cleoside analogues, [8][9][10] the only established treatment option Hepatitis B virus (HBV) replicates via an intermediate to prevent reinfection is the administration of polyclonal hep-RNA step. High frequency of polymerase errors with adatitis B surface antigen antibody (anti-HBs) (hepatitis B imditional selection pressure leads to mutations in the mune globulin [HBIG]). HBIG reduces the rate of reinfection HBV genome. We investigated the number, type, and anfrom about 90% to less than 30% and improves the long-term tigenic effects of mutations in the coding region of the outcome of patients who underwent OLT for HBV-related HBV surface antigen in eight patients who underwent disease. 2-4orthotopic liver transplantation (OLT) for HBV-related A number of explanations for graft infection have been end-stage liver disease and were experiencing infection proposed. First, virions from the explanted liver are circulatof the graft and who received hepatitis B surface antigen ing in the blood during or soon after transplantation. Second, antibody (anti-HBs) prophylaxis (hepatitis B immune virions are replicating at extrahepatic sites. HBIG interferes globulin [HBIG]) after OLT. Controls were chronic HBV with this process and probably prevents virions from entering patients who underwent kidney transplantation and rehepatocytes. 11 The mechanisms that lead to reinfection in ceived the same immunosuppressive regime but no 30% of patients receiving HBIG after OLT are not under-HBIG. The S-gene was amplified from serum before and stood. after transplantation, sequenced, and changes in the ge-HBV employs reverse transcriptase for its replication; this nome were analyzed. In the five patients who experilacks proofreading capability, and thus leads to a higher enced reinfection while receiving anti-HBs, clear mutanumber of mutations in the HBV genome. 12 Some of these tions occurred in the S-gene. In the patient who did not variants may have a replication advantage and become domireceive HBIG and those who experienced reinfection nant. From the pool of variants with similar replication poonly after termination of HBIG, no mutations were tential, some will be positively selected by forces such as found in the S-gene. In the kidney recipients, mutations the humoral or cellular immune response 13; these are termed in the S-gene occurred in only one of eight patients. Beescape mutants. Evolution of viruses under antibody prescause the a determinant contains neutralizing epitopes, sure, either monoclonal or polyclonal, has been well studied this region was chosen for antibody binding to quantify both in vitro and in vivo. The addition of neutralizing antibodantigenic effects of the mutations. The two patients who ies to virus cultures regularly results in isolates that are not selected mutations in the a determinant and became reneutralized by the added antibodies. This is particularly true infected while receiving HBIG had reduced antibody with monoclonal reagents, because the change in viral antibinding after OLT. Our results...
The proteins predicted to be encoded by varicella-zoster virus (VZV) genes 47 and 66 display sequence similarity to the serine/threonine family of protein kinases. Homologues ofgene 47 exist in c~-, fl-and ~-herpesviruses but homologues of gene 66 are specific to the ~-herpesviruses. Monospecific rabbit antisera were raised against two separate fusion proteins constructed from a portion of each protein fused to the carboxy terminus of fl-galactosidase. These antisera were used to characterize the 47 and 66 proteins in VZV-infected cells and in cells infected with vaccinia virus recombinants expressing each protein. The 47 protein is a 54K phosphoprotein which is distributed between the cytoplasmic and nuclear compartments of VZV-infected cells and is associated with the capsid/tegument fraction of purified VZV particles. Gene 66 encodes a 48K phosphoprotein when expressed by VZV or a vaccinia virus recombinant, and, in the latter case, the 66 protein was located exclusively in the cytoplasm. The 47 protein immunoprecipitated from VZV-infected cells could be phosphorylated in vitro, but the same protein produced by in vitro transcription and translation could not. This and other evidence indicates that additional proteins induced or encoded by VZV may be involved in the phosphorylation of the 47 protein.
The distribution and temporal and clinical features of amino acid substitutions of the core protein of hepatitis B (HB) virus were analyzed, using at least 2 sequential samples from 27 patients. Six patients seroconverted from HBe antigen (HBeAg)-positive to anti-HBe-positive (3 went into remission), and 21 were continuously anti-HBe positive with progressive hepatitis. Precore mutations, which terminate HBeAg translation, all appeared by the second sample. Most core mutations occurred between the first and second samples; significantly fewer occurred after the second. In seroconverters who went into remission, mutations occurred in the T helper epitope from aa 50 to 69 (P = .00045); for anti-HBe-positive patients with ongoing disease, mutations occurred in B cell epitopes (P = .0007 for aa 74-83). An ineffective anti-HBc B cell response accounts for ongoing disease and selection of mutations after seroconversion. In those who remit, mutations in the major T helper epitope allow immune escape, thus minimizing immune-mediated hepatitis.
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