To both of you: My knowledge of microbiology and biochemistry is almost non-existent. So I actually very much welcome pushback on the threat itself. I also feel that I should grasp the science behind mirror bacteria at least on some very preliminary level. That said, I always want to understand things “completely” so I started looking for specific places in the immune system where reversed chirality would mess things up and started with the TLR4 receptor and could not conclude that well that chirality would play a role for 2 reasons: 1 - It seems the TLR4 could bind to quite a variety of “form factors” so it is unclear why it would be much less effective for mirror pathogens 2 - I then looked at TLR2 and am hoping to learn from someone expert in this why the binding of NAM (I hope I got that right) and the attached lipid is likely to fail with mirror bacteria. This avenue of study led me to discover 2 things that some bacteria actually uses reverse chirality amino acids in their cell walls exactly to be resistant to degradation, and, that the TLR structures seem to actually flex in space, meaning they have at least some flexibility in the spatial arrangement of whatever they seek to recognize.
The evidence I am now chasing is somewhere scientists actually swapped some lipid or sugar for its mirror equivalent and then looked at the resulting binding or failure to bind to e.g. a TLR.
That said, there is a lot of intellectual power behind that report and it has been peer reviewed so I would be surprised if I find something that invalidates it. And I think the main message is that “we don’t know, but it does not look promising” and the authors state that they would love for people to engage with their assertions.
You cannot completely understand the immune system; that is something you learn early on in immunology.
That being said, the key understanding on mirror bacteria evading the immune system is that the immune system generally relies on binding to identify foreign invaders, and if they cannot bind then they cannot respond. Bacteria generally share a number of molecules on their surface, so the innate immune system has evolved to bind and detect these molecules. If they were mirrored, they would not bind as well, and would be harder to detect and respond to.
That being said, you did find the insight that they are not completely invisible. There are also systems that can detect the damage done by the infection and start a counterattack, even if they can’t see the invaders themselves. But much of the counterattack would not be able to affect the mirror bacteria.
What matters in the report is that the immune system of all animals and plants will likely be (much) less effective against mirror bacteria. This doesn’t mean it’s an untreatable disease, as we have antibiotics that should still be effective against the mirror bacteria. But it does mean that if the mirror bacteria finds its way into the environment it is unlikely that anything can fight back well.
I agree about it being hard to understand the immune system completely, i should have written “understand one single process well enough to have high confidence”. So i just wanted to understand one step, such as the binding of something to just one of the TLRs. And the understanding could be empirical too—I would be confident if researchers could robustly repeat a failure of some mirror component to bind to a TLR, for example.
To both of you: My knowledge of microbiology and biochemistry is almost non-existent. So I actually very much welcome pushback on the threat itself. I also feel that I should grasp the science behind mirror bacteria at least on some very preliminary level. That said, I always want to understand things “completely” so I started looking for specific places in the immune system where reversed chirality would mess things up and started with the TLR4 receptor and could not conclude that well that chirality would play a role for 2 reasons:
1 - It seems the TLR4 could bind to quite a variety of “form factors” so it is unclear why it would be much less effective for mirror pathogens
2 - I then looked at TLR2 and am hoping to learn from someone expert in this why the binding of NAM (I hope I got that right) and the attached lipid is likely to fail with mirror bacteria. This avenue of study led me to discover 2 things that some bacteria actually uses reverse chirality amino acids in their cell walls exactly to be resistant to degradation, and, that the TLR structures seem to actually flex in space, meaning they have at least some flexibility in the spatial arrangement of whatever they seek to recognize.
The evidence I am now chasing is somewhere scientists actually swapped some lipid or sugar for its mirror equivalent and then looked at the resulting binding or failure to bind to e.g. a TLR.
That said, there is a lot of intellectual power behind that report and it has been peer reviewed so I would be surprised if I find something that invalidates it. And I think the main message is that “we don’t know, but it does not look promising” and the authors state that they would love for people to engage with their assertions.
You cannot completely understand the immune system; that is something you learn early on in immunology.
That being said, the key understanding on mirror bacteria evading the immune system is that the immune system generally relies on binding to identify foreign invaders, and if they cannot bind then they cannot respond. Bacteria generally share a number of molecules on their surface, so the innate immune system has evolved to bind and detect these molecules. If they were mirrored, they would not bind as well, and would be harder to detect and respond to.
That being said, you did find the insight that they are not completely invisible. There are also systems that can detect the damage done by the infection and start a counterattack, even if they can’t see the invaders themselves. But much of the counterattack would not be able to affect the mirror bacteria.
What matters in the report is that the immune system of all animals and plants will likely be (much) less effective against mirror bacteria. This doesn’t mean it’s an untreatable disease, as we have antibiotics that should still be effective against the mirror bacteria. But it does mean that if the mirror bacteria finds its way into the environment it is unlikely that anything can fight back well.
I agree about it being hard to understand the immune system completely, i should have written “understand one single process well enough to have high confidence”. So i just wanted to understand one step, such as the binding of something to just one of the TLRs. And the understanding could be empirical too—I would be confident if researchers could robustly repeat a failure of some mirror component to bind to a TLR, for example.