Virions release from host cell

Once the mature virion has been assembled, it is ready for release from the cell. The release of certain viruses (c.g. poliovirus) is accompanied by lysis of the ho.st cell membrane and cell death. Some of the enveloped viruses, however. are released by budding m exocyloyis. a process involving fusion between the viral envelope and the cell mcmbiaiK This process is nearly a reversal nf the entry process the host cell membrane remains intact under these cxinditioos and the cell may survive. 

Virions are composed of a core of genetic material, which can either be in the form of DNA or ribonucleic acid (RNA), and a protein coat or capsid. In some vimses (enveloped vimses) the capsid is surrounded by a lipid bilayer membrane. Attached to these membranes are specific proteins, which may play a role in the attachment of the virion to the host cell, or release from the host. Thus, haemagglutinin and neuraminidase are two important enzymes present in the envelope of the influenza vims. 

Sialidase or NA is the second glycoprotein on the virion surface. One of the most important functions of sialidase is associated with the release of virus progeny from infected host cells to repeat the cycle of infection [6, 50], The enzyme catalyzes the hydrolysis of sialic acid residues from glycoconjugates on the cell surface with either Neu5Ac(a2 3)Gal or Neu5Ac(a2 6)Gal linkages (Gal=galactose) [60, 61]. 

Table 2 lists various types of biopharmaceutical products from animal cell cultures. Viral vaccines are usually produced by first culturing the host cells (e.g., MRC-5 and WI-38) to form a cell layer on the surface of substratum. Seed virus is then added and incubated for about 3 weeks for replication in the host cells without killing them. After washing to remove the medium components, the cells are lysed to release the virions for harvesting and purification. The inactivated viral vaccine is produced by inactivation with formaldehyde and adsorption onto aluminum hydroxide adjuvant. 

Despite the diversity in the structures of viruses and the types of host cell that are infected, there are several basic steps in the life cycle of all viruses infection (penetration of the virion or its nucleic acid into the host cell), replication (expression of the viral genome), maturation (assembly of viral components into virions), and release (the emission of new virions from the host cell). Because viruses usually possess only enough genetic information to specify the synthesis of their own components, each type must exploit some of the normal metabolic reactions of its host cell to complete the life cycle. For this reason there are numerous variations on these basic steps. This point can be illustrated by comparing the life cycles of two well-researched viruses the T4 bacteriophage and the human immunodeficiency virus (HIV). 

Rather uniquely, ICAM-1 is also subverted as receptor by human pathogens in at least three different ways. Major group rhinoviruses and A-type coxsackieviruses use ICAM-1 to release their RNA into the host cell cytoplasm. Erythrocytes infected by the malarial parasite Plasmodium falciparum, are able to bind ICAM-1 in the surface of endothelial cells (Berendt et al., 1992 Ockenhouse et al., 1992), and use this cytoadherence to sequester themselves in deep vascular beds, including the brain, minimizing exposure of the parasite to immune surveillance. Finally, human immunodeficiency virus-1 (HIV-1), uses ICAM-1 as a coreceptor (Bastiani et al., 1997 Fortin et al., 1997 Rizzuto and Sodroski, 1997). HIV-1 acquires several host cell membrane proteins when it buds from infected cells, making it possible for ICAM-1 to be incorporated into the envelope of the virions. This results in an increase of subsequent virus-cell interactions, enhancement of virus infectivity, and extension of the host cell range. 

The outcome of infection of cells by simian virus 40 depends on the nature of the cells. When primate cells are infected, the large-T protein is produced, and its presence ultimately leads to the production of new viral DNA and coat proteins. New virus particles are assembled and released the death of the host cell takes place when the new virions are released. When rodent cells are infected, the viral genome is incorporated into the cell DNA. (Adapted from Dealing with Genes The Language of Heredity, by Paul Berg and Maxine Singer, 1992 by University Science Books.)... 

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