58
been infected.4 Reduction of number of partners may not be an easy option for women for whom this is a part of their strategy for social and economic survival.6 Women’s subordinate position may not allow them to negotiate successfully the use of safe sex even when they perceive the risk correctly. 7,8 This process is also influenced by men’s attitudes and by notions of masculinity.7 Women’s knowledge, perceptions, choices, and ability to negotiate change with their partners should be understood in the context of the power balance in gender relationships and against its wider historical and cultural basis (Brooke GS, et al, unpublished). An effective contribution to facilitate change towards safer practices for women will need a better understanding of the conditions of transmission to all women, not just those in at-risk categories, of the social and cultural norms that shape women’s perception of risk, and of the constraints that women face to change their risk behaviour and to negotiate safer sex practices with their partners. This in turn will help to develop strategies to redress the lack of power of women to protect themselves against HIV infection and to negotiate safer sex with their partners.8 This lack of power is most often real, not merely perceived, as you suggest in your note. Oxfam, 274 Banbury Road, Oxford OX2 7DZ, UK, and London School of Hygiene and Tropical Medicine, London WC1
CLAUDIA GARCÍA MORENO LAURA C. RODRIGUES
1. Garda Moreno C. AIDS: women and not just transmitters. In: Wallace T, March C, eds. Changing perceptions: gender in development. Oxford: Oxfam, 1990. 2. Carovano K. More than mothers and whores: redefining the AIDS prevention needs of women. Int J Health Ser 1991; 21: 131-42. 3. Rodrigues LC, Garcia Moreno C HIV transmission to women in stable relationships. N Engl J Med 1991; 325: 966. 4. Lindam C, Allen S, Carael M, et al. Knowledge, attitudes, and perceived risk of AIDS among urban Rwandan women: relationship to HIV infection and behaviour change. AIDS 1991; 5: 993-1002. 5. Worth D. Sexual decision-making and AIDS: why condom promotion among vulnerable women is likely to fail. Stud Fam Plann 1989; 20: 297-307. 6. Bassett MT, Mhloyi M. Women and AIDS in Zimbabwe: the making of an epidemic. Int J Health Ser 1991; 21: 143-56. 7. Ankrah EM. AIDS and the social side of health. Soc Sci Med 1991; 32: 967-80. 8. Ulin PR. African women and AIDS: negotiating behavioural change. Soc Sci Med
1992; 34: 63-73.
p
SIR,-Professor Lecatsas and Professor Alexander’s (June 6, 1427) suggestion that the simultaneous appearance of HIV-1and
HIV-2 is evidence for the contamination of poliovirus vaccine being the origin of AIDS is flawed. They need to explain several points. How did two distantly related viruses contaminate the poliovaccine ? Why did this affect African countries more than others with much higher poliovaccine coverage? And why has long-term follow-up of people who received retrovirus-contaminated batches of poliovaccine failed to demonstrate ill health?l A simpler explanation for the simultaneous appearance of two dissimilar viruses lies in the main route of transmission. Since the end of colonialism there have been major social and economic changes in African countries.2 Those relevant to the HIV epidemic include rapid urbanisation across the continent, new road building improving communications, and the mass movement of people as a result of civil war and starvation. Urbanisation is likely to have brought HIV-1and HIV-2 into the cities and towns. Accompanying this urbanisation is greater sexual freedom from loss of tribal traditions, the migrant worker system which encourages multiple sexual partners and stimulates demand for prostitution, along with the growing poverty of many urban women increasing the numbers engaging in prostitution.2 These social factors lead to an increase in the number of new sexual partners, which allows any sexually transmitted disease, especially one with a long duration of infectivity to produce an epidemic. The developing road system allowed the virus to be moved across the continent. The high prevalence in truck drivers testifies to this potential. When people live in small social groups with little movement, as in rural villages, the spread of sexually transmitted diseases is much less than in large heterogeneous populations. HIV-1 has a low probability of infectivity, 0.1 to 0-2 for each relationship,3 and is dependent on the long duration of infectivity to maintain the infection. Major spread could only occur when the behaviour of the population changed, which happened with urbanisation. This theory explains how 2 dissimilar viruses, both sexually transmitted, have suddenly appeared and rapidly produced
major epidemics. Westbrook House, Sharrow Vale Road, Sheffield S11 8EU, UK
AIDS in India SIR,-It is gratifying to note, as your Round-the-World correspondent says (May 9, p 1162), that the Indian Government will be initiating a national control plan for AIDS with the monies given by the World Bank and the World Health Organisation. The plan is necessary because very few preventive measures are being undertaken, despite evidence that the infection is spreading. Although the initiative overcomes governmental reluctance to accept AIDS as a serious public health issue in India, there are several other difficulties that pose a greater challenge. Successful health education campaigns in developed countries may not work very well in India in view of low literacy levels, limited access to radio and television, and large rural populations. Added to these is the growing nationwide problem of alcohol consumption, which encourages casual sex. What is needed, therefore, is an active attempt to educate and modify behaviour through personal intervention. This has been successfully achieved in other communicable diseases and in maternal and child health. There has to be a national programme with community health workers whose primary aim is to inform people of the risks of AIDS and how these risks can be avoided. This may mean also a free distribution of condoms for safer sex which can also be an effective birth control method. Some use of existing communication channels needs to be undertaken simultaneously, aimed especially at urban populations. India needs a comprehensive and complex plan to prevent the spread of AIDS infection, and this may mean personal contact with 900 million people over some time. The current initiative can only be a starting point. Poole
Hospital, Nunthorpe, Middlesbrough, Cleveland TS7 ONJ, UK
Origins of HIV
R. S. RAMAIAH
KEITH NEAL
1. Beale AJ. Polio vaccines: time for a change in immunisation policy? Lancet 1990; 335: 839-42. 2. Larson A. Social context of human immunodeficiency virus transmission in Africa: historical and cultural bases of east and central African sexual relations. Rev Infect
Dis 1989; 2: 716-31. 3.
European Study Group on Heterosexual transmission of HIV. Comparison of female to male and male to female transmission of HIV in 563 stable couples. BMJ 1992; 304: 809-13.
Peripartum HIV seroconversion: a cautionary tale SIR,-A bottle-fed child aged 4 months was admitted to hospital with a provisional diagnosis of bronchiolitis. The child deteriorated and he required ventilation. On day 5 a tracheal aspirate was found to be positive for Pneumocystis carinii by a fluorescence antibody test and on day 6 a serum sample was reported positive for HIV-1/2 antibody. The child died on hospital day 27. The blood was sent to a reference laboratory for confirmatory tests for anti-HIV-1/2 and both gave low positive results. Immunoblot testing was indeterminate but there was reactivity to proteins p24, gp 120, and gp 160; the bands on the blot were definite but not strong, and could be consistent with low antibody level. The polymerase chain reaction (PCR) for HIV RNA was positive and p24 antigen was detected by enzyme immunoassay. During 1991, when this child was born, no HIV antibody positive newborn babies were found in Aberdeen by anonymous Guthrie card testing. The batch of Guthrie cards pertaining to this birth was retested by the department of child health, Yorkhill, Glasgow, and found to be HIV antibody negative. This was confirmed by a reference laboratory. The mother denied that she might be HIV positive. Later her general practitioner was able to discuss with her the death of her
59
child and the HIV testing of her blood. She and this was confirmed
HIV-1/2 seropositive,
was
by
found to be the reference
laboratory (ELISA and
western blot). A p24 test was weakly not be could neutralised and was of uncertain clinical but positive significance. A sample of her blood that had been sent for rubella antibody testing during the first trimester had been stored in the virus laboratory. This was tested and found to be negative for HIV-1/2 antibody by EIA and for HIV p24 antigen. The mother seroconverted towards the end of her pregnancy or immediately afterwards, and the associated viraemia resulted in a massive infection of her baby. There are several lessons to be learned from this case. Antenatal testing may not identify those who are HIV seropositive if testing is done in the "window" before seroconversion. The Guthrie card screening in this case was correct (the result was not a false negative) but the danger to staff from such a mother and baby identified as HIV negative at the time of delivery illustrates the need for strict policies for all deliveries, remembering the general caution that "blood is dangerous". Medical staff need to be aware of the possibility of HIV infection in a child when the differential diagnosis proves difficult. The HIV infection ran a very rapid course in this child and the presumed high level of viraemia poses a risk for carers.
We thank the virus
laboratory, department
of medical
on
stored
serum
by RT-PCR.
A = negative buffer control; B=serum from seronegative control; C-F seronegative sera samples from donor (C=Aug 8, D =June 27, E=April 17, F =Feb 6) Arrow indicates specific segment amplified with SK38/ SK39 and hybridised with SK19; PR = unreacted SK19
microbiology,
Foresterhill, Aberdeen; Dr John F. Peutherer, department of bacteriology, University of Edinburgh; and Dr E. A. C. Follett, Ruchill Hospital, Glasgow, for their help
Department of Public Health Medicine, Grampian Health Board, Aberdeen AB9 8QP
J. S. BERKELEY
General Practice, Aberdeen
P. C. FOGIEL
Department of Paediatrics, Aberdeen Royal Infirmary
A. D. KINDLEY
Department of Virology, Royal Infirmary
M. A. J. MOFFAT
Aberdeen
Detection of HIV-1 RNA
Transmission of HIV-1 from seronegative but PCR-positive blood donor SIR,-Seroconversion to HIV-1 usually occurs within 6 months of exposure1 but because there is a serological "window" transmission from infected donors screened as seronegative for HIV-1is still encountered.2,3 The polymerase chain reaction (PCR) permits identification of HIV-1sequences in patients who have not yet seroconverted.4 A seronegative individual has been shown to have transmitted HIV-1 to organ recipients.sWe describe here a transmission of HIV-1from a seronegative but PCR-positive blood donor; PCR on serum stored from previous donations permitted retrospective detection of HIV-1infection before seroconversion. A 22-year-old man complained at the end of August, 1991, of fever without other symptoms. He had generalised lymphadenopathies. He had had unprotected sex with multiple male partners. He had antibodies to HIV-1(enzyme immunoassay [EIA] and western blot) on a blood sample drawn on Aug 20,1991. Between June, 1990, and August, 1991, he had donated blood four times (June 27,1990, and Feb 6, April 17, and Aug 8,1991). The four donations had been screened negative for HIV-1by EIA. He had denied risk factors for HIV-1 infection in questionnaires completed before every donation and never used the confidential unit exclusion procedure. Serum from the four seronegative donations, which had been kept at - 70°C, were analysed by PCR for HIV-1RNA. RNA was extracted with guanidinium, subjected to reverse transcription (RT), and amplified with SK38/SK39 (RT-PCR).6 Amplified products were detected with 32P-labelled SK19 after gel
electrophoresis (see figure). The Aug 8, 1991, serum was positive. PCR without the RT step was negative (not shown), reflecting absence of proviral DNA. The same serum was re-tested for HIV-1 antibodies and found to be negative by EIA and western blot; a weak gpl60 band was noticed on radioimmunoprecipitation assay;
p24 antigen was undetectable. Two recipients of blood products from the PCR-positive donation were identified. One had died, of a disease unrelated to
HIV-1,3 weeks after the transfusion. The other, the recipient of a platelet unit and having no risk factors for HIV-1 infection, seroconverted after the transfusion. A recipient of packed red blood cells from the April 17, 1991, donation (seronegative and PCR negative for HIV-1) was seronegative after that transfusion. Donors in the phase preceding seroconversion may be viraemic and their blood could transmit HIV-1.3,4 Since serum rarely contains proviral DNA4,6 detection of viral genome needs RT-PCR. This observation demonstrates that in investigation of recipient seroconversion after blood transfusion combined RT and PCR on stored donor sera may sometimes identify an infectious seronegative donor. Departments of Infectious Diseases and Microbiology, Hôpital Notre-Dame, Montreal, Quebec, Canada H2L 4M1; and Hôpital Saint-Luc, Montreal, Canadian Red Cross Society, Blood Services (Montreal Centre), and Federal Centre for AIDS, Ottawa
FRANCOIS COUTLÉE GILLES DELAGE FRANCOIS LAMOTHE SHARON CASSOL FRANCINE DÉCARY
Horsburgh CR, Jason J, Longini IM, et al. Duration of human immunodeficiency virus infection before detection of antibody. Lancet 1989; ii: 637-40. 2. Ward JW, Holmberg SD, Allen JR, et al. Transmission of human immunodeficiency virus (HIV) by blood transfusion screened as negative for HIV antibody. N Engl J 1.
Med 1988; 318: 473-78. 3. Irani MS, Dudley AW, Lucco LJ. Case of HIV-1 transmission by antigen-positive antibody-negative blood. N Engl J Med 1991; 325: 1174. 4. Hewlett IK, Gregg RA, Ou C-Y, et al. Detection in plasma of HIV-1 specific DNA and RNA by polymerase chain reaction before and after seroconversion. J Clin
Immunoassay 1988; 11: 161-64. RJ, Holmberg SD, Hurwitz RL, et al. Transmission of human immunodeficiency virus type 1 from a seronegative organ donor. N Engl J Med
5. Simonds
1992; 326: 726-32. 6.
Holodniy M, Katzenstein DA, Israelski DM, Mengan TC. Reduction in plasma human immunodeficiency virus ribonucleic add after dideoxynucleoside therapy as determined by the polymerase chain reaction. J Clin Invest 1991; 88: 1755-59.
Betel nut
chewing and asthma
SIR,-Dr Taylor and colleagues (May 9, p 1134) report two Asian patients who were often admitted with acute severe asthma, probably linked to betel nut chewing immediately before the attacks. In the same report, in-vitro studies with methacholine and arecoline, a major alkaloid of betel nut, showed dose-related contractions of human bronchial smooth-muscle; a double-blind study showed inhaled arecoline to cause bronchoconstriction in six of seven asthma subjects; and betel nut challenges produced a significant (30%) drop in the forced expiratory volume in 1 s (FEV 1) in one of four asthmatic patients who regularly chewed the nut. These findings are very similar and corroborate those of a study that my colleague (A. Saweri) and I completed last year (unpublished). Taylor et al, however, say that, to their knowledge, bronchoconstriction due to arecoline has not been reported
been infected.4 Reduction of number of partners may not be an easy option for women for whom this is a part of their strategy for social and economic survival.6 Women’s subordinate position may not allow them to negotiate successfully the use of safe sex even when they perceive the risk correctly. 7,8 This process is also influenced by men’s attitudes and by notions of masculinity.7 Women’s knowledge, perceptions, choices, and ability to negotiate change with their partners should be understood in the context of the power balance in gender relationships and against its wider historical and cultural basis (Brooke GS, et al, unpublished). An effective contribution to facilitate change towards safer practices for women will need a better understanding of the conditions of transmission to all women, not just those in at-risk categories, of the social and cultural norms that shape women’s perception of risk, and of the constraints that women face to change their risk behaviour and to negotiate safer sex practices with their partners. This in turn will help to develop strategies to redress the lack of power of women to protect themselves against HIV infection and to negotiate safer sex with their partners.8 This lack of power is most often real, not merely perceived, as you suggest in your note. Oxfam, 274 Banbury Road, Oxford OX2 7DZ, UK, and London School of Hygiene and Tropical Medicine, London WC1
CLAUDIA GARCÍA MORENO LAURA C. RODRIGUES
1. Garda Moreno C. AIDS: women and not just transmitters. In: Wallace T, March C, eds. Changing perceptions: gender in development. Oxford: Oxfam, 1990. 2. Carovano K. More than mothers and whores: redefining the AIDS prevention needs of women. Int J Health Ser 1991; 21: 131-42. 3. Rodrigues LC, Garcia Moreno C HIV transmission to women in stable relationships. N Engl J Med 1991; 325: 966. 4. Lindam C, Allen S, Carael M, et al. Knowledge, attitudes, and perceived risk of AIDS among urban Rwandan women: relationship to HIV infection and behaviour change. AIDS 1991; 5: 993-1002. 5. Worth D. Sexual decision-making and AIDS: why condom promotion among vulnerable women is likely to fail. Stud Fam Plann 1989; 20: 297-307. 6. Bassett MT, Mhloyi M. Women and AIDS in Zimbabwe: the making of an epidemic. Int J Health Ser 1991; 21: 143-56. 7. Ankrah EM. AIDS and the social side of health. Soc Sci Med 1991; 32: 967-80. 8. Ulin PR. African women and AIDS: negotiating behavioural change. Soc Sci Med
1992; 34: 63-73.
p
SIR,-Professor Lecatsas and Professor Alexander’s (June 6, 1427) suggestion that the simultaneous appearance of HIV-1and
HIV-2 is evidence for the contamination of poliovirus vaccine being the origin of AIDS is flawed. They need to explain several points. How did two distantly related viruses contaminate the poliovaccine ? Why did this affect African countries more than others with much higher poliovaccine coverage? And why has long-term follow-up of people who received retrovirus-contaminated batches of poliovaccine failed to demonstrate ill health?l A simpler explanation for the simultaneous appearance of two dissimilar viruses lies in the main route of transmission. Since the end of colonialism there have been major social and economic changes in African countries.2 Those relevant to the HIV epidemic include rapid urbanisation across the continent, new road building improving communications, and the mass movement of people as a result of civil war and starvation. Urbanisation is likely to have brought HIV-1and HIV-2 into the cities and towns. Accompanying this urbanisation is greater sexual freedom from loss of tribal traditions, the migrant worker system which encourages multiple sexual partners and stimulates demand for prostitution, along with the growing poverty of many urban women increasing the numbers engaging in prostitution.2 These social factors lead to an increase in the number of new sexual partners, which allows any sexually transmitted disease, especially one with a long duration of infectivity to produce an epidemic. The developing road system allowed the virus to be moved across the continent. The high prevalence in truck drivers testifies to this potential. When people live in small social groups with little movement, as in rural villages, the spread of sexually transmitted diseases is much less than in large heterogeneous populations. HIV-1 has a low probability of infectivity, 0.1 to 0-2 for each relationship,3 and is dependent on the long duration of infectivity to maintain the infection. Major spread could only occur when the behaviour of the population changed, which happened with urbanisation. This theory explains how 2 dissimilar viruses, both sexually transmitted, have suddenly appeared and rapidly produced
major epidemics. Westbrook House, Sharrow Vale Road, Sheffield S11 8EU, UK
AIDS in India SIR,-It is gratifying to note, as your Round-the-World correspondent says (May 9, p 1162), that the Indian Government will be initiating a national control plan for AIDS with the monies given by the World Bank and the World Health Organisation. The plan is necessary because very few preventive measures are being undertaken, despite evidence that the infection is spreading. Although the initiative overcomes governmental reluctance to accept AIDS as a serious public health issue in India, there are several other difficulties that pose a greater challenge. Successful health education campaigns in developed countries may not work very well in India in view of low literacy levels, limited access to radio and television, and large rural populations. Added to these is the growing nationwide problem of alcohol consumption, which encourages casual sex. What is needed, therefore, is an active attempt to educate and modify behaviour through personal intervention. This has been successfully achieved in other communicable diseases and in maternal and child health. There has to be a national programme with community health workers whose primary aim is to inform people of the risks of AIDS and how these risks can be avoided. This may mean also a free distribution of condoms for safer sex which can also be an effective birth control method. Some use of existing communication channels needs to be undertaken simultaneously, aimed especially at urban populations. India needs a comprehensive and complex plan to prevent the spread of AIDS infection, and this may mean personal contact with 900 million people over some time. The current initiative can only be a starting point. Poole
Hospital, Nunthorpe, Middlesbrough, Cleveland TS7 ONJ, UK
Origins of HIV
R. S. RAMAIAH
KEITH NEAL
1. Beale AJ. Polio vaccines: time for a change in immunisation policy? Lancet 1990; 335: 839-42. 2. Larson A. Social context of human immunodeficiency virus transmission in Africa: historical and cultural bases of east and central African sexual relations. Rev Infect
Dis 1989; 2: 716-31. 3.
European Study Group on Heterosexual transmission of HIV. Comparison of female to male and male to female transmission of HIV in 563 stable couples. BMJ 1992; 304: 809-13.
Peripartum HIV seroconversion: a cautionary tale SIR,-A bottle-fed child aged 4 months was admitted to hospital with a provisional diagnosis of bronchiolitis. The child deteriorated and he required ventilation. On day 5 a tracheal aspirate was found to be positive for Pneumocystis carinii by a fluorescence antibody test and on day 6 a serum sample was reported positive for HIV-1/2 antibody. The child died on hospital day 27. The blood was sent to a reference laboratory for confirmatory tests for anti-HIV-1/2 and both gave low positive results. Immunoblot testing was indeterminate but there was reactivity to proteins p24, gp 120, and gp 160; the bands on the blot were definite but not strong, and could be consistent with low antibody level. The polymerase chain reaction (PCR) for HIV RNA was positive and p24 antigen was detected by enzyme immunoassay. During 1991, when this child was born, no HIV antibody positive newborn babies were found in Aberdeen by anonymous Guthrie card testing. The batch of Guthrie cards pertaining to this birth was retested by the department of child health, Yorkhill, Glasgow, and found to be HIV antibody negative. This was confirmed by a reference laboratory. The mother denied that she might be HIV positive. Later her general practitioner was able to discuss with her the death of her
59
child and the HIV testing of her blood. She and this was confirmed
HIV-1/2 seropositive,
was
by
found to be the reference
laboratory (ELISA and
western blot). A p24 test was weakly not be could neutralised and was of uncertain clinical but positive significance. A sample of her blood that had been sent for rubella antibody testing during the first trimester had been stored in the virus laboratory. This was tested and found to be negative for HIV-1/2 antibody by EIA and for HIV p24 antigen. The mother seroconverted towards the end of her pregnancy or immediately afterwards, and the associated viraemia resulted in a massive infection of her baby. There are several lessons to be learned from this case. Antenatal testing may not identify those who are HIV seropositive if testing is done in the "window" before seroconversion. The Guthrie card screening in this case was correct (the result was not a false negative) but the danger to staff from such a mother and baby identified as HIV negative at the time of delivery illustrates the need for strict policies for all deliveries, remembering the general caution that "blood is dangerous". Medical staff need to be aware of the possibility of HIV infection in a child when the differential diagnosis proves difficult. The HIV infection ran a very rapid course in this child and the presumed high level of viraemia poses a risk for carers.
We thank the virus
laboratory, department
of medical
on
stored
serum
by RT-PCR.
A = negative buffer control; B=serum from seronegative control; C-F seronegative sera samples from donor (C=Aug 8, D =June 27, E=April 17, F =Feb 6) Arrow indicates specific segment amplified with SK38/ SK39 and hybridised with SK19; PR = unreacted SK19
microbiology,
Foresterhill, Aberdeen; Dr John F. Peutherer, department of bacteriology, University of Edinburgh; and Dr E. A. C. Follett, Ruchill Hospital, Glasgow, for their help
Department of Public Health Medicine, Grampian Health Board, Aberdeen AB9 8QP
J. S. BERKELEY
General Practice, Aberdeen
P. C. FOGIEL
Department of Paediatrics, Aberdeen Royal Infirmary
A. D. KINDLEY
Department of Virology, Royal Infirmary
M. A. J. MOFFAT
Aberdeen
Detection of HIV-1 RNA
Transmission of HIV-1 from seronegative but PCR-positive blood donor SIR,-Seroconversion to HIV-1 usually occurs within 6 months of exposure1 but because there is a serological "window" transmission from infected donors screened as seronegative for HIV-1is still encountered.2,3 The polymerase chain reaction (PCR) permits identification of HIV-1sequences in patients who have not yet seroconverted.4 A seronegative individual has been shown to have transmitted HIV-1 to organ recipients.sWe describe here a transmission of HIV-1from a seronegative but PCR-positive blood donor; PCR on serum stored from previous donations permitted retrospective detection of HIV-1infection before seroconversion. A 22-year-old man complained at the end of August, 1991, of fever without other symptoms. He had generalised lymphadenopathies. He had had unprotected sex with multiple male partners. He had antibodies to HIV-1(enzyme immunoassay [EIA] and western blot) on a blood sample drawn on Aug 20,1991. Between June, 1990, and August, 1991, he had donated blood four times (June 27,1990, and Feb 6, April 17, and Aug 8,1991). The four donations had been screened negative for HIV-1by EIA. He had denied risk factors for HIV-1 infection in questionnaires completed before every donation and never used the confidential unit exclusion procedure. Serum from the four seronegative donations, which had been kept at - 70°C, were analysed by PCR for HIV-1RNA. RNA was extracted with guanidinium, subjected to reverse transcription (RT), and amplified with SK38/SK39 (RT-PCR).6 Amplified products were detected with 32P-labelled SK19 after gel
electrophoresis (see figure). The Aug 8, 1991, serum was positive. PCR without the RT step was negative (not shown), reflecting absence of proviral DNA. The same serum was re-tested for HIV-1 antibodies and found to be negative by EIA and western blot; a weak gpl60 band was noticed on radioimmunoprecipitation assay;
p24 antigen was undetectable. Two recipients of blood products from the PCR-positive donation were identified. One had died, of a disease unrelated to
HIV-1,3 weeks after the transfusion. The other, the recipient of a platelet unit and having no risk factors for HIV-1 infection, seroconverted after the transfusion. A recipient of packed red blood cells from the April 17, 1991, donation (seronegative and PCR negative for HIV-1) was seronegative after that transfusion. Donors in the phase preceding seroconversion may be viraemic and their blood could transmit HIV-1.3,4 Since serum rarely contains proviral DNA4,6 detection of viral genome needs RT-PCR. This observation demonstrates that in investigation of recipient seroconversion after blood transfusion combined RT and PCR on stored donor sera may sometimes identify an infectious seronegative donor. Departments of Infectious Diseases and Microbiology, Hôpital Notre-Dame, Montreal, Quebec, Canada H2L 4M1; and Hôpital Saint-Luc, Montreal, Canadian Red Cross Society, Blood Services (Montreal Centre), and Federal Centre for AIDS, Ottawa
FRANCOIS COUTLÉE GILLES DELAGE FRANCOIS LAMOTHE SHARON CASSOL FRANCINE DÉCARY
Horsburgh CR, Jason J, Longini IM, et al. Duration of human immunodeficiency virus infection before detection of antibody. Lancet 1989; ii: 637-40. 2. Ward JW, Holmberg SD, Allen JR, et al. Transmission of human immunodeficiency virus (HIV) by blood transfusion screened as negative for HIV antibody. N Engl J 1.
Med 1988; 318: 473-78. 3. Irani MS, Dudley AW, Lucco LJ. Case of HIV-1 transmission by antigen-positive antibody-negative blood. N Engl J Med 1991; 325: 1174. 4. Hewlett IK, Gregg RA, Ou C-Y, et al. Detection in plasma of HIV-1 specific DNA and RNA by polymerase chain reaction before and after seroconversion. J Clin
Immunoassay 1988; 11: 161-64. RJ, Holmberg SD, Hurwitz RL, et al. Transmission of human immunodeficiency virus type 1 from a seronegative organ donor. N Engl J Med
5. Simonds
1992; 326: 726-32. 6.
Holodniy M, Katzenstein DA, Israelski DM, Mengan TC. Reduction in plasma human immunodeficiency virus ribonucleic add after dideoxynucleoside therapy as determined by the polymerase chain reaction. J Clin Invest 1991; 88: 1755-59.
Betel nut
chewing and asthma
SIR,-Dr Taylor and colleagues (May 9, p 1134) report two Asian patients who were often admitted with acute severe asthma, probably linked to betel nut chewing immediately before the attacks. In the same report, in-vitro studies with methacholine and arecoline, a major alkaloid of betel nut, showed dose-related contractions of human bronchial smooth-muscle; a double-blind study showed inhaled arecoline to cause bronchoconstriction in six of seven asthma subjects; and betel nut challenges produced a significant (30%) drop in the forced expiratory volume in 1 s (FEV 1) in one of four asthmatic patients who regularly chewed the nut. These findings are very similar and corroborate those of a study that my colleague (A. Saweri) and I completed last year (unpublished). Taylor et al, however, say that, to their knowledge, bronchoconstriction due to arecoline has not been reported
