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Having effectively invaded Earth, the Martians will not be able to continue their plans of world domination - all because of a novel virus, which has been created - The Wells Virus. This virus contains the essential features which will make it a successful pathogen. It is unlike any other known virus due to its combination of unique structure and infectious pathogenic path, thus, making the Wells Virus a truly enigmatic and infectious pathogen. The Martians will never stand a chance.
The Wells Virus like any other virus is an obligate intracellular parasite. It must hijack a host cell in order to replicate. New viral components are synthesised and assembled in the host cell. Viruses do not replicate by division.
It consists of a double-stranded ribonucleic acid (dsRNA) genome, and like all other viruses, the genome is packaged into a protective protein coat, referred to as a capsid. Capsids are formed around the viral genome and can have either helical or icosohedral symmetry. This novel virus contains a capsid with helical symmetry. The capsid is formed from structural subunits, which associate to form capsomeres, which self-assemble to form a helix around the genome. In the Wells Virus, you can see the proteins of the nucleocapsid are arranged like the steps of a spiral staircase and the linear RNA genome fills the central core
This feature is similar to that of the Tobacco Mosaic Virus ; however, the Wells Virus is also surrounded by a lipoprotein envelope, which consists of glycoproteins and a membrane. The membrane is derived from portions of the host cell membrane, through which the virus matures by budding . Glycoproteins present on the Wells Virus surface have the expected role of identifying and binding to receptor sites on susceptible host cell membranes.
Examples of such enveloped viruses with helical morphology are observed within most negative-sense, single stranded RNA viruses ((-) ssRNA), such as Paramyxoviruses. This makes the Wells Virus unique in its attack as it contains dsRNA, but has the structure of viruses containing ss-RNA.
Another feature which makes the Wells Virus unique, are the various proteins it contains. The capsid protein it contains is similarly found in another (-) ssRNA virus - Orthomyxoviruses . The membrane structure contains two types of glycoproteins, haemagglutinin (HA) and neuraminidase (NA) . These proteins extend outwards. HA forms a spike shaped trimer and has several roles including promoting fusion with the host cell membrane, acting as the viral attachment protein, hemagglutinating red blood cells, and eliciting antibody responses. NA is a glycoprotein tetramer and has enzymatic roles, such as cleaving the sialic acid on cell surfaces, which prevents clumping and is important for the release of new progeny. These glycoproteins are in equal proportion on the Wells Viral surface. The membrane which lies underneath the envelope contains membrane proteins.
The Wells virus contains 2 core proteins found in the core of the virus and produce non-structural proteins: 5'methyl guanosine mRNA capping enzyme and RNA dependent RNA polymerase. It requires the latter as it is double stranded; therefore the virus must package the polymerase in order to function as mRNA and because the host cell having a DNA genome, will not have this polymerase. This feature is also found in Rotaviruses.
The Wells virus also has a segmented genome and each gene encodes for only a single protein. Thus, replication can be described as monocistronic, which is common for most eukaryotic mRNA.
Once the Wells Virus has entered the body, target cell recognition and attachment (adsorption) takes place due to the glycoprotein attachment protein (HA) on the viral surface. The HA receptors on the viral surface binds to complimentary sialic acid receptors on a susceptible host cell. The HA undergoes a dramatic conformational change, exposing hydrophobic parts of the cell that allow membrane fusion. The nucleic acid is directly released into the cell's cytoplasm.
Now that the virus has penetrated the host cell, it has entered the eclipse period of the early phase. As is the case with enveloped viruses, the Wells virus becomes uncoated on fusion with cell membrane. The genome remains in the capsid which also contains the necessary RNA polymerase . The genome also remains in the cytoplasm and is not delivered to the nucleus, which is what happens with DNA viruses.
The late phase and Type III (Baltimore Classification) replication now begins as the nucleic acid core is released into the cytoplasm, and as discussed before, the Wells Virus cannot function as an mRNA, because it is double stranded, therefore the initial step is the transcription of the negative strand of dsRNA into a positive strand, using RNA polymerase. The mRNA is capped by the 5'methyl guanosine mRNA capping enzyme, and it provides an effective way of tagging mRNA for translation to the ribosomes. The mRNA is also mythelated before leaving the core for translation into more structural viral proteins, synthesised to make more RNA dependent RNA polymerase. Some viral proteins assemble to from an immature capsid and once RNA polymerase has been packaged into this new core, they are then copied to form dsRNA once again . This mode of reproduction is similar to that seen in the reovirus and rotavirus.
The Wells Virus can either then continue to form more viral proteins, or it can exit the cell by budding, and using the cell membrane to produce an envelope . Continuous budding will slowly use up the cell membrane and eventually lead to the demise of the cell .
Entry of this virus is through both inhalation and any cuts or damage to the skin. Its first point of replication is the upper respiratory tract, and then spreads throughout the body particularly to dermal tissue, causing skin lesions. As well as cell-to-cell contact, the virus can also spread via the bloodstream, thus the virus develops much quicker should it enter through the skin via a cut, and bring it closer to the bloodstream. The nature of the Wells Virus initially resembles that of poxviruses, as well as this; it is the only DNA virus which replicates in the cytoplasm. The virus can be transmitted either by aerosols, or by fomites, where the virus can live in tissues outside the cell . Both these mechanisms allow for easy spread of the virus from one person to the next.
The virus causes a persistent chronic infection, causing cellular senescence and then cell death. The Wells Virus causes viral cytopathogenesis through inhibiting protein synthesis, and by syncytia formation. Forming these giant multinucleate host cells, by fusing infected ones together allows the virus to effectively spread and not be affected by the immune system.
The virus incubation period should be used as a diagnostic tool in the fact that there is an incubation period of 1-3 days before the 1st appearance of symptoms appears. In this case, symptoms related to a common cold and flu infection appear, due to a natural immune response to what it thinks is a reoccurrence of a cold or flu infection. However, there is after a further incubation period of 5-14 days before respiratory infections such as laryngitis, bronchitis and pneumonia can also be experienced. As well this, there is development of blisters and lesions, which present themselves on any epidermal tissue and the mouth. These are similar symptoms seen by Herpes Virus sufferers. Unfortunately due to the virus' ability to establish viremia, the disease spreads and as the infection grows, sufferers become septic. Moreover, through the development of different strains, sufferers may also see the development of the rash into raised papules, eventually forming pustules. These pustules may be mistaken for the same rash exhibited by smallpox sufferers. They are filled with pus and cell debris, as it causes necrosis of immune cells.
Excluding Martians, the major population groups at risk are mainly those who have frequent contact with contaminated surfaces . Those working in hospitals with frequent exposure to the virus, and the immunocompromised are more at risk, since they have a weaker defence system, and already more prone to infection. Risk groups also depend on each individual depending on age, personal habits, and the level of cleanliness they maintain. The virus can be found worldwide, and during the winter months because of lack of light and UV radiation, airborne viruses may be more likely to survive and therefore be transmitted .
Modes of control for the Wells Virus, should the human population be infected include antiviral drugs. The drugs must be administered before the development of raised papules. Improvement in hygiene, including washing hands, disinfecting contaminated objects, and healthcare professionals should wear gloves in order to help prevent spread.
The wells Virus is a unique pathogen, and has all the characteristics which will make it an effective pathogen against the Martians. Although it may have the structure of (-) ssRNA viruses, the Wells Virus replicates like that of a dsRNA virus. Its combination of proteins, allows it to have distinct features when entering and leaving the cell. Its enveloped structure adds the advantage of increasing the speed the viral cells are taken up. RNA viruses mutate more frequently than DNA which means the Wells virus has the potential to cause an extremely virulent strain. Although essentially a RNA virus, the Wells Virus infects and has the pathogenicity similar to various DNA viruses, like Poxviruses, and Herpesviruses. Again, this is simply another feature which makes this a novel virus.
To conclude, the Wells Virus is a force to be reckoned with. It will be an extremely effective virus due its unique features, and for what appears to be a complicated enigmatic virus; it is simply the virus that will, in effect, save the world.
- Klug, A. (1999) The tobacco mosaic virus particle: structure and assembly. Philos. Trans. R. Soc. Lond. B. Biol. Sci., 354, 1383, 531-535
- Suzuki Y. (2005) Sialobiology of influenza: molecular mechanism of host range variation of influenza viruses. Biol. Pharm. Bull., 28, 3, 399-408
- Pornillos, O., Jennifer E. Garrus, J. E. and Sundquist, W. I. (2002) Mechanisms of enveloped RNA virus budding. TRENDS in Cell Biology, 12, 12, 569-579
- Boone, S. A. and Gerba, C. P. (2007) Significance of Fomites in the Spread of Respiratory and Enteric Viral Disease. Applied and Environmental Microbiology, 73, 6, 1687-1696
- Lowen, A. and Peter Palese, P. (2009) Transmission of influenza virus in temperate zones is predominantly by aerosol, in the tropics by contact A hypothesis, PLoS. Curr. Influenza, PMCID: PMC2762697
Abstract can be viewed: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762697/
- Medical Microbiology (2009) Murray, P. R., Rosenthal, K. S. and Pfaller, M.A., Sixth Edition., Elsevier Mosby.