Original Paragraph _____________________________
In a world where bats and pigs recombine diseases to create contagions that would leave The Hulk a quivering mess, what hope does our immune system really have in fighting off these new super invaders? Well, motivated by the entirely reasonable belief that what we don’t know really could kill us, researchers in The Netherlands have shown that a certain virus called ‘emerging human Coronavirus’ interacts with an immune regulatory protein called dipeptidyl peptidase 4 (DPP4) and can use it to sneak into and infect our cells through a metaphorical ‘back door’ (Raj et.al., Nature 2013). This new human coronavirus is closely related to the infamous SARS respiratory virus from China that the World Health Organisation reported killed 774 people in 2002 and 2003 (see Alcami et. al. 2000). When a virus like this mutates and embellishes itself, just like SARS it could cause life-threatening illness in humans. This is where DPP4 comes in. Associate Professor Mark Gorrell of Sydney University says that, “This molecule [DPP4] has been closely studied in terms of its role in the immune system, especially lymphocytes. The coronavirus will attack the immune system using DPP4 as its doorway into the immune cells.” This effectively means that the virus will target and infect the very immune cells, or lymphocytes, that are designed to destroy pathogens. Dr. Gorrell is a prominent expert in DPP4 and studies many proteins involved in immune function and liver disease. He thinks that, based on the research done in the Netherlands, and from previous research in his own lab, “we already have antibodies specifically targeted to the part of DPP4 that this coronavirus binds to, and hence potentially could develop a drug that can block viral infection”. Although our immune system is enormously adept at battling the myriad invaders we face every day, if we didn’t have the help of scientific innovations like these and the development of medicines that give our immune system a bit of a superhero boost, we could all succumb to sneaky little mutants just waiting for their chance.
Edited paragraph _____________________________
In a world where bats and pigs recombine diseases to create contagions that would leave The Hulk a quivering mess, what hope does our immune system really have in fighting off these new super invaders? Well, motivated by the entirely reasonable belief that what we don’t know really could kill us, researchers in the Netherlands have shown that a certain virus called ‘emerging human Coronavirus’ interacts with an immune regulatory protein called dipeptidyl peptidase 4 (DPP4) and can use it to sneak into and infect our cells though a metaphorical ‘back door’ (Raj et.al., Nature 2013). This new human coronavirus is closely related to the infamous SARS respiratory virus from China that the World Health Organisation reported killed 774 people in 2002 and 2003 (see Alcami et. al. 2000). When a virus like this mutates and embellishes itself, just like SARS it could cause life-threatening illness in humans. This is where DPP4 comes in. Associate Professor Mark Gorrell of Sydney University says that, “This molecule [DPP4] has been closely studied in terms of its role in the immune system, especially lymphocytes. The coronavirus will attack the immune system using DPP4 as its doorway into the immune cells.” This effectively means that the virus will target and infect the very immune cells, or lymphocytes, that are designed to destroy disease causing agents like viruses. Dr. Gorrell is a prominent expert in DPP4 and studies many proteins involved in immune function and liver disease. He thinks that, based on the research done in the Netherlands, and from previous research in his own lab, “we already have antibodies specifically targeted to the part of DPP4 that this coronavirus binds to, and hence potentially could develop a drug that can block viral infection”. Although our immune system is enormously adept at battling the myriad invaders we face every day, with a little help from scientific innovations like these our immune cells can get the superhero boost they sometimes need to stop sneaky little mutants in their tracks.
New Paragraph
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You may then wonder: if our immune system is usually so amazingly adept, how is it that pathogens like viruses can get past it? The answer is that even the terribly clever immune system we have in our employ can be fooled with equally clever trickery. After discovering that emerging human coronavirus had a specialised mechanism for hoodwinking our immune cells by binding to DPP4, researchers focused on answering the very important question of how this mechanism worked. The main focus was on the tiny section of the
DPP4 protein that allowed the binding. It is a little like the old ‘key and lock’ adage – researchers from Beijing in China showed that the mechanism involves a small section of DPP4 that acts as the ‘lock’ that sticks out of the lymphocyte cell wall, and the individual coronavirus particles (or virions), hone in and bind to this little protruding arm of the DPP4 protein; this viral binding then acts as the ‘key’ that tricks the immune cell into inviting the virus inside the cell (Lu. et.al, Nature 2013). Once inside the immune cell, the coronavirus rapidly replicates itself thousands of times and kills the lymphocyte it infected, stopping it from protecting our body. Doing this in thousands of cells at a time, the now many millions- strong virus breaks out and goes on to invade and infect even more immune cells. What this all means is that the virus has sneakily evolved to bind to DPP4, a protein present ubiquitously in tissue in our bodies, and avoid our immune system by directly infecting and killing the very lymphocytes that would normally kill the virus. It is little wonder that this process makes us feel sick! According to World Health Organisation data as of July 2013, this coronavirus has a mortality rate of almost 50%. Dr. Mark Gorrell of Sydney University says that, “…something particularly fascinating is that even if DPP4 is ‘switched off’, and its protein function stopped using very specific drugs, the virus can still use the inactive DPP4
to wiggle its way into the target lymphocytes.” This is very important because this particular coronavirus, just like SARS, specifically targets lymphocytes in our respiratory tract – this is the main reason infected people develop fluid-filled lungs and a characteristic racking cough. With further research and some nifty engineering, a vaccine could potentially be used to prevent this binding, and therefore also prevent viral infection by using targeted antibodies to kill the virus before it can attack.
Reflection __________________________
In completing the coursework for this unit I have become very aware of stylistic choices for communicating concepts to different audiences. The feedback I received from my partner was very useful in terms of stylistic revision and higher order concerns, as well as furthering my understanding of how genre can be interpreted very differently depending on a person’s own experiences. I suppose I had an expectation that my partner would be able to identify the genre of my review paragraph, and I can reasonably attribute this expectation to my own familiarity with popular science magazines and my own cultural context. The fact is, however, that when considered with respect to my partner’s own experiences, he interpreted that it appeared to be for a formal academic audience. This made me consider just how audience specific and targeted the genre of scientific journalism is, and that a particular interpretation of a written style is not only connected to cultural context, but also to exposure and the diversity of individual experiences with different kinds of literature.
The majority of the feedback I was given for this task did not fit with the genre my paragraph was written in and I therefore chose not to incorporate many of the review comments into my edited paragraph. I did consider each point that was made in the feedback very carefully, and as my partner suggested, I simplified the term ‘pathogens’ to ‘disease causing agents’ in order to clarify my meaning. This made the sentence more appropriate to a general audience by using descriptive and more commonly utilised words.
I also think my partner’s suggestion to change and formalise the colloquialism ‘through a metaphorical back door’ was interesting to consider. I interpreted this request for specificity as being linked to a curiosity about the actual mechanism for DPP4 binding, and as this detail would have been inappropriate to add in my introductory paragraph I decided to make it the focus of my second paragraph. The research on this mechanism is very recent and directly related to my first paragraph, so it flows on very easily and maintains the essential contextual and stylistic elements of a journalistic genre.
I tried to keep the style of this new paragraph the same as for my previous writing. The magazine genre needs to be attention grabbing and punchy, so emotional language like ‘attack’, ‘terribly clever’ and ‘killing’ stop the writing from feeling too dry and scientific by
adding pathos, whilst still allowing efficient communication of the point I wish to get across. I used words and phrases throughout the paragraph like ‘how is it…?’ ‘the answer is’, ‘the main focus’, ‘what this all means’ and ‘this is very important’ that linked my ideas and made clear statements of what I wanted the ‘take home’ messages to be, and furthermore the ideas that were important to understanding the paragraph and preparing the reader for subsequent statements.
I experimented with some of the stylistic techniques discussed in this course to emphasise and clarify my ideas and target my writing to my audience. I incorporated another quote and reference to increase the ethos of my writing, and I used parallelism in sentence five with ‘acts as the lock’ and ‘acts as the key’ to keep the progression of ideas logical in a long sentence. I also used an exclamation mark to emphasise a short and punchy statement about ‘feeling sick’ that I thought gave the reader a key idea in a strongly guided format. I was careful to consider the context in which I used different punctuation and how the writing sounded when read aloud, as well as incorporating ideas and feedback from both my tutor and my partner in each paragraph. By integrating all of these techniques I feel I have made my writing more credible, logical and fluid, and that I have a better understanding of how to make use of rhetoric to convey my ideas effectively.
References (for new paragraph): ____________________________
Lu, G., Hu, Y., Wang, Q., Qi, J., Gao, F., Li, Y., Zhang, Y., Zhang, W., Yuan, Y., Bao, J., Zhang, B., Shi, Y., Yan, J., Gao, G. F. (2013). Molecular basis of binding between novel human coronavirus MERS-CoV and its receptor CD26. Nature. 07/07/13 advance online publication, doi:10.1038/nature12328
- Gorrell (personal communication, July 12, 2013) supported his claims about DPP4 binding coronavirus.
Middle East respiratory syndrome coronavirus (MERS-CoV) – update (2013). World Health Organisation. Retrieved from http://www.who.int/csr/don/2013_07_21/en/ on July 25, 2013.
