ISSN:0300-5526    

DOI:10.1159/000150288

出版商:S. Karger AG    

年代:1993

数据来源: Karger

ISSN:0300-5526    

DOI:10.1159/000150289

出版商:S. Karger AG    

年代:1993

数据来源: Karger

ISSN:0300-5526    

DOI:10.1159/000150290

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

By describing 100 years of virus research (the era of adventure, the era of consolidation, and the era of unknown future), the author attempts to change concepts held toward virology.

ISSN:0300-5526    

DOI:10.1159/000150291

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

Influenza A viruses continue to emerge from the aquatic avian reservoir and cause pandemics. Phylogenetic analysis of the nucleotide sequence of all eight influenza A virus RNA segments indicates that all of the influenza viruses in mammalian hosts originate from the avian gene pool. In contrast to the rapid progressive changes in both the nucleotide and amino acid sequences of mammalian virus gene lineages, avian virus genes show far less variation and, in most cases, appear to be in evolutionary stasis. There are periodic exchanges of influenza virus genes or whole viruses between species giving rise to pandemics of diseases in humans, lower animals and birds. The periodic emergence of influenza viruses in mammalian species has been illustrated by the appearance of a new influenza virus in horses in northern China in 1989. Phylogenetic analysis of classical H1N1, avian-like H1N1 and human H3N2 viruses circulating in Italian pigs reveals that genetic reassortment is taking place between avian- and human-like viruses in the European pig population. These studies provide evidence supporting the possibility that pigs serve as a mixing vessel for reassortment between influenza viruses in mammalian and avian hosts and raise the question of whether the next pandemic of influenza will emerge in Europe!

ISSN:0300-5526    

DOI:10.1159/000150292

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

Epstein-Barr virus (EBV) as a member of the herpesvirus family persists lifelong in the human body and causes diseases associated with virus replication (infectious mononucleosis, oral hairy leukoplakia) as well as neoplastic conditions such as nasopharyngeal carcinoma, B-cell lymphoma, Hodgkin’s disease associated with viral latency. This complex biology relates to a highly regulated control of the persisting virus. Still, EBV is lytically produced in certain compartments of the human body. Epithelial cells were found to be of key importance for this. Various routes (cell fusion, IgA receptor-mediated uptake) were described for EBV to enter epithelial cells in the absence of CR2 receptor. Viral entry into cells, however, via CR2 receptor fusion or IgA mediated was not found to be sufficient for viral production. The molecular mechanisms for the lack of viral production in most target cells are primarily the presence of silencer activities and the early elimination of cells entering the lytic cycle. Only terminally differentiated epithelial cells are capable of supporting an efficient lytic cycle of EBV replication. EBV-mediated suppression of apoptosis as well as down-regulation of cellular and viral gene products, such as HLA molecules, which mediate recognition by the immune system, are important contributing factors to the development of these neoplasias where viral genes, possibly via interaction with anti-oncogenes, such as p53, in context with genetic and environmental factors play a key role. Novel diagnostic tools and a vaccine have been developed which could help to control EBV-related disease

ISSN:0300-5526    

DOI:10.1159/000150293

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

Mutations of viral genomes are normal biological events and result in the coexistence of viral genotypes in infected individuals (‘quasispecies’). Hepatitis B virus (HBV) and the related animal hepadnaviruses have a mutation rate which is intermediate between DNA and RNA viruses because they replicate asymmetrically via reverse transcription of an RNA intermediate. HBV mutants affecting all known reading frames of the viral genome have been demonstrated in patients with acute fulminant or chronic HBV infection. Some of the mutations identified to date suggest a contribution to viral latency, low level HBV infection, the severity of liver disease and vaccine escape. Since most viral genomes carry more than one mutation and most individuals are infected by more than one variant, the demonstration of a causal relationship between a single mutation and a biological or pathobiological effect requires the in vitro and in vivo analysis of genetically defined mutants. Such analyses should allow a molecular understanding of the genetic contribution of HBV to the variable natural course of HBV infection, ranging from an asymptomatic healthy carrier state to acute or even fulminant hepatitis, chronic liver disease, liver cirrhosis and hepatocellular carcin

ISSN:0300-5526    

DOI:10.1159/000150294

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

The complex etiology of mucosal disease of cattle has been unravelled by experimental reproduction of the fatal syndrome, thereby validating Koch’s postulates. The causal virus, bovine virus diarrhea virus (BVDV), has two biotypes, noncytopathogenic and cytopathogenic; the former can infect the early bovine fetus, induce immunotolerance and a lifelong persistent viremia (pv), whereas the latter biotype can superinfect the pv cattle and induce mucosal disease. The cytopathogenic biotype appears able to originate de novo from the persisting virus by molecular rearrangement (e.g. template switching) and has been shown to arise in a case of spontaneous mucosal disease. The animal had been maintained in isolation for an extended perio

ISSN:0300-5526    

DOI:10.1159/000150295

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

Infections with persistent viruses such as herpesviruses have become of significant clinical importance with the increasing number of immunocompromized patients at risk to suffer from severe disease. As antiviral chemotherapy is available for herpesvirus infections, the diagnostic methods for rapid and sensitive detection of symptomatic infection have been developed and recently refined. In human cytomegalovirus (HCMV), the use of recombinant viral antigens provides a rationale to improve serological assays. This may be of use for the discrimination of primary versus secondary infection. Early diagnosis of symptomatic HCMV infection in immuno-suppressed patients can be most effectively achieved by the detection of a viral tegument protein, pp65, in peripheral blood leukocytes. This early diagnosis has been shown to be of major importance for the effective treatment of these patients. HCMV infection in solid organs can be demonstrated by immunohistochemistry using monoclonal antibodies against viral proteins. HCMV involvement in diseases of the central nervous system in AIDS patients can be verified by the detection of very small amounts of HCMV DNA in cerebrospinal fluid by polymerase chain reaction. This method may prove useful for monitoring HCMV encephalitis and neuropathy.

ISSN:0300-5526    

DOI:10.1159/000150296

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

Patients with hepatocellular carcinoma (HCC) develop autoantibodies to nuclear and nucleolar antigens (ANAs) which can be readily detected by immunofluorescence on cell substrates. The frequency of ANAs in HCC is 31 % (57/184). The identity of three autoantigens was established as: NOR-90, nucleolus organizer region (doublet) polypeptides involved in RNA polymerase I transcription; fibrillarin, a component of nucleolar U3 RNP involved in pre-ribosomal RNA processing, and nucleophosmin/protein B23, a nucleolar protein involved in ribosome maturation and cell proliferation. Changes in ANAs were observed in some patients during transition from chronic liver disease to HCC and were manifested as seroconversion from ANA-negative to ANA-positive status by an increase in titers and changes in ANA specificities. Serum from a patient during this transition period was used to isolate a cDNA clone encoding a novel nuclear protein with structural motifs characteristic of a family of splicing factors. These observations support the notion that ANA responses in HCC might be driven by intracellular events related to transformation from the stage of chronic injury to the stage of malignancy. Changes in ANA profiles which were observed to precede clinically diagnosed HCC in some patients might be early markers of transformation.

ISSN:0300-5526    

DOI:10.1159/000150297

出版商:S. Karger AG    

年代:1993

数据来源: Karger