Since the discovery of Australia antigen and its association with type B hepatitis, molecular characterization of the components making up hepatitis B virus (RBV) have been pursued with worldwide interest. Over the past two decades, such characterization has led to the development of sensitive assays to screen and exclude contaminated units from blood banks and has recently resulted in the licensing of several RBV vaccines. That more than 200 million people worldwide are chronically infected with RBV, and that they are at a high risk for the development of chronic hepatitis and hepatocellular carcinoma, still represent formidable problems in our understanding of host-virus relationships on the molecular level. In the absence of a suitable tissue culture system, and with a very limited host range of infection, characterization of RBV on the molecular level has made remarkable progress recently with the advent of genome cloning, sequencing and expression of individual virus genes by recombinant DNA technology. The presence of hepatitis B-like viruses in an expanding number of animal hosts, and the possibility of virus replication in cells other than hepatocytes, provide great promise that future work will elucidate the molecular mechanisms operative in the various outcomes of RBV infection.
The early, organ-specific diagnosis of malignancy continues to be a major unmet medical need. Clearly the ability to establish an early diagnosis of cancer is dependent upon an intimate knowledge of the cancer's biology, which if understood at the molecular level should identify key diagnostic and therapeutic manipulation points. Advances in recombinant gene technology have provided significant understanding of the mechanisms of action of oncogenic viruses, as well as of cancer-associated genomic sequences (oncoÂ genes). This text will explore the known molecular genetic, biologÂ ical, and clinical knowledge of selected human neoplasms that demonstrate association with suspected oncogenic virus and those cytogenetic alterations that either cause or are caused by oncogene activation. The text first reviews the cytogenetics of human cancers linkÂ ing classical cytogenetics and molecular genetics. Avery A. SandÂ berg (Roswell Park Memorial Institute, Buffalo, New York) reviews the leukemias and lymphomas, followed by S. Pathak (M. D. Anderson Hospital and Tumor Institute, Houston, Texas), who reviews solid tumors. Functional consideration of oncogenes is highlighted by Keith C. Robbins and Stuart A. Aaronson (NO, Bethesda, Maryland) through their description of the v-sis locus sis and its gene product p.28 ; a protein that closely resembles human platelet-derived growth factor (PDGF).
The purpose ofthis book isto provide acritical appraisal oftheconcept thatschizophreniacan becaused by viralinfections. The ability of viruses to cause psychiatric symptoms is not in question - the mental depression following a bout with mononucleosis or hallucinations associated with herpesencephalitisarewell-described examples. However,aviraloriginfor chronic disorders such as autism, schizophrenia, and bipolar disorder, is another matter. The claim of an infectious etiology for these disorders has beenmetinthemainstream scientific community byavagueskepticism that occasionally erupts into stringent criticism. Too often, however, the viral hypotheses of these disorders is simply disregarded; marginalized with the hopethat itwillgoaway sothatthe "serious" researchaimed atuncovering therealcauseoftheseillnesses willnotloseitsfocus.This beingsaid,much of the criticism is valid, and as a researcher with formal training in both neuroscience and viral immunology, I view the proposed viral etiology of thesedisorderswithaskepticaleye. Nevertheless, one cannot ignore the growing number of well-performed studies pointing to the role of viral infections as important antecedents of schizophreniaand other disorders inthe schizophreniaspectrum. Inthe last 30 years there have been hundreds of articles in peer-reviewed journals presenting evidenceorpositingtheoriestosuggestthatatleastsomecasesof schizophrenia have a viral origin. Moreover, many schizophrenia experts have been calling for the recognition that schizophrenia isa heterogeneous group of disorders that may have different causes. This idea of disease heterogeneity is reaching a crescendo, and there is undoubtedly a place for viruses among alternative etiologies; but we have to look. The intellectual climate tolooknowisbetterthanitwas20yearsago,inpartbecause inthe last 2 decades a number of chronic diseases of unknown etiology (e.g. gastric ulcers, Kaposi's sarcoma, hepatocellular carcinoma) have been ascribedtoinfectiouscauses.
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