Differences between Viruses and Bacteria - Case Study Example

Virus Name Institution Date Introduction A virus is considered as an infectious particle that is submicroscopic made up of a nucleic acid core and a protein coat (Fields, Knipe & Howley, 2007). Viruses are related in size and in diameter they are normally less than 200nm. Like cells, viruses carry genetic material encoded within their nucleic acid (Fields et al, 2007). They can go through mutations as well as reproduce; on the other hand, they are not able to execute metabolism, and hence are not regarded alive. In terms of classification, viruses are grouped according to the nucleic acids’ type they entail, as well as their protein capsule’s shape (Tortora, Funke & Case, 2010). Differences between viruses and bacteria Viruses are the established smallest and uncomplicated form of life (Saunders & Carter, 2007). They are actually 10-100 times tinier than bacteria (Tortora et al, 2010). The leading difference between bacteria and virus is that viruses ought to have a host that is living, like an animal or a plant, in order to multiply, whereas most bacteria are able to grow on surfaces that are not living (Fields et al, 2007). Bacteria are considered intercellular organisms meaning they reside in-between cells; while viruses are considered intracellular organisms i.e. they penetrate the cell of the host and live within the cell (Fields et al, 2007). They transform the genetic material of the host cell from its usual role to creating the virus. There exist some beneficial bacteria although all viruses are actually harmful. Antibiotics are able to destroy bacteria but viruses cannot be killed by antibiotics. One example of an illness that bacteria can cause is strep throat and the flu is one example of a disease that a virus causes (Saunders & Carter, 2007). Bacteria carry every cell organelle (machinery) required for their multiplication and growth (Tortora et al, 2010). Bacteria normally reproduce asexually. With regards to sexual reproduction, particular plasmids genetic information is able to be transferred between bacteria. On the contrary, viruses carry majorly information, for instance, RNA or DNA, packaged within a membranous and/or a protein coat (Tortora et al, 2010). Viruses attach to the machinery of the host cell to reproduce. The structural organization of viruses Every virus has at least 2 parts. An external capsid, made up of subunits of protein, surrounds an internal hub of either RNA or DNA, but not together (Fields et al, 2007). The genome of the virus is mainly numerous hundred genes. Contrary, a cell of a human contains more than 30,000 genes (Fields et al, 2007). A particle of a virus may as well contain numerous proteins, particularly enzymes like polymerases, required to generate viral RNA or DNA (Saunders & Carter, 2007). How viruses multiply A virus is an intracellular parasite that is obligate and can be sustained basically within living cells (Tortora et al, 2010). Obligate in this instance means that viruses ought to behave in a particular manner. Because viruses are considered obligate parasites that are intracellular, they ought to perform their reproduction through parasitizing a cell of a host. They are not able to multiply externally, they can just replicate within a definite host (Tortora et al, 2010). Viruses get access to and are definite to a specific host cell since capsid’s portions (or the envelope’s spikes) attach to particular sites of receptor on the plasma membrane of the host cell (Tortora et al, 2010). The nucleic acid thereby gains entry to the cell, and the genome of the virus codes for protein units’ production within the capsid. The host cell is invaded by the bacteriophages that become in charge of the cell and start replicating viruses, finally bursting or lysing the cell of the host, releasing fresh viruses that infect more cells (Tortora et al, 2010). Other bacteriophages are able to infect a host thereby inserting their DNA in the host DNA (Tortora et al, 2010). With respect to specific circumstances the viral DNA is able to detach and control new virus’s replication, ultimately killing the cell of the host. The nucleic acid takes one of two ways: lysogenic or lytic, once within the host cell (Tortora et al, 2010). Virus might contain genes for some special enzymes required for reproduction of the virus and detach from the cell of the host. The virus depends on host ribosomes, enzymes, ATP, and transfer RNA (tRNA) for the replication (Fields et al, 2007). The lytic phase involves the virus taking over the bacterium operation upon invading it, with the new viruses’ production and their succeeding release killing the bacterium (Fields et al, 2007). On the other hand, the lysogenic cycle occurs when the virus integrates its DNA in the bacterium one, with a few delays until new viruses are produced (Fields et al, 2007). After attachment and invasion, viral DNA turns out to be incorporated into bacterial DNA without host DNA’d destruction (Tortora et al, 2010). When this happens, the phage becomes latent, hence the viral DNA is referred to as prophage. Replication of this prophage takes place together with host DNA, thus every subsequent cell generated by the cell that is infected although latent (lysogenic cell) takes a prophage’s copy (Tortora et al, 2010). Specific environmental elements (for instance, ultraviolent radiation) trigger the prophage to go into the lytic cycle’s biosynthesis stage; thereafter maturation as well as release takes place. Still some viruses infect animal cells, multiply without destroying the cells of the host immediately. Fresh viruses are released through budding from the plasma membrane of the host cell (Tortora et al, 2010). The retrovirus like the human immunodeficiency virus (HIV) that brings about AIDS, multiplies in this manner. Animal viruses multiply just like bacteriophages do, even though with modifications (Tortora et al, 2010). In case the virus entails an envelope, spikes from the glycoprotein first attach to receptors of the plasma membrane. The whole virus then enters the cell of the host through endocytosis (Tortora et al, 2010). The capsid and envelope are lost by the virus the moment the virus is inside the cell of the host. Viral particles that are newly assembled are released by budding. The host range of viruses The host specificity or host range of a parasite involves the set of hosts which an organism is able to use as an associate (Fields et al, 2007). Usually the host range is a function of the virus inability to effectively adsorb or penetrate cells due to incompatibility involving capsid proteins of the virus (or envelope proteins of the virus) and the receptor molecule of the host (Fields et al, 2007). Additionally, the host range is an incompatibility function between the virus biochemistry and the host’s biochemistry (Tortora et al, 2010). Surface receptors of the cell (transmembrane receptors, membrane receptors) are particular fundamental membrane proteins that participate in communication that involves the external world and the cell (Greenacre, 2005). Commensal is a term used for a type of symbiosis where one organism gains whereas the other does not gain (Greenacre, 2005). The host’s first line of defense entails and not limited to the surface receptors like the CD4, glycophorin, mucus, low pH, complement receptors, skin, cellular and humoral components (Greenacre, 2005). The virus’s host range will rely upon the availability of the listed receptors. In case a host does not have a virus’s receptor, or in case the cell of the host does not have a couple of component essential for a virus’s replication, the host may not be infected by the virus inherently (Fields et al, 2007). For instance, mice do not have polio viruses’ receptors and hence cannot be infected by the polio virus. In the same way, humans are naturally resistant to animal and plant viruses. A brief description of how viruses are cultured Viral culture means a laboratory examination where samples are put with a type of a cell that viruses being examined for are able to cause infection (Greenacre, 2005). In case the cells indicate changes, referred to as cytopathic effects, this will indicate positivity of the culture. Conventional viral culture has generally been superseded by culture that is shell vial, where the sample of the virus is centrifuged on the cells’ single layer and the growth of the virus is measured through antigen detection approaches (Tortora et al, 2010). This greatly decreases the period to recognition for viruses that are slow growing like cytomegalovirus. Additionally, the step in centrifugation during shell vial culture promotes this method’s sensitivity because following centrifugation; the sample’s particles of the virus are near the cell’s proximity (Greenacre, 2005). In both shell vial and traditional viral culture, cells from the monkey and human are used. Types of human viruses that are able to be identified through viral culture entail cytomegalovirus, herpes simplex virus, parainfluenza virus, enteroviruses, adenovirus, measles, mumps, influenza virus, varicella zoster virus, rhinovirus, and respiratory syncytial virus (Saunders & Carter, 2007). The final method of identification for these is generally through immunofluorescence, with exclusion of rhinovirus and cytomegalovirus, whose viral culture identification are established through cytopathic effects (Saunders & Carter, 2007). Reference Saunders, V. A., & Carter, J. (2007). Virology. Chichester: John Wiley. Greenacre, C. B. (2005). Virology. Philadelphia: W.B. Saunders. Fields, B. N., Knipe, D. M., & Howley, P. M. (2007). Fields virology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Tortora, G. J., Funke, B. R., & Case, C. L. (2010). Microbiology: An introduction. New York: Custom Pub. Read More