Host cell early

Early steps in replication of the virus nucleic acid, in which the host cell biosynthetic machinery is altered as a prelude to virus nucleic acid synthesis. Virus-specific enzymes may be made ... 

Exit of the virus from the cell occurs as a result of cell lysis. The phage codes for a lytic enzyme, the T4 lysozyme, which causes an attack on the peptidoglycan of the host cell. The burst size of the virus (the average number of phage particies per cell) depends upon how rapidly lysis occurs. If lysis occurs early, then a smaller burst size occurs, whereas slower lysis leads to a higher burst size. The wild type phage exhibits the phenomenon of lysis inhibition, and therefore has a large burst size, but rapid lysis mutants, in which lysis occurs early, show smaller burst sizes. 

Infection-induced cell cycle re-entry and suspension in G2/M occur early in infection and are likely to influence regulation of some of the other host cell effects (Jasmer, 1993). The earliest indication that 7. spiralis induces terminally differentiated skeletal muscle cells to re-enter the cell cycle came... 

The structure of an alphavirus particle is simpler than that of all known cellular organelles, but it is built according to the same principles. This is because the viral genome is small and the virus must use for its construction those cellular components normally engaged in the biogenesis of host cell membranes. This means that studies of viral replication can be exploited to study cellular functions at the molecular level. Naturally viral infections also perturb cellular physiology, but there is usually enough time early in infection for studies to be carried out before cellular malfunction becomes a source of error. 

Note that the protein kinase, which phosphorylates the IF-GDP complex is structurally similar to the protein kinase that is activated by double-stranded RNA, i.e. the genome of some viruses. This protein kinase phosphorylates the IF-GDP complex in an infected host cell, so that viral peptide synthesis is inhibited and the virus cannot multiply. Synthesis of this kinase is stimulated by the cytokine, interferon, which is released by virus-infected cells as an early-warning system to adjacent cells not yet infected (Chapter 17 see Figure 17.32). 

Viral replication consists of several steps (Figure 49-1) (1) attachment of the vims to receptors on the host cell surface (2) entry of the virus through the host cell membrane (3) uncoating of viral nucleic acid (4) synthesis of early regulatory proteins, eg, nucleic acid polymerases (5) synthesis of new viral RNA or DNA (6) synthesis of late, structural proteins (7) assembly (maturation) of viral particles and (8) release from the cell. Antiviral agents can potentially target any of these steps. 

Restriction endonucleases are found in a wide range of bacterial species. Werner Arber discovered in the early 1960s that their biological function is to recognize and cleave foreign DNA (the DNA of an infecting virus, for example) such DNA is said to be restricted. In the host cell s DNA, the sequence that would be recognized... 

Tn general, the DNA viruses multiply in the nucleus of the host cell. The viral DNA is transcribed in the nucleus and the resultant rnRNA translated into proteins on cytoplasmic ribosomes. Depending upon the virus type, early or late proteins may be synthesized. These proteins may function as enzymes ill replication of the viral DNA. as structural components of progeny virions, or as regulatory proteins. Replication of the viral DNA is semiconservative and, in general, depends upon viral proteins. 

Mechanism of Action. Amantadine and rimantadine appear to inhibit one of the early steps in influenza A replication by blocking the uncoating of the virus and preventing the release of viral nucleic acid within the host cell.42 These drugs may also interfere with the assembly of viral components, thus inhibiting one of the final steps in the replication process42 This dual inhibitory effect on the early and late steps of viral replication accounts for these drugs antiviral effectiveness. 

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