Neutralising sera and association of anti-GAG antibody with prognosis. Lancet 1987; i: 119-22.
HIV ANTIGENAEMIA IN ACUTE HIV INFECTION
SIR,-Human immunodeficiency virus (HIV) infection may as an acute illness, probably occurring shortly after virus acquisition.1.2 Most cases have been diagnosed retrospectively following seroconversion. We have seen two patients with a clinical picture compatible with acute HIV disease, and have tested their acute phase sera for HIV antigen. The first patient was a 38-year-old homosexual man who presented with a 2-day history of fever, sore throat, and diarrhoea. He had palatal ulceration and petechiae, conjunctivitis, cervical adenopathy, and a widespread maculopapular rash. Serum obtained on day 2 of the illness was negative for HIV antibody by a competitive enzyme-linked immunosorbent assay (’Wellcozyme’), present
but seroconversion occurred 6-8 weeks after the onset of illness. The second patient was a 29-year-old homosexual man who presented with a 2t-week history of sore throat and fever. He had conjunctivitis, pharyngitis, a truncal macular rash, and
hepatosplenomegaly. He subsequently had myelopathy.2 Serum obtained on day 17 (after admission) had an equivocal antibody result but was subsequently shown to contain HIV IgM by a capture radioimmunoassay (MACRIA).2,3 Neither patient had serological evidence of active infection with syphilis, Epstein-Barr virus, rubella, cytomegalovirus, adenovirus, toxoplasma, or Mycoplasma pneumoniae. Acute phase sera, stored at - 20°C, was tested for HIV antigen with an enzyme immunoassay (Abbott). Both patients had detectable HIV antigenaemia at the time of acute illness when tests for HIV antibody were negative or equivocal (table). DETECTION OF HIV ANTIGENAEMIA IN ACUTE PHASE SERA
HIV ANTIGEN DETECTION IN ROUTINE BLOOD DONOR SCREENING
SIR,—After human immunodeficiency virus (HIV) infection HIV antigen seems to appear in serum some weeks before antibodies become detectable.1,2 While HIV infection is on the increase, HIV antigenaemia can be anticipated in some blood donors, and antibody screening cannot exclude every infected unit donated at an early stage of infection. To reduce further the risk of transfusion-associated HIV infection we introduced routine HIV testing by Abbott enzyme immunoassay on Dec 19,1986. The test takes about 24 hours but we accepted this disadvantage because of the severe consequences of HIV infection. To date 2096 blood donors have been tested for HIV besides anti-HIV. Negative samples have had a mean extinction value of 0.053 (SD 0-012).9 sera were repeatedly reactive (0-43%) but none of them could be neutralised, indicating false-positive reactions. Although blood transfusion and blood products are not common routes of spreading HIV infection, HIV antigen testing should be used to close the diagnostic "window" between infection and antibody production. Of the 2096 blood donors tested so far none has been positive for HIV antibody or for HIV antigen but we see no reason for stopping this screening policy. Saarland Blood Bank, Saarbrucken, West Germany
6600
REINHARD STUTE
1. Goudsmit J,
de Wolf F, Paul DA, et al. Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic
infection. Lancet 1986; ii: 177-80. 2. Allain JP, Laurian Y, Paul DA. Senn
D, Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs. Lancet 1986; ii: 1233-36.
DETECTION OF HIV ANTIGENS IN ELUATES FROM WHOLE BLOOD COLLECTED ON FILTERPAPER
SIR,—The detection of virus antigens in the serum or plasma from individuals infected with human immunodeficiency virus (HIV)1,2 can supplement tests for antibodies in the diagnosis ofHIV infection because antigens are often detectable in blood weeks to months before antibodies appear.1 HIV antigen measurements also seem to have prognostic relevance.2 Analysis of eluates of whole blood dried on filterpaper is useful for antibody assays when only small amounts of blood can be taken or when cold storage and transportation present special problems, as often happens in developing countries. To study the possibility of HIV antigen detection by filterpaper method we have tested for antigen in 76 paired sera and eluates from drops of blood dried on filterpaper. 37 samples were from patients with AIDS or AIDSrelated disorders and 39 were from healthy individuals at risk of
haematologists
Royal College of Pathologists, 2 Carlton House Terrace,
BARBARA E. CLAYTON,
London SW1Y 5AF
President
SIR,—In the UK blood transfusion is part of the specialty of haematology, and training programmes are approved and monitored by the JCHMT on whose Specialist Advisory Commitee (SAC) sit representatives of the Royal Colleges of Physicians, the Royal College of Pathologists, and the British Society for Haematology. The SAC has always included a regional blood transfusion director. A successful applicant for a consultant post will, after two to three years’ general medical training, normally have completed a JCHMT approved higher specialist training programme lasting at least three years which will include at least six months in a blood transfusion centre or, exceptionally, three months in a transfusion centre and
three months in an approved hospital transfusion service. Completion of this training will normally be marked by success in the final MRC Path examination in haematology. This examination includes a compulsory question on blood transfusion in the written paper, at least half a day spent solving practical blood transfusion problems, a clinical examination involving patients, and a searching oral examination. The criticism, from a Council of Europe working party, of lack of coordination, fragmentation, and inadequate clinical monitoring is not merited in the UK. There is no room for complacency but a new specialty "with a distinct training programme" hardly seems necessary. The clinical aspects of blood transfusion are essentially hospital based and are the responsibility of consultant haematologists. Regional transfusion centres and hospital blood transfusion services already work closely together and consultants in regional centres frequently have sessions in neighbouring hospitals and regularly advise on transfusion matters. Your suggestion that the certificate of transfusion medicine of the Royal College of Physicians of Edinburgh is an important step in the development of transfusion medicine as a recognised clinical specialty is hardly supported by the modest entry requirement of two years’ postgraduate medical experience plus at least twelve months’ experience of hospital blood banking or other experience approved by the examination board. Haematology requires a basic knowledge that extends into immunology, virology, obstetrics, therapeutics, chemical
and good manufacturing practice. Haematologists heavily involved in areas such as plasmapheresis, cardiac surgery, and paediatrics. The training is exacting and not likely to be improved significantly by the creation of a new specialty manned by holders of a certificate of transfusion medicine. Apart from this particular recommendation the general tenor of your proposals for the practice and development of blood transfusion are consistent with current UK practice and training in haematology and blood transfusion.
planned not only to satisfy the technical requirements but also to ensure a living environment that would contribute to the wellbeing of both patients and staff. Corridors, rooms, and operating theatres got colour schemes that made them works of art in themselves; the sculptural aspects were integrated with the architecture, and even the uniforms of the staff were planned as part of the overall scheme. The enthusiasm of all concerned was terrific-all, that is, except the bureaucrats. There would be some extra costs. I still remember my brother’s rage and grief when the first model rooms and corridors were enveloped in "hospital grey" from floor to ceiling. Paintings, lithographs, and sculptures are fine, but it takes more than that to make traditional hospital architecture worth living in. 43 avenue du Lignon, 1219 Le Lignon, Switzerland
EILIF LIISBERG
HIV ANTIGEN TESTING
SIR,—Following infection with human immunodeficiency virus type 1 (HIV-1) the viral antigen p24 can be detected in serum before antibody develops’ and also later in the infection especially if the individual becomes ill.2 We have assessed the prevalence of HIV antigen (HIV Ag) and antibodies in sera from patients in high-risk groups (mostly homosexual/bisexual men) and in low-risk controls.
We used an antigen capture ELISA (Abbott Laboratories) and sought antibodies to the p24 (core) and gp41 (envelope) proteins by competitive ELISA (Abbott) with recombinant antigens.’ Table I shows the HIV Ag/HIV Ab patterns found in patients with AIDS, persistent generalised lymphadenopathy, and AIDSrelated complex; in high-risk symptomless individuals who were positive or negative in a competitive ELISA for anti-HIV (Wellcome Diagnostics); and in patients (controls) with diseases such as rheumatoid arthritis, systemic lupus erythematosus, and hepatitis B or other viral infections. Specificity was checked by a neutralisation test with prior treatment of serum by a human polyclonal antibody to HIV-1. This abolished the reactivity in the antigen test in all individuals who had other serological evidence of HIV infection. 3 of the 68 controls (2 rheumatoid arthritis, 1 hepatitis B) had a positive reaction for HIV Ag on initial and repeat testing but this was unaffected by pretreatment with specific antibody. This neutralisation test is important to confirm the specificity of the antigen test. TABLE I-HIV ANTIGEN AND ANTIBODY* TEST RESULTS
°
engineering, bacteriology, are
also
department of Haematology, Manchester Royal Infirmary,
J. E. MACIVER,
Manchester M13 9WL
President, British Society for Haematology
HOSPITAL DESIGN
SIR,-Dr Baron’s article on art in hospitals (Dec 20/27, p 1438) reminded me of my late brother’s fight in 1953 with bureaucracy when trying-for the first time in history-to plan and build a hospital in close collaboration with patients, artists, and hospital staff. Painters, sculptors, and colour psychologists worked closely with the architect (my brother), who believed, with all the vision of a 25-year-old, that hospitals were meant to be more than square metres of rooms and high technology. The total environment was
*E=ann-gp41 (envelope), C=anti p24 (core); += antibody positive, —=antibody negative. t3 were antigen positive, not confirmable by neutralisation. tAIDS =acquired immunodeficiency syndrome (Centers for Disease Control group IV, subgroups Cl or D); PGL=persistent generalised lymphadenopathy (group Ii1); ARC = AIDS-related complex (group IV, subgroups A or C2).
Of the 32 patients with ARC (table I) 26 were a cohort recruited February and November, 1985, and all have so far been followed up for 13-23 months. There appeared to be a significant association between HIV Ag positivity and/or p24 antibody negativity in patients with ARC and progression to AIDS in this cohort (table 11). This supports the possible predictive value of HIV Ag testing2 and correlates with the reduction in p24 antibody levels demonstrated in HIV-infected patients in whom clinical manifestations developed.3 This new test may be used to select patients for clinical trials of drugs active against retroviruses and may also provide a more direct between
566 TABLE II-ARC PATIENTS: OUTCOME AFTER
13-23 MONTHS OF
FOLLOW UP
approach than reverse transcriptase assay as a method of assessing viral culture. However, the presence or absence of HIV antigen or p24 antibody does not yet have any certain predictive value: individuals may remain antigen positive for a long time without progressing to AIDS while those with p24 antibody may progress to AIDS without becoming antigen positive. We thank Dr A. J. Pinching, Dr J. R. W. Harris and the staff of St Mary’s Hospital for their cooperation, Abbott Laboratories for the use of kits and equipment, and Ms D. Patel for clerical assistance.
C. KENNY
J. PARKIN Departments of Virology and Immunology, St Mary’s Hospital Medical School, London W2 1PG; and Praed Street Clinic, St Mary’s Hospital
G. UNDERHILL
HIV antigenaemia has been detected before HIV antibody appearance4.5 but not temporally linked to acute disease. The HIV antigen test is useful for an early definitive diagnosis of acute HIV disease. Particularly in acute encephalopathy,6 an early aetiological diagnosis may obviate the need for unnecessary procedures and therapy. As HIV infection spreads beyond the currently recognised high-risk groups, detection of HIV antigenaemia will become increasingly useful in many clinical and laboratory situations. Departments of Microbiology and Infectious Diseases, Northwick Park Hospital and Clinical Research Centre, Harrow HA1 3UJ
R. A. WALL D. W. DENNING A. AMOS
Cooper DA, Gold J, Maclean P, et al. Acute AIDS retrovirus infection. Definition ofa clinical illness associated with seroconversion. Lancet 1985; i: 537-40. 2. Denning DW, Anderson J, Rudge P, Smith H Acute myelopathy associated with primary infection with human immunodeficiency virus. Br Med J 1987; 294: 1.
143-44.
(GACRIA) for anti HTLV LAV and its use as a Virol 1986; 14: 387-97. 4. Allain JP, Laurian Y, Paul DA, Senn D. Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs Lancet 1986; ii: 1233-36. 5. Goudsmit J, de Wolf F, Paul D, et al. Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic infection. Lancet 1986; ii: 177-80. 6. Carne CA, Tedder RS, Smith A, et al. Acute encephalopathy coincident with seroconversion for anti-HTLV-III. Lancet 1985; ii 1206-08. 3.
Parry JV. An IgG capture
assay
confirmatory test. J Med
N. SHAH B. BURNELL
E. OSBORNE D.
J. JEFFRIES
Allain JP, Laurian Y, Paul DA, Senn D. Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs. Lancet 1986; ii: 1233-36. 2. Lange JMA, Paul DA, Huisman HG, et al. Persistent HIV antigenaemia and decline 1.
of HIV core antibodies associated with transition to AIDS. Br Med J 1986; 293: 1459-62. 3. Weber JN, Clapham PR, Weiss RA, et al. Human immunodeficiency virus infection in two cohorts of homosexual men: Neutralising sera and association of anti-GAG antibody with prognosis. Lancet 1987; i: 119-22.
HIV ANTIGENAEMIA IN ACUTE HIV INFECTION
SIR,-Human immunodeficiency virus (HIV) infection may as an acute illness, probably occurring shortly after virus acquisition.1.2 Most cases have been diagnosed retrospectively following seroconversion. We have seen two patients with a clinical picture compatible with acute HIV disease, and have tested their acute phase sera for HIV antigen. The first patient was a 38-year-old homosexual man who presented with a 2-day history of fever, sore throat, and diarrhoea. He had palatal ulceration and petechiae, conjunctivitis, cervical adenopathy, and a widespread maculopapular rash. Serum obtained on day 2 of the illness was negative for HIV antibody by a competitive enzyme-linked immunosorbent assay (’Wellcozyme’), present
but seroconversion occurred 6-8 weeks after the onset of illness. The second patient was a 29-year-old homosexual man who presented with a 2t-week history of sore throat and fever. He had conjunctivitis, pharyngitis, a truncal macular rash, and
hepatosplenomegaly. He subsequently had myelopathy.2 Serum obtained on day 17 (after admission) had an equivocal antibody result but was subsequently shown to contain HIV IgM by a capture radioimmunoassay (MACRIA).2,3 Neither patient had serological evidence of active infection with syphilis, Epstein-Barr virus, rubella, cytomegalovirus, adenovirus, toxoplasma, or Mycoplasma pneumoniae. Acute phase sera, stored at - 20°C, was tested for HIV antigen with an enzyme immunoassay (Abbott). Both patients had detectable HIV antigenaemia at the time of acute illness when tests for HIV antibody were negative or equivocal (table). DETECTION OF HIV ANTIGENAEMIA IN ACUTE PHASE SERA
HIV ANTIGEN DETECTION IN ROUTINE BLOOD DONOR SCREENING
SIR,—After human immunodeficiency virus (HIV) infection HIV antigen seems to appear in serum some weeks before antibodies become detectable.1,2 While HIV infection is on the increase, HIV antigenaemia can be anticipated in some blood donors, and antibody screening cannot exclude every infected unit donated at an early stage of infection. To reduce further the risk of transfusion-associated HIV infection we introduced routine HIV testing by Abbott enzyme immunoassay on Dec 19,1986. The test takes about 24 hours but we accepted this disadvantage because of the severe consequences of HIV infection. To date 2096 blood donors have been tested for HIV besides anti-HIV. Negative samples have had a mean extinction value of 0.053 (SD 0-012).9 sera were repeatedly reactive (0-43%) but none of them could be neutralised, indicating false-positive reactions. Although blood transfusion and blood products are not common routes of spreading HIV infection, HIV antigen testing should be used to close the diagnostic "window" between infection and antibody production. Of the 2096 blood donors tested so far none has been positive for HIV antibody or for HIV antigen but we see no reason for stopping this screening policy. Saarland Blood Bank, Saarbrucken, West Germany
6600
REINHARD STUTE
1. Goudsmit J,
de Wolf F, Paul DA, et al. Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic
infection. Lancet 1986; ii: 177-80. 2. Allain JP, Laurian Y, Paul DA. Senn
D, Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs. Lancet 1986; ii: 1233-36.
DETECTION OF HIV ANTIGENS IN ELUATES FROM WHOLE BLOOD COLLECTED ON FILTERPAPER
SIR,—The detection of virus antigens in the serum or plasma from individuals infected with human immunodeficiency virus (HIV)1,2 can supplement tests for antibodies in the diagnosis ofHIV infection because antigens are often detectable in blood weeks to months before antibodies appear.1 HIV antigen measurements also seem to have prognostic relevance.2 Analysis of eluates of whole blood dried on filterpaper is useful for antibody assays when only small amounts of blood can be taken or when cold storage and transportation present special problems, as often happens in developing countries. To study the possibility of HIV antigen detection by filterpaper method we have tested for antigen in 76 paired sera and eluates from drops of blood dried on filterpaper. 37 samples were from patients with AIDS or AIDSrelated disorders and 39 were from healthy individuals at risk of