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Hepatitis C virus antibody in HIV-1 infected Ugandan mothers
551
CLINICAL AND VIROLOGICAL DETAILS OF FIRST INDIAN PATIENTS WITH HIV-2 OR UNRESOLVED HIV-1/2 INFECTION
+=positive,= negative, (+) = cross-reaction; ’ = not done or in progress. L= lymphocyte culture, M = lymphocyte/macrophage mixed culture7,. Staging according to WHO system 9’°
Blood products must be tested for both HIV-1and HIV-2 in India, and Asia can no longer be considered free from HIV-2. We thank Dr Wiegand-Kanzaki, Max-Mueller-Bhavan Goethe Institution, Bombay; and Mrs M. Landersz and Mrs D. Kunstle for technical assistance. The Georg-Speyer-Haus is supported by the Hessische Ministerum fur Wissenschaft und Kunst and the Bundesministerium fur Jugend, Familie und Gesundheit.
Chemotherapy Research Institute, Georg-Speyer-Haus, 6000 Frankfurt 70, Germany
H. RÜBSAMEN-WAIGMANN H. V. BRIESEN
Hospital and STD Clinic, Bombay, India
J. K. MANIAR
Chemotherapy Research Institute, Georg-Speyer-Haus, Frankfurt
C. SCHOLZ A. PFÜTZNER
G.T
P. K. RAO
1. Dumasia A, Kulkarni
S, Joshi SH, Gupte S, Apte SV. Women receiving anti-Rh(D) immunoglobulin containing HIV antibodies. Lancet 1989; ii: 459. 2. Singhvi A, Pulimood RB, John TD, et al. The prevalence of markers for hepatitis B and human immunodeficiency viruses, malaria parasites and microfilaria in blood donors m a large hospital in south India. J Trop Med Hyg 1990; 93: 178-82. 3. Seth P, Malaviya
AN, Kiran U, et al. Lack of evidence of endemicity of human immunodeficiency virus infection in northern India. Indian J Med Res 1988; 87:
108-12. 4. Anon. India: prostitutes and the
spread of AIDS. Lancet 1990; 335: 1238. 5. Santos-Ferreira MO, Cohen T, Lourenco MH, Almeida MJ, Chamaret S, Montagnier L. A study of seroprevalence of HIV-1 and HIV-2 in six provinces of People’s Republic of Angola: clues to the spread of HIV infection. J AIDS 1990; 3: 780-86. 6. De Cock KM, Odehouri K, Colebunders RL, et al. A comparison of HIV-1 and HIV-2 infections in hospitalized patients in Abidjan, Côte d’Ivoire. AIDS 1990; 4: 443-48. 7. Rubsamen-Waigmann H, Becker WB, Helm EB, et al. Isolation of variants of lymphoadenopathic retroviruses from the peripheral blood and cerebrospinall fluid of patients with ARC and AIDS. J Med Virol 1986; 19: 335-44. 8. Rübsamen-Waigmann H, von Briesen H, Regeniter A, et al. Indicators of HIV-disease progression I. Relations to viral cultures on lymphocytes and macrophages and to a decrease of serum cholesterol. The Microbiologist 1990; 1: 90-97. 9. WHO Weekly Epidemiol Rec 1990, no 29. 10. MMWR 1987; 36: 225-36.
Hepatitis C virus antibody in HIV-1 infected Ugandan mothers SIR,-In Europe and
the United States the
prevalence of
hepatitis C virus (HCV) antibody positivity is generally reported to be less than 1-5% in blood donors’-3 and up to 77% in drug users infected with HIV-1.4 Preliminary data suggest that HIV-1 may enhance the risk of maternal HCV transmission to newborn babies.’ Hepatitis B and HIV-1 infection are endemic in much of sub-Saharan Africa, including Uganda,6,7 but the contribution of HCV is not known. To evaluate the role, if any, of HCV as a complicating factor in HIV-1infected mothers we tested the plasma of 160 selected mothers seen at the antenatal and paediatric clinics in Old Mulago Hospital, Kampala, Uganda, over 2 weeks in July, 1990. Plasma samples were tested with licensed HIV-1 and HCV
antibody enzyme immunoassays (EIA) (Abbott). HIV-1 reactive samples were confirmed by western blot (Bio-Rad) and samples repeatedly reactive for anti-HCV were confirmed by measuring blocking of reactivity with a truncated C-100 antigen expressed in
Escherichia coli and/or by the presence of reactivity to an HCV C-100 synthetic peptide." 96 mothers (60%) were HIV-1 antibody positive but only 4 (2-5%) were repeatedly reactive for HCV antibody, none was confirmed by the peptide assay or neutralisation procedure. None of these 4 mothers was HIV-1antibody positive. Our results indicate that antibody to the C-100 antigen of HCV is uncommon in this part of Africa despite the high prevalence of HIV-1 infection. Preliminary data suggest high prevalences of HCV in Africa, but these results were to a large extent attributed to false reactions related to increased IgG and/or malarial infection.9 In the absence of valid supplementary assays to discriminate between true and false positivity, HCV reactivity should be interpreted with great care. This low seroprevalence of HCV contrasts with the rate of 51 % in HIV-1 infected Italian mothers who transmitted HCV to their infants 44% of the time.s It is reassuring that HCV is unlikely to be another complicating factor in HIV-1-infected mothers and children in this part of the world. Our data suggest that the prevalence of HCV infection in Uganda is the same or perhaps less than that in the general populations of Europe and the United States.
J. BROOKS JACKSON Departments of Pathology and Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106, USA
LAURA GUAY
JOHANNA GOLDFARB
Departments of Paediatrics and Obstetrics, Makerere University, Kampala, Uganda
KAREN OLNESS CRISTOPHER NDUGWA FRANCIS MMIRO PETER KATAAHA
Abbott Laboratories, North Chicago, Illinois
JEAN-PIERRE ALLAIN
1. Esteban JI, Gonzalez A, Hernandez JM, et al. Evaluation of antibodies to hepatitis C virus in a study of transfusion-associated hepatitis. N Engl J Med 1990; 323: 1107-12. 2. Weiner AJ, Truett MA, Rosenblatt J, et al. HCV testing in low-risk population. Lancet
1990; 336: 695. 3. Zuck TF, Rose GA, Dumaswala UJ, Geer NJ. Experience with a transfusion recipient education program about hepatitis C. Transfusion 1990; 30: 759-61. 4. Van den Hoek JAR, Van Haastrecht HJA, Goudsmit J, De Wolf F, Coutinho RA. Prevalence, incidence, and risk factors of hepatitis C virus infection among drug users in Amsterdam. J Infect Dis 1990; 162: 823-26. 5. Giovannini M, Tagger A, Ribero ML, et al. Maternal-infant transmission of hepatitis C virus and HIV infections: a possible interaction. Lancet 1990; 335: 1166. 6. Sobeslavsky O. Prevalence of markers of hepatitis B virus infection in various countries: a WHO collaborative study. Bull WHO 1980; 58: 621-28. 7. Goodgame RW. AIDS in Uganda: clinical and social features. N Engl J Med 1990; 323: 383-89. 8. Wong DC, Diwan AR, Rosen L, et al. Non-specificity of anti-HCV test for seroepidemiological analysis. Lancet 1990; 336: 750-51. 9. Aceti A, Taliani G, De Bac C, Sebastiani A. Anti-HCV false positivity in malaria. Lancet 1990; 336: 1442-43.
Second
generation (RIBA) test in diagnosis of chronic hepatitis C
SiR,—The first generation (ELISA)
test
for antibodies
to
C virus (anti-HCV) is positive in about 75% of patients with chronic non-A, non-B hepatitis.’ The similar clinical, biochemical, and histological features in patients with anti-HCV positive and anti-HCV negative chronic non-A, non-B hepatitis
hepatitis
CLINICAL AND VIROLOGICAL DETAILS OF FIRST INDIAN PATIENTS WITH HIV-2 OR UNRESOLVED HIV-1/2 INFECTION
+=positive,= negative, (+) = cross-reaction; ’ = not done or in progress. L= lymphocyte culture, M = lymphocyte/macrophage mixed culture7,. Staging according to WHO system 9’°
Blood products must be tested for both HIV-1and HIV-2 in India, and Asia can no longer be considered free from HIV-2. We thank Dr Wiegand-Kanzaki, Max-Mueller-Bhavan Goethe Institution, Bombay; and Mrs M. Landersz and Mrs D. Kunstle for technical assistance. The Georg-Speyer-Haus is supported by the Hessische Ministerum fur Wissenschaft und Kunst and the Bundesministerium fur Jugend, Familie und Gesundheit.
Chemotherapy Research Institute, Georg-Speyer-Haus, 6000 Frankfurt 70, Germany
H. RÜBSAMEN-WAIGMANN H. V. BRIESEN
Hospital and STD Clinic, Bombay, India
J. K. MANIAR
Chemotherapy Research Institute, Georg-Speyer-Haus, Frankfurt
C. SCHOLZ A. PFÜTZNER
G.T
P. K. RAO
1. Dumasia A, Kulkarni
S, Joshi SH, Gupte S, Apte SV. Women receiving anti-Rh(D) immunoglobulin containing HIV antibodies. Lancet 1989; ii: 459. 2. Singhvi A, Pulimood RB, John TD, et al. The prevalence of markers for hepatitis B and human immunodeficiency viruses, malaria parasites and microfilaria in blood donors m a large hospital in south India. J Trop Med Hyg 1990; 93: 178-82. 3. Seth P, Malaviya
AN, Kiran U, et al. Lack of evidence of endemicity of human immunodeficiency virus infection in northern India. Indian J Med Res 1988; 87:
108-12. 4. Anon. India: prostitutes and the
spread of AIDS. Lancet 1990; 335: 1238. 5. Santos-Ferreira MO, Cohen T, Lourenco MH, Almeida MJ, Chamaret S, Montagnier L. A study of seroprevalence of HIV-1 and HIV-2 in six provinces of People’s Republic of Angola: clues to the spread of HIV infection. J AIDS 1990; 3: 780-86. 6. De Cock KM, Odehouri K, Colebunders RL, et al. A comparison of HIV-1 and HIV-2 infections in hospitalized patients in Abidjan, Côte d’Ivoire. AIDS 1990; 4: 443-48. 7. Rubsamen-Waigmann H, Becker WB, Helm EB, et al. Isolation of variants of lymphoadenopathic retroviruses from the peripheral blood and cerebrospinall fluid of patients with ARC and AIDS. J Med Virol 1986; 19: 335-44. 8. Rübsamen-Waigmann H, von Briesen H, Regeniter A, et al. Indicators of HIV-disease progression I. Relations to viral cultures on lymphocytes and macrophages and to a decrease of serum cholesterol. The Microbiologist 1990; 1: 90-97. 9. WHO Weekly Epidemiol Rec 1990, no 29. 10. MMWR 1987; 36: 225-36.
Hepatitis C virus antibody in HIV-1 infected Ugandan mothers SIR,-In Europe and
the United States the
prevalence of
hepatitis C virus (HCV) antibody positivity is generally reported to be less than 1-5% in blood donors’-3 and up to 77% in drug users infected with HIV-1.4 Preliminary data suggest that HIV-1 may enhance the risk of maternal HCV transmission to newborn babies.’ Hepatitis B and HIV-1 infection are endemic in much of sub-Saharan Africa, including Uganda,6,7 but the contribution of HCV is not known. To evaluate the role, if any, of HCV as a complicating factor in HIV-1infected mothers we tested the plasma of 160 selected mothers seen at the antenatal and paediatric clinics in Old Mulago Hospital, Kampala, Uganda, over 2 weeks in July, 1990. Plasma samples were tested with licensed HIV-1 and HCV
antibody enzyme immunoassays (EIA) (Abbott). HIV-1 reactive samples were confirmed by western blot (Bio-Rad) and samples repeatedly reactive for anti-HCV were confirmed by measuring blocking of reactivity with a truncated C-100 antigen expressed in
Escherichia coli and/or by the presence of reactivity to an HCV C-100 synthetic peptide." 96 mothers (60%) were HIV-1 antibody positive but only 4 (2-5%) were repeatedly reactive for HCV antibody, none was confirmed by the peptide assay or neutralisation procedure. None of these 4 mothers was HIV-1antibody positive. Our results indicate that antibody to the C-100 antigen of HCV is uncommon in this part of Africa despite the high prevalence of HIV-1 infection. Preliminary data suggest high prevalences of HCV in Africa, but these results were to a large extent attributed to false reactions related to increased IgG and/or malarial infection.9 In the absence of valid supplementary assays to discriminate between true and false positivity, HCV reactivity should be interpreted with great care. This low seroprevalence of HCV contrasts with the rate of 51 % in HIV-1 infected Italian mothers who transmitted HCV to their infants 44% of the time.s It is reassuring that HCV is unlikely to be another complicating factor in HIV-1-infected mothers and children in this part of the world. Our data suggest that the prevalence of HCV infection in Uganda is the same or perhaps less than that in the general populations of Europe and the United States.
J. BROOKS JACKSON Departments of Pathology and Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106, USA
LAURA GUAY
JOHANNA GOLDFARB
Departments of Paediatrics and Obstetrics, Makerere University, Kampala, Uganda
KAREN OLNESS CRISTOPHER NDUGWA FRANCIS MMIRO PETER KATAAHA
Abbott Laboratories, North Chicago, Illinois
JEAN-PIERRE ALLAIN
1. Esteban JI, Gonzalez A, Hernandez JM, et al. Evaluation of antibodies to hepatitis C virus in a study of transfusion-associated hepatitis. N Engl J Med 1990; 323: 1107-12. 2. Weiner AJ, Truett MA, Rosenblatt J, et al. HCV testing in low-risk population. Lancet
1990; 336: 695. 3. Zuck TF, Rose GA, Dumaswala UJ, Geer NJ. Experience with a transfusion recipient education program about hepatitis C. Transfusion 1990; 30: 759-61. 4. Van den Hoek JAR, Van Haastrecht HJA, Goudsmit J, De Wolf F, Coutinho RA. Prevalence, incidence, and risk factors of hepatitis C virus infection among drug users in Amsterdam. J Infect Dis 1990; 162: 823-26. 5. Giovannini M, Tagger A, Ribero ML, et al. Maternal-infant transmission of hepatitis C virus and HIV infections: a possible interaction. Lancet 1990; 335: 1166. 6. Sobeslavsky O. Prevalence of markers of hepatitis B virus infection in various countries: a WHO collaborative study. Bull WHO 1980; 58: 621-28. 7. Goodgame RW. AIDS in Uganda: clinical and social features. N Engl J Med 1990; 323: 383-89. 8. Wong DC, Diwan AR, Rosen L, et al. Non-specificity of anti-HCV test for seroepidemiological analysis. Lancet 1990; 336: 750-51. 9. Aceti A, Taliani G, De Bac C, Sebastiani A. Anti-HCV false positivity in malaria. Lancet 1990; 336: 1442-43.
Second
generation (RIBA) test in diagnosis of chronic hepatitis C
SiR,—The first generation (ELISA)
test
for antibodies
to
C virus (anti-HCV) is positive in about 75% of patients with chronic non-A, non-B hepatitis.’ The similar clinical, biochemical, and histological features in patients with anti-HCV positive and anti-HCV negative chronic non-A, non-B hepatitis
hepatitis