Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stored donor and recipient sera from prospective studies of post-transfusion hepatitis were analysed for the presence of human T-cell lymphotropic virus type-III/lymphadenopathy associated virus (HTLV-III/LAV) antibodies as determined by enzyme-linked immunosorbent assays (ELISA). Of 3961 donor samples given to 461 patients, only 2 (0.05%) contained specific HTLV-III/LAV antibodies as determined by an avidin-biotin-enhanced western blot tech nique. Anti-HTLV-III/LAV was measured before and 3 and 6 months after transfusion in 295 recipients of anti-HTLV-III-negative blood, 7 recipients of ELISA-positive blood which was western blot negative, and 2 recipients of ELISA-positive blood confirmed as specific by western blot. Only the last 2 recipients became infected with HTLV-III/LAV, as assessed by antibody seroconversion (p less than 0.0001). Serocon version occurred early (6 and 8 weeks after transfusion) and was characterised first by antibody to p24 and later by antibody to p41. AIDS has not developed in either patient, but one has a T4/T8 ratio of 0.4 and impaired mitogen responses; the second patient has no evidence of immune dysfunction 4 years after exposure. This study confirms that HTLV-III/LAV infection can be transmitted by blood transfusion and supports the advisability of anti-HTLV-III/LAV testing of all blood donors. It also confirms the validity of western blot testing for HTLV-III/LAV specificity and suggests that ELISA-positive, western-blot-negative blood may not be infectious.
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PMID:Importance of western blot analysis in predicting infectivity of anti-HTLV-III/LAV positive blood. 286 66

We tested serum samples from Swiss subjects by three different assays based on enzyme-linked immunosorbent assay (ELISA) and Western blot techniques for antibodies to proteins associated with the recently discovered human T-cell leukemia/lymphoma virus HTLV-III, the putative etiologic agent for the acquired immunodeficiency syndrome (AIDS). Of 10 patients with AIDS and 10 with pre-AIDS, all were antibody-positive. Furthermore, 37 of 103 intravenous-drug addicts (36 per cent), 4 of 40 healthy homosexual men (10 per cent), 7 of 83 patients with various types of hepatitis (8.4 per cent), but none of 83 healthy blood donors or 10 other controls were antibody-positive. Antibodies to the major viral protein p24 were found consistently and at high titers in the seropositive members of the groups at risk and in those with pre-AIDS but were dramatically reduced in patients with AIDS. In contrast, antibodies to another virus-associated protein, p41, were present in all cases of AIDS and pre-AIDS but were absent in nearly 10 per cent of seropositive persons at risk. Whereas p41 and p24 thus appear to be the targets of choice for future screening tests, the ELISA test that is currently available is a useful screening tool.
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PMID:Antibodies to HTLV-III in Swiss patients with AIDS and pre-AIDS and in groups at risk for AIDS. 298 7

Antibodies against HTLV-III, neopterin levels in blood and urine, TH/TS ratio and hepatitis marker were determined in 34 clinically symptom-free persons known to be intravenous drug abusers. 15 persons were positive in the ELISA and Western-blot tests. There was a strong reaction to protein p24 compared with that to protein p41. In 12 of 14 persons who were antibody-positive the neopterin level in morning urine was elevated; an abnormal TH/TS ratio was present in nine of 13 persons. In future, determination of neopterin and of antibodies against certain proteins of HTLV-III may make it possible to provide a simple way of prognosticating on the course of an HTLV-III infection.
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PMID:[HTLV-III in persons with intravenous drug abuse. Correlation of antibodies against HTLV-III with neopterin and TH/TS]. 300 78

Syncytial giant-cell hepatitis is a rare but severe form of hepatitis that is associated with autoimmune diseases, drug reactions, and viral infections. We used serologic, molecular, and immunohistochemical methods to search for an infectious cause in a case of syncytial giant-cell hepatitis that developed in a liver-transplant recipient who had latent infection with variant B of human herpesvirus 6 (HHV-6B) and who had received the organ from a donor with variant A latent infection (HHV-6A). At the onset of the disease, the detection of HHV-6A (but not HHV-6B) DNA in plasma, in affected liver tissue, and in single micromanipulated syncytial giant cells with the use of two different polymerase-chain-reaction (PCR) assays indicated the presence of active HHV-6A infection in the patient. Expression of the HHV-6A-specific early protein, p41/38, but not of the HHV-6B-specific late protein, p101, was demonstrated only in liver syncytial giant cells in the absence of other infectious pathogens. The same markers of HHV-6A active infection were documented in serial follow-up samples from the patient and disappeared only at the resolution of syncytial giant-cell hepatitis. Neither HHV-6B DNA nor late protein was identified in the same follow-up samples from the patient. Thus, HHV-6A may be a cause of syncytial giant-cell hepatitis.
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PMID:HHV-6A in syncytial giant-cell hepatitis. 1868 40