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Viruses of genome

The genome of viruses carries fewer genes than does that of bacteria. Thus, in a fixed amount of DNA (say several viral genome equivalents), viral genes would be present in more copies than would individual bacterial genes. Different genes have different nucleotide sequences, but various sequences would be repeated more frequently in the viral DNA i.e., it would have less sequence heterogeneity. [Pg.224]

At the moment, more than 4,000 different miRNAs are identified or predicted in the genomes of viruses, plants and animals, of which some 700 may occur in man (Griffiths-Jones et al. 2006). Some mammalian miRNAs are located within gene introns and appear to be transcribed within the primary transcript, only to be released during RNA processing (Shivdasani 2006). [Pg.13]

Unlike the genome of viruses, the bacterial genome is able to orient bacterial cells correctly (purposively) relative to chemical (assimilation) conditions of the external environment in two ways, to some extent opposite in direction. [Pg.357]

Very few self-sufficient viruses have only 60 protein chains in their shells. The satellite viruses do not themselves encode all of the functions required for their replication and are therefore not self-sufficient. The first satellite virus to be discovered, satellite tobacco necrosis virus, which is also one of the smallest known with a diameter of 180 A, has a protein shell of 60 subunits. This virus cannot replicate on its own inside a tobacco cell but needs a helper virus, tobacco necrosis virus, to supply the functions it does not encode. The RNA genome of the satellite virus has only 1120 nucleotides, which code for the viral coat protein of 195 amino acids but no other protein. With this minimal genome the satellite viruses are obligate parasites of the viruses that parasitize cells. [Pg.329]

Fig. 1 Classification of viruses by their genome replication strategy according to Baltimore (Baltimore 1971), Examples for important human pathogens falling into the respective class are listed above, Black DNA, gray RNA arrows to the right (+) strand polarity (i,e, corresponding to mRNA) arrows to the left (—(strands asterisk enveloped viruses... Fig. 1 Classification of viruses by their genome replication strategy according to Baltimore (Baltimore 1971), Examples for important human pathogens falling into the respective class are listed above, Black DNA, gray RNA arrows to the right (+) strand polarity (i,e, corresponding to mRNA) arrows to the left (—(strands asterisk enveloped viruses...
Second, the INSTl, but not an RTl, may conceivably inhibit the virus production from the pool of resting CD4 T cells that are in a state of pre-integration latency (Murray et al. 2007). Upon activation, the preformed pro-viral DNA that is already located in the nucleus integrates into the genome of these cells, allowing them to contribute to the viral load. [Pg.161]

The nonnucleoside reverse transcriptase inhibitors (NNRTIs), used in the treatment of AIDS, provide interesting examples of clinically relevant noncompetitive inhibitors. The causative agent of AIDS, HIV, belongs to a virus family that relies on an RNA-based genetic system. Replication of the vims requires reverse transcription of the viral genomic RNA into DNA, which is then incorporated into the genome of the infected host cell. Reverse transcription is catalyzed by a virally encoded nucleic acid polymerase, known as reverse transcriptase (RT). This enzyme is critical for viral replication inhibition of HIV RT is therefore an effective mechanism for abrogating infection in patients. [Pg.59]

When a virus multiplies, the genome becomes released from the coat. This process occurs during the infection process. The present chapter is divided into three parts. The first part deals with basic concepts of virus structure and function. The second part deals with the nature and manner of multiplication of the bacterial viruses (bacteriophages). In this part we introduce the basic molecular biology of virus multiplication. The third part deals with important groups of animal viruses, with emphasis on molecular aspects of animal virus multiplication. [Pg.108]

Virus messenger RNA In order for the new virus-specific proteins to be made from the virus genome, it is necessary for new virus-specific RNA molecules to be made. Exactly how the virus brings about new mRNA synthesis depends upon the type of virus, and especially upon whether its genetic material is RNA or DNA, and whether it is single-stranded or double-stranded. Which copy is read into mRNA depends upon the location of the appropriate promoter, since the promoter points the direction that the RNA polymerase will follow. In cells (uninfected with virus) all mRNA is made on the DNA template, but with RNA viruses the situation is obviously different. [Pg.127]

Viruses may also cause latent infection of a host. In a latent infection, there is a delay between infection by the virus and the appearance of symptoms. Fever blisters (cold sores), caused by the herpes simplex virus, result from a latent viral infection the symptoms reappear sporadically as the virus emerges from latency. The latent stage in viral infection of an animal cell is generally not due to the integration of the viral genome into the genome of the animal cell, as is the case with latent infections by temperate bacteriophages. [Pg.164]


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See also in sourсe #XX -- [ Pg.201 , Pg.244 , Pg.245 , Pg.246 , Pg.247 , Pg.1714 , Pg.1715 ]

See also in sourсe #XX -- [ Pg.201 , Pg.244 , Pg.245 , Pg.246 , Pg.247 ]

See also in sourсe #XX -- [ Pg.201 , Pg.244 , Pg.245 , Pg.246 , Pg.247 ]




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