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Molecular virology is the study of viruses on a molecular level. Viruses are submicroscopic parasites that replicate inside host cells. They are able to successfully infect and parasitize all kinds of life forms- from microorganisms to animals and plants - and as the result viruses have more biological diversity than the rest of the animal, plant, and bacterial kingdoms combined. Studying this diversity is the key to a better understanding of how viruses interact with their hosts, replicate inside them, and causes diseases.

Viral Replication
'''Viral populations do not grow through cell division, because they are acellular. Instead, they use the machinery and metabolism of a host cell to produce multiple copies of themselves, and they assemble in the cell.(virus)'''

Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must first get into the cell before viral replication can occur. From the perspective of the virus, the purpose of viral replication is to allow production and survival of its kind. By generating abundant copies of its genome and packaging these copies into viruses, the virus is able to continue infecting new hosts. Most DNA viruses assemble in the nucleus while RNA viruses tend to develop solely in cytoplasm.

David Baltimore, a Nobel Prize-winning biologist, devised a system called the Baltimore Classification System to classify different viruses based on their unique replication strategy. There are seven different replication strategies based on this system (Baltimore Class I, II, III, IV, V, VI, VII). The seven classes of viruses are listed here briefly and in generalities.[2]

Replication between viruses is greatly varied and depends on the type of genes involved in them. In this respect, viruses can be divided into seven groups. Such a division was first proposed by David Baltimore in 1971:
 * Class I; "Double-stranded DNA". Depending on the location of genome replication, this class can be subdivided into two groups: (a) ones in which replication happens exclusively in the nucleus and is thus relatively dependent on cellular factors; (b) viruses replicating in cytoplasm (e.g., the Poxviridae), in which case they have evolved (or acquired) all the necessary factors for transcription and replication of their genomes and are therefore largely independent of the cellular machinery.
 * Class II; "Single-stranded DNA". In these viruses replication occurs in the nucleus, involving the formation of a double-stranded intermediate that serves as a template for the synthesis of single-stranded progeny DNA.
 * Class III; "Double-stranded RNA". These viruses have segmented genomes. Each segment is transcribed separately to produce individual monochromatic mRNAs.
 * Class IV; "Single-stranded RNA". These viruses can be subdivided into two groups depending on their translation process : (a) viruses with polycistronic mRNA where the genomic RNA forms mRNA and translates into poly protein products; (b) viruses with complex transcription, for which two rounds of translation or subgenomic RNAs are necessary to produce the genomic RNA.

Viral pathogenesis
Viral pathogenesis, a specialized field of study in virology, is the study of how biological viruses cause diseases in their target hosts on the molecular level. Viral disease is a sum of the effects on the host caused by the replication of the virus and of the host's subsequent immune response.

In the past few decades, molecular genetic analysis has contributed enormously to our understanding of virus pathogenesis.The function of all cells is regulated by controlled expression of their genetic information and the subsequent degradation of the molecules produced. Such control relies on a delicate and dynamic balance between synthesis and decay, which determines the intracellular levels of all the important molecules in the cell. This is particularly true of the control of the cell cycle, which determines the behavior of dividing cells (see “Cell Transformation by DNA Viruses,” later). In general terms, a number of common phenotypic changes can be recognized in virus-infected cells. These changes are often referred to as the cytopathic effects (c.p.e.) of a virus, and include:
 * Altered shape: Adherent cells that are normally attached to other cells (in vivo) or an artificial substrate (in vitro) may assume a rounded shape different from their normal flattened appearance. The extended processes (extensions of the cell surface resembling tendrils) involved in attachment or mobility are withdrawn into the cell.
 * Detachment from the substrate: For adherent cells, this is the stage of cell damage that follows that just described. Both of these effects are caused by partial degradation or disruption of the cytoskeleton that is normally responsible for maintaining the shape of the cell.


 * Lysis: This is the most extreme case, where the entire cell breaks down. Membrane integrity is lost, and the cell may swell due to the absorption of extracellular fluid and finally break open. This is an extreme case of cell damage, and it is important to realize that not all viruses induce this effect, although they may cause other cytopathic effects. Lysis is beneficial to a virus in that it provides an obvious method of releasing new virus particles rom an infected cell; however, there are alternative ways of achieving this, such as release by budding.


 * Membrane fusion: The membranes of adjacent cells fuse, resulting in a mass of cytoplasm containing more than one nucleus, known as a syncytium, or, depending on the number of cells that merge, a giant cell. Fused cells are short lived and subsequently lysedapart from direct effects of the virus, they cannot tolerate more than one nonsynchronized nucleus per cell.


 * Membrane permeability: A number of viruses cause an increase in membrane permeability, allowing an influx of extracellular ions such as sodium. Translation of some virus mRNAs is resistant to high concentrations of sodium ions, permitting the expression of virus genes at the expense of cellular messages.

Viral immunology
Viral immunology by antibodies results from a number of mechanisms, including conformational changes in the virus capsid caused by antibody binding, or blocking of the function of the virus target molecule (e.g. receptor binding) by steric hindrance. A secondary consequence of antibody binding is phagocytosis of antibody-coated (opsonized) target molecules by mononuclear cells or polymorphonuclear leukocytes. This usually results from the presence of the Fc receptor on the surface of these cells. However, in some cases opsonization of a virus can result in enhanced virus uptake by the binding of nonneutralizing antibodies. An example of such opsonization is observable in rabies virus and in human immunodeficiency virus (HIV). In the latter case, opsonization promotes uptake of the virus by macrophages.

Virus outbreaks

Viral vaccines contain inactivated or killed viruses which have lost their ability to replicate. Furthermore, these vaccines have more antigen than live vaccines so that they can cause a stronger response from the immune system. By contrast, attenuated or live vaccines contain the live form of the virus. These viruses are not pathogenic but are able to induce an immune response.

The alternative to vaccination is to attempt to treat virus infections using drugs that block virus replication. Historically, the discovery of antiviral drugs was largely due to luck. Spurred on by successes in the treatment of bacterial infections with antibiotics, drug companies launched huge blindscreening programs to identify chemical compounds with antiviral activity, with relatively little success. The key to the success of any antiviral drug lies in its specificity. Almost any stage of virus replication can be a target for a drug, but the drug must be more toxic to the virus than to the host. This is measured by the chemotherapeutic index, given by :
 * $$\frac{\hbox{Dose of drug that inhibits virus replication}}{\hbox{Dose of drug that is toxic to host}}$$

The smaller the value of the chemotherapeutic index, the better the efficacy of the drug. In practice, a difference of several orders of magnitude between the two toxicity values is usually required to produce a safe and clinically useful drug.

Additional links

 * molecular biology
 * phage, the virus of bacteria/prokaryotes
 * viral plaque
 * Important publications in virology
 * Virus classification