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- Pathology: The arms race between viruses and humankind ☢️
Pathology: The arms race between viruses and humankind ☢️
Plus: How do we know things are different? 🤷♂️, and more...
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Here’s a taste of what we’re serving today:
Medicine: The arms race between viruses and humankind ☢️
Linguistics: How do we know things are different? 🤷♂️
Biology: Aposematism and Mimicry 🦋
[MEDICINE] Pathology: The arms race between viruses and humankind ☢️

Viruses infamously outsmart the human body regularly. For example, influenza vaccinations have to be changed each year to fit whichever strain is predicted to be most prevalent. You may have heard of the new BA.2.86 Covid variant, which can render previously-acquired immunity less effective. One of the key reasons for this dynamic nature is the rate at which viruses reproduce. While human generations last about 20 years, viruses can reproduce 200 times in 30 minutes (such as bacteriophage T4). This increased rate of replication opens the door for more frequent mutations and more phenotypic variation to arise in a viral population, some of which may be advantageous to the virus and thus, are positively selected. With our relatively slow replication rate, viruses would naturally out-compete our adaptations with ease. However, we have modern medicine on our side, such as antiviral pharmaceuticals and, more commonly, induced immunity (in the form of a vaccination). These protect us at the point of use, however, also provide a selection pressure to these rapidly mutating viruses, meaning they can evolve to withstand our treatment attempts. Evading this is fundamentally difficult and viruses may always outsmart us…
💡 Things to consider
The advanced machinery and choreographed attack procedure of viruses: The fast turnover rate of viruses allows them to possess a range of attack strategies, despite their small and simple composition. They hijack body cells to exploit their replication machinery at that cell’s expense, acting as a passive protection from immune surveillance. The number of ways that viruses have adapted to overcome our immune system is almost too many to list. Examples include the production of vIL-10 (vIL = viral interleukin: a glycoprotein that regulates immune response) from EBV, which directs the immune system to a response that is less potent against viruses (Th2 polarisation). Membrane modification then allows cell-cell viral spread without it having to enter the extracellular space, where it can more easily be spotted by immune cells.
What affects how well-equipped a virus is?: It goes without saying that some viruses naturally adapt more rapidly than others: you have a measles vaccine (MMR) when you’re very young and you’re set for life, but influenza needs an annual vaccine. The stability of viruses affects to what extent they can outcompete human defence: those that are less stable acquire more mutations that may allow them to evade any attempt kill them. Factors that affect how stable a virus is includes whether it is enveloped or not, its size, and its genome (DNA/RNA, single/double-stranded…).
Why don’t we use antivirals as much as antibiotics?: Earlier, I alluded to antiviral medications. While most people can name a few antibiotics or have at least been prescribed them at some point, antivirals are seemingly harder to come by. There are a number of reasons for this. First of all, the success of viral vaccination programmes and herd immunity means that most people are able to fight off a viral infection easily, without the need for drugs, given the higher amount of virus-specific immune cells circulating in their blood (memory T-lymphocytes). Another, arguably more important reason, is the difference in how bacteria and viruses act in the body. Bacteria are self-contained organisms, while viruses enter our body cells to hijack replicative machinery. Antibiotics can therefore target bacteria - and just the bacteria - while antivirals may have to kill infected body cells, leading to more severe side effects.
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[LINGUISTICS] Saussure: How do we know things are different? 🤷♂️
You would almost certainly know the difference between a dress, a guitar, and a table, if somebody mentioned them to you in conversation. But have you ever stopped to wonder why you know this? Ferdinand de Saussure did, and his Course in General Linguistics was fundamental to the field we now call post-structuralism.

Our bestie Ferdinand de Saussure
Saussure created different categories in language: the sign, the signifier, and the signified. The signifier is the sound of a word as it is spoken (aloud or in our heads), the signified is the concept that this word evokes in our minds, and the sign is the combination of the two. To use ‘cat’ as an example, the signifier is the sound this word makes when you say it, the signified is the cute, furry animal, and the sign is the two put together, which make up the word you see on your screen.
In Saussure’s view, the only reason why we know that a ‘cat’ is a furry animal is because it has a sound that is different to ‘hat’. No language has meaning by itself – all language only has meaning because it is different to everything else in the linguistic system. So we only know that ‘cat’ is the furry animal because we know it isn’t a hat, or a dress, or a guitar, or a table.
💡 Things to consider
Re-signification: According to Saussure, language systems only work if everybody who participates in the language system agrees on what the signifiers refer to. If some people started calling what we know to be a ‘cat’ a ‘dog’ instead, then they might begin the process of re-signification, where a concept that is signified is given a new name, or signifier. How quickly do you think this process could happen? Do the names we give things impact how we understand them?
Arbitrariness: Saussure makes it clear that the connection between the signifier and the signified is arbitrary. There is no reason for the sound we make when we say a word to indicate the concept behind that word. How does this impact how we think about language? If language doesn’t inherently have any meaning, who (or what) gives it meaning? Does it matter?
Different languages: The French bleu and the German blau both express the same thing as the English blue. But do all of these signifiers have exactly the same signified concept? How do we know if an English person and a German person think about the colour in the same way?
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[BIOLOGY] Aposematism and Mimicry 🦋
There are many signals animals can use with each other to communicate a wide scope of information. One such method of signalling is known as aposematism, which is what many prey species use to conspicuously identify to predators themselves as difficult to kill and eat. This is an example of predator avoidance. Animals that have evolved to use aposematism are very brightly coloured. For example, monarch butterflies have evolved to have very brightly coloured wings, resplendent orange hues set against a dark background. This makes them obvious to a predator and signals they should not be eaten, for it will not be a pleasant snack. Aposematic animals quite often evolve to aggregate as well, which is theorised to be because predators quickly learn to associate their bright colour patterns with their toxicity and thus stop eating them. The evolution of aposematism also allows for the evolution of mimicry, whereby mimic species can evolve to look like model aposematic species.

💡 Things to consider
In keeping with the monarch butterfly example, viceroy butterflies are a species which exploit predator associations of monarch butterfly markings and toxicity to their own advantage. By mimicking the monarch butterfly, they can signal their own distastefulness to predators and so reinforce the honest warning signal to predators, helping naïve predators learn more quickly and mutually benefitting both species. This is known as a Mullerian mimic. Batesian mimics cheat the system and mimic distasteful species while they themselves have no secondary defences (such as toxins or spines), so essentially piggyback off the honest signals broadcast by the aposematic species. Can you think of any advantages of engaging in Mullerian mimicry? What selection pressures do you think would cause this type of mimicry to evolve between two (or more) species?
The effectiveness of Batesian mimicry is dependent on the abundance of the mimic species relative to the model species. Knowing this information, how do you think the effectiveness of this signal will vary if mimics become more or less abundant compared to model species? How do you think abundances of mimic species would respond? And how might changes in abundance of the model species affect abundance of mimic species, perhaps in the face of climate change?
As mentioned, aposematic animals tend to be very brightly coloured. Why do you think it is important that aposematic signals have evolved to use bright colours? What aspects of predator physiology and psychology do you think this targets?
🔎 Find out more
Smith, J. M. & Harper, D., 2011. Animal Signals. Oxford: Oxford University Press.
The Writers at National Geographic Education, 2023. Camouflage. [Online] Available at: https://education.nationalgeographic.org/resource/camouflage/
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That’s it for this week! We’d like to thank this week’s writers: Rob Folkard (Medicine), Eva Bailey (Linguistics), Oliver Eyre (Biology), and Gabriel Pang (Philosophy).
As ever, feel free to hit the REPLY button - we really love hearing from you! Have a happy Monday 😎
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