{"title":"Defective interfering RNAs and defective viruses associated with multipartite RNA viruses of plants","authors":"Michael V. Graves , Judit Pogany , Javier Romero","doi":"10.1006/smvy.1996.0048","DOIUrl":"10.1006/smvy.1996.0048","url":null,"abstract":"<div><p>Defective interfering (DI) RNAs and defective viruses have been described for a variety of multipartite RNA viruses of plants. At present, the DI RNAs of broad bean mottle bromovirus (BBMV) have been the most characterized defective elements of multipartite viruses. Several naturally occurring and artificial DI RNAs derived from BBMV RNA2 have been studied to determine the minimum requirements in the RNA sequence and the presence of an open reading frame (ORF) for efficient accumulation of the defective molecule. Sequence/structural elements of BBMV RNA that may be involved in DI RNA formation have been analysed as well. Additional DI RNAs found associated with members of the<em>Bromoviridae</em>family and other virus groups as well as defective viruses are also described. Several general features of DI RNAs and defective viruses derived from multipartite RNA viruses of plants are becoming apparent. In general, for a given virus, the defective element appears to be derived preferentially from only one of the RNA components. DI RNAs are formed via simple, single deletions that preserve some form of an ORF. Finally, when selective conditions have been altered, multipartite RNA viruses can form defective viruses quite rapidly by deleting substantial portions of the viral genome. This last point indicates that the entire viral genome is subject to continual selection pressure.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 6","pages":"Pages 399-408"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51138990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recombination in large RNA viruses: Coronaviruses","authors":"Michael M.C. Lai","doi":"10.1006/smvy.1996.0046","DOIUrl":"10.1006/smvy.1996.0046","url":null,"abstract":"<div><p>Coronaviruses contain a very large RNA genome, which undergoes recombination at a very high frequency of nearly 25% for the entire genome. Recombination has been demonstrated to occur between viral genomes and between defective-interfering (DI) RNAs and viral RNA. It provides an evolutionary tool for both viral RNAs and DI RNA and may account for the diversity in the genomic structure of coronaviruses. The capacity of coronaviruses to undergo recombination may be related to its mRNA transcription mechanism, which involves discontinuous RNA synthesis, suggesting the nonprocessive nature of the viral polymerase. Recombination is used as a tool for the mutagenesis of viral genomic RNA.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 6","pages":"Pages 381-388"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51139282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Formation and evolution ofTombusvirusdefective interfering RNAs","authors":"K.Andrew White","doi":"10.1006/smvy.1996.0049","DOIUrl":"10.1006/smvy.1996.0049","url":null,"abstract":"<div><p>Defective interfering (DI) RNAs associated with members of the genus<em>Tombusvirus</em>are among the most extensively characterized. These molecules, which represent replicable deletion mutants of viral genomes, are able to accumulate to high levels in viral infections and have the effect of suppressing virus accumulation and attenuating virus-induced symptoms in host plants. Numerous studies have led to a greater understanding of how these molecules are formed and what factors influence their accumulation. Here an overview is provided of what is currently known about the structure, formation and evolution of this important class of sub-viral replicon.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 6","pages":"Pages 409-416"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51139029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Richard F. Allison , William L. Schneider , Ann E. Greene
{"title":"Recombination in plants expressing viral transgenes","authors":"Richard F. Allison , William L. Schneider , Ann E. Greene","doi":"10.1006/smvy.1996.0050","DOIUrl":"10.1006/smvy.1996.0050","url":null,"abstract":"<div><p>When a segment of a specific viral genome is expressed in a transgenic plant, the plant is often resistant to that virus. This promising method of deriving virus resistance appears also to provide an opportunity for RNA recombination. Several reports confirm that the viral transgenic transcript is available to a challenging virus for recombination. Using cowpea chlorotic mottle virus as a model, modifications of the transgene significantly reduced the recovery of viable recombinants from transgenic plants. Several recommendations are made for reducing the involvement of the transgene in RNA recombination events.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 6","pages":"Pages 417-422"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51139125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Different mechanisms of homologous and nonhomologous recombination in brome mosaic virus: role of RNA sequences and replicase proteins","authors":"Jozef J. Bujarski , Peter D. Nagy","doi":"10.1006/smvy.1996.0044","DOIUrl":"https://doi.org/10.1006/smvy.1996.0044","url":null,"abstract":"<div><p>Brome mosaic bromovirus, a tripartite, positive-stranded RNA virus of plants, can generate both homologous and nonhomologous recombinants<em>in vivo</em>. Recombination signals in the RNAs were different for these two recombination types. Nonhomologous recombination requires the formation of local double-stranded regions between the RNA templates. In contrast, homologous recombination is facilitated by AU-rich sequences and upstream GC-rich regions common in the recombining RNAs. Mutations within the replicase proteins affect homologous and nonhomologous recombination in different ways, confirming the involvement of BMV replicase proteins in both types of events as well as the differences in their pathways. Replicase-driven template-switching models are discussed in relation to supporting evidences.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 6","pages":"Pages 363-372"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137195607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Human herpesvirus 8 and the biology of Kaposi's sarcoma","authors":"Don Ganem","doi":"10.1006/smvy.1996.0040","DOIUrl":"https://doi.org/10.1006/smvy.1996.0040","url":null,"abstract":"<div><p>Kaposi's sarcoma (KS) is the leading neoplasm of AIDS patients and also occurs at a lower frequency in HIV-negative hosts. Epidemiologic evidence suggests that a sexually transmitted agent or cofactor other than HIV plays a key role in KS development. The DNA of a novel herpesvirus (termed human herpesvirus 8 (HHV8) or KS-associated herpesvirus (KSHV)) is regularly associated with both the AIDS-related and HIV-negative forms of the disease. Seroepidemiologic studies suggest that HHV8 is sexually transmitted and show that HHV8 infection is tightly linked to KS risk. Infection precedes tumor development and targets the spindle (endothelial) cell component of the tumor, thought to be the dominant cell in KS pathogenesis. Most such cells are latently infected, but tumors also appear to harbor a small subpopulation of productively infected cells. Thus, mounting evidence supports the view that HHV8 is the sexually transmitted cofactor predicted by the epidemiology of KS. In addition, HHV8 also infects B lymphocytes and is associated with several uncommon lymphoproliferative syndromes in AIDS patients.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 5","pages":"Pages 325-332"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137335077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eberhard Hildt, Peter Hans Hofschneider, Stephan Urban
{"title":"The role of hepatitis B virus (HBV) in the development of hepatocellular carcinoma","authors":"Eberhard Hildt, Peter Hans Hofschneider, Stephan Urban","doi":"10.1006/smvy.1996.0041","DOIUrl":"https://doi.org/10.1006/smvy.1996.0041","url":null,"abstract":"<div><p>Based on epidemiological data and experimental results, mammalian hepadnaviruses, in particular hepatitis B virus (HBV) and woodchuck hepatitis virus (WHV), have to be considered as a causative factor in the development of hepatocellular carcinoma (HCC), despite the fact that they lack a complete viral oncogene. Integrated viral DNA is found regularly in woodchuck and human HCC. In woodchucks an activation in<em>cis</em>of c-myc and N-myc is almost always observed. By contrast, in humans, a pleiotropic activation in<em>trans</em>of cellular genes by integrated genes encoding HBV transactivators, namely the X protein (HBx) and the PreS2 activators (the large surface protein (LHBs) and truncated middle surface proteins (MHBs<sup>t</sup>)), has been described as a general mechanism. Mimicking chemical tumour promoters, i.e. TPA, the viral transactivators trigger PKC/Raf-controlled signalling pathways, finally activating transcription factors such as AP-1 and NF-κB which control genes relevant for proliferation. Moreover, ‘HBV-transactivated’ hepatocytes may give rise to a new epigenetic situation in the form of an ‘immortalized’ inflammatory process which may then pave the way for further critical events such as mutations and chromosomal aberrations.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 5","pages":"Pages 333-347"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137335075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Multiple targets of HTLV-1 for dysregulation of host cells","authors":"Mitsuaki Yoshida","doi":"10.1006/smvy.1996.0042","DOIUrl":"https://doi.org/10.1006/smvy.1996.0042","url":null,"abstract":"<div><p>A retrovirus, human T-cell leukemia virus type 1 (HTLV-1), contains the genes coding for non-structural regulatory proteins. These genes comprise a unique control system for viral gene expression. One of these genes, tax, has also been implicated in the tumorigenesis of adult T-cell leukemia (ATL). The tax gene immortalizes T cells and transforms fibroblasts<em>in vitro</em>. The molecular mechanisms underlying the tumorigenesis might include its pleiotropic effects on multiple regulatory proteins of cells. Target molecules include positive (CREB, NF-κB, SRF) and negative (IκB) regulators of transcription, a basic transcription factor, a cell cycle inhibitor (p16<sup>INK</sup>) and a protein kinase C. Functional roles of Tax in the viral replication and abnormal growth of HTLV-1-infected cells are summarized and compared with other tumorigenic viruses.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 5","pages":"Pages 349-360"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136994450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Human papillomaviruses target differentiating epithelia for virion production and malignant conversion","authors":"Laimonis A. Laimins","doi":"10.1006/smvy.1996.0038","DOIUrl":"10.1006/smvy.1996.0038","url":null,"abstract":"<div><p>Human papillomaviruses infect stratified epithelial cells and induce hyperproliferative lesions. Over 70 different HPV types have been identified and each targets epithelia at distinct body locations. A subset, including HPV types 16, 18, 31, 45 and 54, target the genital tract and are the etiological agents of cervical cancers. While viral infection is a necessary prerequisite for the development of most cervical cancers, it is not by itself sufficient indicating that secondary mutational events are also required. The viral life is closely linked to epithelial differentiation and this process is disrupted in the development of malignancies. In a productive infection, vegetative replication and production of virions is restricted to highly differentiated suprabasal cells. Analysis of the mechanisms regulating the viral life cycle in differentiating epithelia provides insight into why certain types induce cancers of the genital tract.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 5","pages":"Pages 305-313"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51138257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pathogenesis of Epstein–Barr virus and its associated malignancies","authors":"Nancy Raab-Traub","doi":"10.1006/smvy.1996.0039","DOIUrl":"https://doi.org/10.1006/smvy.1996.0039","url":null,"abstract":"<div><p>Epstein–Barr virus (EBV) is a human herpesvirus that establishes a latent infection in lymphoid cells and replicates in epithelial cells. EBV is linked to the development of several human cancers and causes lymphoma in immunocompromised patients. EBV infection<em>in vivo</em>is a complex mixture of latent, reactivated, transforming, or replicative types of infection. It is marked by sporadic viral excretion in the oropharynx and persistent latent infection in the bone marrow and peripheral blood lymphocytes. Factors that contribute to the development of cancer possibly affect the type of viral infection in the differing cell types. The EBV latent membrane protein 1 is a critical factor in EBV pathogenesis as it induces cellular growth and affects cellular growth control mechanisms.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 5","pages":"Pages 315-323"},"PeriodicalIF":0.0,"publicationDate":"1996-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137335076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}