Biological Sciences
Retroviruses
Retroviruses are a type of RNA virus that can integrate their genetic material into the DNA of the host cell. They are known for their ability to cause diseases such as HIV/AIDS and certain types of cancer. Retroviruses have a unique enzyme called reverse transcriptase, which allows them to convert their RNA into DNA once inside a host cell.
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10 Key excerpts on "Retroviruses"
eBook - PDF- Shailendra K. Saxena(Author)
- 2016(Publication Date)
- IntechOpen(Publisher)
Section 1 Retrovirus - Molecular Biology and Pathogenesis Chapter 1 Molecular Biology and Pathogenesis of Retroviruses Shailendra K. Saxena and Sai V. Chitti Additional information is available at the end of the chapter http://dx.doi.org/10.5772/62885 Abstract Retroviruses consist of a varied family of enveloped RNA viruses with positive-sense RNAs that replicate in a host cell through the process of reverse transcription. Retrovirus‐ es belong to the Retroviridae family that typically carries their genetic material in the form of ribonucleic acid, while the genetic material of their hosts is in the form of deoxy‐ ribonucleic acid. Infections with a number of Retroviruses can lead to serious conditions, such as AIDS, a range of malignancies, neurological diseases, and added clinical condi‐ tions. In addition, some can even become integrated as DNA in the germ line and passed as endogenous viruses from generation to generation. Surprisingly, Retroviruses do not appear to straightforwardly activate host innate defenses. On the other hand, attention in these viruses extends beyond their disease causing capabilities. For example, studies on the Retroviruses led to the discovery of oncogenes, understanding of mechanisms that regulate eukaryotic gene expression, and these are proving to be valuable research tools in molecular biology and have been used successfully in gene therapy. The central goals of retrovirology today are the treatment and the prevention of human and non-human diseases and to use this virus in research. Keywords: retrovirus, Retroviridae, reverse transcriptase, replication, immune responses, ART 1. Introduction During the past few decades retrovirus has done an adequate amount of harm to the human life and became a big threat globally.
No longer available |Learn moreGene and Cell Therapy
Therapeutic Mechanisms & Applications
- (Author)
- 2014(Publication Date)
- The English Press(Publisher)
____________________ WORLD TECHNOLOGIES ____________________ Chapter- 2 Retrovirus Retroviruses Virus classification Group: Group VI (ssRNA-RT) Family: Retroviridae Genera Subfamily : Orthoretrovirinae Alpharetrovirus Betaretrovirus Gammaretrovirus Deltaretrovirus Epsilonretrovirus Lentivirus Subfamily : Spumaretrovirinae Spumavirus A retrovirus is an RNA virus that is replicated in a host cell via the enzyme reverse transcriptase to produce DNA from its RNA genome. The DNA is then incorporated into the host's genome by an integrase enzyme. The virus thereafter replicates as part of the host cell's DNA. Retroviruses are enveloped viruses that belong to the viral family Retroviridae . A special variant of retroviri are endogenous retroviri which are integrated into the genome of the host and inherited across generations. The virus itself stores its nucleic acid in the form of a +mRNA (including the 5'cap and 3'PolyA inside the virion) genome and serves as a means of delivery of that genome into cells it targets as an obligate parasite, and constitutes the infection. Once in the host's cell, the RNA strands undergo reverse transcription in the cytoplasm and are integrated into ____________________ WORLD TECHNOLOGIES ____________________ the host's genome, at which point the retroviral DNA is referred to as a provirus. It is difficult to detect the virus until it has infected the host. Simply, DNA is usually transcribed into RNA, and RNA is translated into protein. However, Retroviruses function differently - their RNA is reverse-transcribed into DNA, which is integrated into the host cell's genome (when it becomes a provirus), and then undergoes the usual transcription and translational processes to express the genes carried by the virus. Therefore, the order of steps from a retroviral gene to a retroviral protein is: RNA ➝ DNA ➝ RNA ➝ Protein. Structure Virions of Retroviruses consist of enveloped particles about 100 nm in diameter.
eBook - PDFViral Vectors
Gene Therapy and Neuroscience Applications
- Michael G. Kaplitt, Arthur D. Loewy(Authors)
- 1995(Publication Date)
- Academic Press(Publisher)
Genetics and Biology of Retroviral Vectors Rajat Bannerii Department of Molecular Biology MemoriaI-Sloan Kettering Cancer Center New York, New York In this chapter, retroviral vectors, based on the Moloney murine leukemia virus, are discussed as a method for delivering genes into target cells. This vector system offers the advantages of highly efficient gene transfer and stable gene expression in the target cell by virtue of the integration of the vector genome into the host chromosomal DNA. Other vector systems including adenovirus vectors, vaccinia virus vectors, and nonviral methods, such as lipo- somes, may allow only transient gene expression (Mulligan, 1993). Adeno- associated virus vectors do have the ability to stabily integrate into the host genome and will be discussed elsewhere (see Samulski, this volume). Helper- free retroviral vectors infect only once and do not spread in vivo, in contrast to other viral vector methods which employ attenuated viruses that may retain the ability to infect other cells. Retroviral vectors have a wide host range, both in terms of species and cell types (Hartley and Rowe, 1976; Rasheed et al., 1976; Luciw and Leung, 1992), but are limited to infecting only dividing cells (Varmus et al., 1977; Fritsch and Temin, 1977; Humphries et al., 1981). Overall, retroviral vectors offer an excellent gene delivery system available for stable gene transfer and expression. Retroviruses are single-stranded RNA viruses encoding a characteristic RNA-dependent DNA polymerase (reverse transcriptase, see Baltimore, 1970; Temin and Mizutani, 1970). They initially were identified as RNA tumor viruses by Peyton Rous, who was working at the Rockefeller Institute on a spontaneous chicken sarcoma (Rous, 1911). Since the discovery of the Rous sarcoma virus (RSV), many tumor causing Retroviruses have been found in a variety of vertebrates including reptiles, birds, and mammals.
eBook - PDF- Nigel J. Dimmock, Andrew J. Easton, Keith N. Leppard(Authors)
- 2015(Publication Date)
- Wiley-Blackwell(Publisher)
J. 2010. Defective interfering viruses and their potential as antiviral agents. Reviews in Medical Virology 20, 51–62. Marriott, A.C., Easton, A. J. 2000. Paramyxoviruses. In, reverse genetics of RNA viruses. Advances in Virus Research 53, 312–340. Portela, A., Digard, P. 2002. The influenza virus nucleoprotein: a multifunctional RNA-binding protein pivotal to virus replication. Journal of General Virology 83, 723–734. Taylor, J. M. 1992. The structure and replication of hepatitis delta virus. Annual Review of Microbiology 42, 253–276. Taylor, J. M. 2003. Replication of human hepatitis delta virus: recent developments. Trends in Microbiology 11, 185–190. Chapter 9 The process of infection: IIC. The replication of RNA viruses with a DNA intermediate and vice versa Some viruses switch their genetic material between RNA and DNA forms during their infectious cycles. The idea of DNA synthesis from an RNA template was once regarded as heresy to the doctrine of information flow from DNA to RNA to protein. However, it now has an established place in molecular biology. Indeed, many mammalian genome DNA sequences (some pseudogenes, many highly repetitive sequences and certain types of transposable elements) are known to have been created in this way. Chapter 9 Outline 9.1 The retrovirus replication cycle 9.2 Discovery of reverse transcription 9.3 Retroviral reverse transcriptase 9.4 Mechanism of retroviral reverse transcription 9.5 Integration of retroviral DNA into cell DNA 9.6 Production of retrovirus progeny genomes 9.7 Spumaviruses: retrovirus with unusual features 9.8 The hepadnavirus replication cycle 9.9 Mechanism of hepadnavirus reverse transcription 9.10 Comparing reverse transcribing viruses This chapter discusses the replication of the Retroviruses and the hepadnaviruses, two important virus families that have their genetic information in both RNA and DNA forms at different stages of their lifecycles.
eBook - PDF- Ellen G. Strauss, James H. Strauss(Authors)
- 2002(Publication Date)
- Academic Press(Publisher)
Although clearly important for our understanding of biology, for many years after their discovery Retroviruses were in some ways biological curiosities because no human disease was known to be associated with retroviral infec-tion. This changed with the discovery of human T-cell leukemia viruses, now known as primate T-lymphotropic viruses (PTLV), which cause leukemia in man. More recently, the appearance of human immunodeficiency virus (HIV) and of acquired immunodeficiency syndrome (AIDS) in the human population has dramatically altered our understanding of the disease-causing potential of retro-viruses. 171 C H A P T E R 5 Viruses Whose Life Cycle Uses Reverse Transcriptase 172 Viruses That Use Reverse Transcriptase Virus Genus MLV FeLV HERV-C WDSV HSRV HIV-1 HIV-2 EIAV VMV MPMV MMTV HERV-K IAP RSV BLV PTLV-1 PTLV-2 Gammaretrovirus Epsilonretrovirus Spumavirus Lentivirus Betaretrovirus Alpharetrovirus Deltaretrovirus new env new env orfA, orfB, orfC bel1, bel2 tat, rev dut sag tax, rex FIGURE 5.1 Phylogenetic tree of the Retroviridae drawn from the amino acid sequences of the reverse transcriptases. The lengths of the branches are proportional to the degree of divergence; the names of the “simple” retrovirus genera are boxed in black, the “complex” genera are boxed in red. The green ovals indi-cate the acquisition of new genes during the evolution of current extant viruses. Most of the virus name abbreviations are found in Table 5.1; HERV-C and HERV-K are defective Retroviruses in the human genome and IAP is a virus-like element in rodent genomes. [Adapted from Coffin et al . (1997, Fig. 6, p. 43) and Fields et al . (1996, p. 1769).] The most important hepadnavirus is hepatitis B virus, which is a major cause of hepatitis in man. Like hepatitis C virus, it often establishes a chronic infection that can result in cirrhosis or hepatocellular carcinoma.
eBook - PDF- Nicholas H. Acheson(Author)
- 2012(Publication Date)
- Wiley(Publisher)
If present in germ line cells, the viral genome (and therefore virus) can be inherited, and will persist by “vertical transmission”. Sequencing of genomes of a many animal species has revealed that a sig- nificant fraction of the genome (8% in humans) is composed of retrovirus DNAs; these are called “endogenous Retroviruses”. In most instances, the viral DNA cannot produce infectious virus because of mutations that disrupt or delete reading frames or gene expression control sequences. Comparative sequencing data show that retroviral DNA has been inserted into germ line genomes at different times during evolution, some occurring after the division of humans and apes. Some genes of endogenous Retroviruses have even been adapted by the host organism for special- ized functions. An example is the env gene of human endog- enous retrovirus W, called syncytin-1. Expressed during fetal development, Syncytin-1 can induce membrane fusion, and is active in the formation of the fused trophoblast layer of cells surrounding the fetus. An even larger fraction of most genomes (41% in humans) is composed of retrovirus-like elements termed retrotransposons. These elements are related to the retro- viruses by their mechanism of replication; they express an RNA that is converted into DNA by reverse transcriptase and is subsequently integrated into the genome. They can there- fore spread within the cell genome, but do not code for pro- teins that allow them to escape the cell. Retrotransposons may have been the precursor of Retroviruses. The two major types of human retrotransposons are designated LINE (long interspersed nuclear element) and SINE (short interspersed nuclear element). Only LINEs encode reverse transcriptase. SINEs are dependent on the reverse transcriptase provided by LINEs for their replication. The large number of endogenous Retroviruses and ret- rotransposons present in the genome have enormous muta- genic potential.
eBook - PDFHuman Evolution
Genes, Genealogies and Phylogenies
- Graeme Finlay(Author)
- 2013(Publication Date)
- Cambridge University Press(Publisher)
Because of its toxicity, HIV kills cells rather than causing derangements in their long-term patterns of prolifer- ation. HIV is not believed to directly cause cancers. Cancer-causing Retroviruses pursue their parasitic lifestyle with elegant sophistication. The first step occurs when the infecting virus particle attaches to a cell. It is able to do this because the virus particle displays a protein called the envelope protein (encoded by the retroviral envelope or env gene) that adheres to a target molecule on the surface of the cell to be infected. This adhesive interaction enables the retroviral membrane to fuse with that of the cell, so that the viral genetic material is delivered into the cytoplasm. The genetic information of Retroviruses is embodied in a mol- ecule called RNA, but Retroviruses possess an enzyme that copies (or transcribes) the RNA version into a DNA one. The flow of infor- mation from RNA to DNA is opposite to that which operates in the genetic expression of cellular organisms. The retroviral enzyme has thus been called a reverse transcriptase, and Howard Temin and David Baltimore received the Nobel Prize for its discovery in 1975 (Figure 1.1 ). Retroviruses are professional mutagens. The freshly synthe- sised viral DNA is spliced into the chromosomal DNA of the infected cell. This process is initiated by another virus-encoded enzyme, an integrase or endonuclease. The enzyme haphazardly selects a target Retroviral genealogy 24 site in the host genome, at which it makes two staggered nicks, four to six bases apart (depending on the type of retrovirus), one nick on each DNA strand. This cleavage event creates a gap in the chromo- somal DNA into which the DNA copy of the retroviral genome inserts itself. The integrase has a very loose preference for the bases in the target site. It favours a sequence environment that is rich in A and T bases, and insertion is also favoured in active regions of the genome, in the vicinity of genes.
eBook - PDF- James Shapiro(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
Moreover, Retroviruses can exchange envelope glycoproteins with some members of the rhabdovirus family, such as vesicular stomatitis virus (VSV) (Zavada, 1972; Weiss, 1982). In general, such exchanges are reciprocal, although it is easier to detect pseudotypes containing VSV genomes and retro-virus coat proteins because of the simpler biological assay for VSV. Phenotypic mixing involving products of genes other than env appears to demand close relations between the viruses. For example, only members of the avian leukosis-sarcoma virus family can supply functionally compatible reverse transcriptase to a pol~ member of the same family (Vogt, 1977). Ε. Retroviral Pathogenesis Retroviruses induce a wide variety of diseases (Section II,A,3, Table I), but efforts to determine pathogenetic mechanisms have been focused largely upon neoplastic diseases, and only neoplasms will be considered here. For a broader perspective on retroviral diseases, the reader is referred to Teich et al. (1982) and Gross (1970). 1. PATHOGENESIS BY v-onc + VIRUSES It is convenient to discuss separately the oncogenic viruses that carry an one sequence (v-onc + ) and those that do not (v-onc~) (see Section II,A,8). Al-though in most cases genetic proof is not yet available, it is commonly assumed 10. Retroviruses 457 that tumor induction by v-onc + viruses is due to proteins partially or completely encoded by v-onc (reviewed by Bishop and Varmus, 1982). These proteins are generally not present in virus particles and hence have been identified by immu-noprecipitation of labeled proteins from extracts of infected cells or by transla-tion of viral RNA in vitro. Appropriate antisera have been easily procured in the several cases in which v-onc sequences are expressed as hybrid proteins also containing gag determinants (Fig. 2D, E), because antisera raised against viral structural proteins can also precipitate the hybrid proteins.
eBook - PDF- Angus G. Dalgleish, Robin A. Weiss(Authors)
- 1999(Publication Date)
- Academic Press(Publisher)
HIV and the New Viruses Second Edition ISBN 0-12-200741-7 Copyright 9 1999 Academic Press All rights of reproduction in any form reserved 486 HIV and the New Viruses Exogenous I Endogenous Bindin~.~ I ! Uncoating'~~ I Reverse ~ ~ transcription ~L and intregration Protein synthes~,~ ~'~ synthesis ~_ ,4 9 at,. 9 %~oq Particle~t / Infection -( /'~ No infection Figure 22.2 Comparison of exogenous and endogenous retrovirus life cycles In addition to the cycles indicated, on rare occasions RNA transcripts can reintegrate into the genome without previously being associated with intracellular virus particles. of retroelements among all eukaryotic kingdoms and the high degree of amino acid homology among all known reverse transcriptases adds support for this hypothesis. Alternatively, ERVs may have evolved as endogenized variants of exogenous viruses. Support for this theory can be taken from certain Retroviruses, such as Jaagsiekte retro- virus and mouse mammary tumour virus (MMTV), which are found as both endoge- nous and exogenous agents in their host species (Coffin, 1982; Palmarini et al, 1996). It may be that these viruses represent viral agents that have yet to become fully endoge- nized. As ERVs form part of the germline DNA they will be inherited in a mendelian manner. Although generally considered to be stable mendelian traits of the host genome, in mice new ERV integrations have been reported (Szabo et al, 1993), suggest- ing that the acquisition of new sequences may still be an ongoing process, albeit a very slow one. Isolation of the infectious Retroviruses, murine leukaemia virus (MLV) and Rous- associated virus (RAV-0), from uninfected murine and avian cells respectively, was taken as the first proof that viruses could form part of the normal genome of cells (Aaronson et al, 1969; Vogt and Friis, 1971).
eBook - PDFRna Viruses: Host Gene Responses To Infections
Host Gene Responses to Infections
- Decheng Yang(Author)
- 2009(Publication Date)
- World Scientific(Publisher)
(Joint United Nations Programme on AIDS). 2. Fauci AS, Desrosiers RC (1997). In Retroviruses , eds. Coffin JM, Hughes SH, Varmus Cold Spring Harbor Laboratory Press, Plainview, NY pp. 587–636. 3. Greene WC, Peterlin BM (2002). Nat Med 8 , 673–680. 4. Bohan CA, Kashanchi F, Ensoli B, Buonaguro L, Boris-Lawrie KA, Brady JN (1992). Gene Expr 2 , 391–407. 98 Z. A. Klase, K.-T. Jeang & F. Kashanchi Figure 2. A model of the complex interactions between viruses and cellular RNAi pathways. Interferon is shown here to have miRNA-independent and miRNA-dependent effects on viral replication. Separately, emerging evidence indicates that cellular miRNAs serve to restrict replication of viruses and that viruses in response have evolved ways to suppress and evade these restrictions. 5. Feinberg MB, Baltimore D, Frankel AD (1991). Proc Natl Acad Sci USA 88 , 4045–4049. 6. Jeang KT, Xiao H, Rich EA (1999). J Biol Chem 274 , 28837–28840. 7. Laspia MF, Rice AP, Mathews MB (1989). Cell 59 , 283–292. 8. Fukumori T, Kagawa S, Iida S,Oshima Y, Akari H, Koyama AH, Adachi A (1999). Int J Mol Med 3 , 297–302. 9. Hope TJ (1997). Chem Biol 4 , 335–344. 10. Hope T, Pomerantz RJ (1995). Curr Top Microbiol Immunol 193 , 91–105. 11. Cullen BR (1991). Faseb J 5 , 2361–2368. 12. Perales C, Carrasco L, Gonzalez ME (2005). Biochim Biophys Acta 1743 , 169–175. 13. Agrawal N, Dasaradhi PV, Mohmmed A, Malhotra P, Bhatnagar RK, Mukherjee SK (2003). Microbiol Mol Biol Rev 67 , 657–685. 14. Bartel DP (2004). Cell 116 , 281–297. 15. Hannon GJ (2002). Nature 418 , 244–251. 16. Bernstein E, Caudy AA, Hammond SM, Hannon GJ (2001). Nature 409 , 363–366. 17. Cullen BR (2004). Mol Cell 16 , 861–865. 18. Gregory RI, Yan KP, Amuthan G, Chendrimada T, Doratotaj B, Cooch N, Shiekhattar R (2004). Nature 432 , 235–240. 19. Lee Y, Ahn C, Han J, Choi H, Kim J, Yim J, Lee J, Provost P, Radmark O, Kim S, et al. (2003). Nature 425 , 415–419. 20. Sigova A, Rhind N, Zamore PD (2004).
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