Viral genetic mutation Viruses undergo genetic change by

Viral genetic mutation Viruses undergo genetic change by several mechanisms. These include a process called : Antigenic drift where individual bases in the DNA or RNA mutate to other bases. Most of these point mutations are "silent" – they do not change the protein that the gene encodes. Antigenic shift occurs when there is a major change in the genome of the virus. This can be a result of recombination or reassortment. When this happens with influenza viruses, pandemics might result.

Segmented genomes confer evolutionary advantages; different strains of a virus with a segmented genome can shuffle and combine genes and produce progeny viruses or (offspring) that have unique characteristics. This is called reassortment or viral sex. Genetic recombination is the process by which a strand of DNA is broken and then joined to the end of a different DNA molecule. This can occur when viruses infect cells simultaneously and studies of viral evolution have shown that recombination has been rampant in the species studied. Recombination is common to both RNA and DNA viruse.

How antigenic shift, or reassortment, can result in novel and highly pathogenic strains of human flu.

The Types of Mutations The types of mutations or alterations of the DNA or RNA that these viruses incur on the host cells include the processes of substitution, insertion, deletion, and frameshift. Substitution occurs when one or more type amino acid is replaced by another. The result can either be a change of protein product, or silent mutation (no change in protein product), or an incomplete and nonfunctional protein. Deletion mutation occurs when a portion of the DNA is taken away, or deleted. Insertion mutation happens when an extra pairs of amino acids are inserted in the sequence. When insertion and deletion mutation occurs, it also causes a frameshift mutation where a gene can no longer be correctly transcribed.

Defective Viruses A defective virus is one that lacks one or more functional genes required for viral replication. Defective viruses require helper activity from another virus for some step in replication or maturation. One type of defective virus lacks a portion of its genome (deletion mutation). The extent of loss by deletion may vary from a short base sequence to a large amount of genome. another category of defective virus required an unrelated replication – competent virus as helper. examples include the adeno-associated satellite viruses and hepatitis d, which replicate only in the presence of coinfecting human adenovirus or hepatitis b virus, respectively.

Pseudovirions, a different type of defective particle, contain host cell DNA rather than the viral genome. During viral replication, the capsid sometimes encloses random pieces of host nucleic acid rather than viral nucleic acid. Such particles look like ordinary viral particles when observed by electron microscopy, but they are not able to replicate. Theoretically might be transduce cellular nucleic acid from one cell to another. Interactions among viruses When two or more virus particles infect the same host cell, they may interact in a variety of ways. They must be sufficiently closely related, usually within the same viral family, for most type of interactions to occur. Genetic interaction results in some progeny that are heritably (genetically) different from either parent.

A. Recombination in the production of progeny virus (recombinant) that carries traits not found together in either parent. The classic mechanism is that the nucleic acid strands break, and part of the genome of the second genome of one parent is joined to part of the second genome of the second parent. A. Complementation This refers to the interaction of viral gene products in cells infected with two viruses, one or both of which may be defective. It results in the replication of one or both under conditions in which replication would not ordinary occur. The basis for complementation is that one virus provide a gene product in which the second is defective, allowing the second virus to grow. The genotypes of the two viruses remain unchanged. If both mutants are defective in the same gene product, they will not be able to complement each other growth.

C- Phenotypic mixing A special case of complementation is phenotypic mixing, this occurs when the genome of one virus becomes randomly incorporated within capsid proteins specified by a different virus or a capsid consisting of components of both viruses. Phenotypic mixing usually occurs between different members of the same virus family. D- Interference Infection of either cell cultures or whole animals with two viruses, an effect called interference. Furthermore, interference does not occur with all viral combinations; two viruses may infect and multiply within the same cell as efficiently as in single infection. Several mechanisms have been elucidated as cause of interference:

1. One virus may inhibit the ability of the second to adsorb to the cell, either by blocking its receptors (retroviruses, enteroviruses) or by destroying its receptors (orthomyxoviuses). 2. One virus may compete with the second for components of the replication apparatus (eg. Polymerase, translation initiation factor). 3. The first virus may cause the infected cell to produce an inhibitor (interferon) that prevents replication of the second virus.

Can Viruses Cause Gene Mutations? Such examples of these are the SV 40 virus (Simian vacuolating virus 40) and the HPV (Human Papilloma Virus), where they inject their RNA or DNA, depending on the type of virus, and mutate the host cell’s genetic code to function and substitute for their metabolic deficiencies. The HPV (Human Papilloma Virus), especially the E 6 and E 7 types, are oncogenes that suppress or inhibit the tumor suppression functions of the p 53 gene. This gene is part of a regulatory pathway that causes damaged cells to die when they cannot be repaired. The E 6 and E 7 proteins inhibits these functions, and allows damaged cells to grow uncontrolled instead of dying off. This can eventually lead to the development of cervical cancer.

The SV 40 virus (Simian vacuolating 40 virus) on the other hand uses the method of caveolin vesicle - via endocytosis, to penetrate the membrane of the host cell and alter the DNA and RNA components resulting in a cell death and an offspring of new SV 40 viruses. These types of virus also have a property that suppresses the suppression functions of the p 53 gene thus resulting again in an uncontrolled cell growth leading to malignant mesothelioma.