Most scholars would agree that viruses, particularly enteroviruses, play a key role in triggering autoimmune diseases like type 1 diabetes. Yet their identities and exact roles remain speculative?
Could an individual be exposed to a virus which attacks the microbiome but not the host directly, changing the microbiota and thus the microbe-immune system interaction, triggering autoimmunity?
So the virus would be indirectly involved, mediated by the microbiome, but not infecting the host so no markers would be left for scientists to pinpoint retrospectively.
All the classic signs of bodily infection at the time and after would be missing, but the immune system would still be auto-activated and lasting changes would occur to the gut bacteria.
There are probably more flaws in this concept than there are bacteria in a human G.I tract but I am interested as to why we cannot definitively describe the role of these viruses!
The answer to the first part of your question
...Could an individual be exposed to a virus which attacks the microbiome but not the host directly?...
is yes. Actually bacteriophages are viruses that affect only bacteria.
While for the second part
...changing the microbiota and thus the microbe-immune system interaction, triggering autoimmunity....
is quite difficult to give an univocal answer.
In fact if a virus attack a bacterial species, we could not exclude an exposure of some exogenous antigenic epitopes by the same bacterium, thus epitopes carried by the virus (ie capside proteins in the bacterial surface, even if very unlikely) could give a possible reverberation on the immunity response of the host infected by the bacterium, but it would be brought by virus antigens, as I already said. However, I think that in your question you referred to an effect of these viruses to the quality/quantity modulation of the microbiome in the host, with the elimination of certain bacterial species or at least in decreasing of the activity of several bacterial species as components of the microbiome. In this regard, by killing some standard bacteria of the gut flora, other bacteria of different species/genus could replace the same niche. These new bacteria could hypothetically carry antigens that mimic endogenous epitopes of some host cell types. In this way the presence of homology to endogenous epitopes, and epitopes of the bacterium (such as membrane proteins) could trigger a response against the bacterium that led also to autoimmunity against the host cells (self). As you can see also in this case, the autoimmunity is not directly triggered by the virus, but by a bacterium.
I would like to tell my experience. Without telling lots of details, we found that there are some proteins secreted by Neisseria that can inhibit the multiplication of HIV, in vitro. Currently, there is a trend that microorganisms may inhibits the growth of each other. Further research is needed to study this area.
Thank you all for your help. Part one of the question= bacteriophages ✔
So the second part, which some of you have touched on, is whether bacteriophages could be responsible for the "hit and run" viral attacks that are believed to trigger type 1 diabetes?
Unbalancing the microbial-immune system balance and triggering autoimmunity, without ever entering the bloodstream and thus not leaving a trace.
Hi team, i moved this question over to diabetology to get their perspective on the second part, here is the link if you want to follow it. Thank you all so much for your input, particularly Dr Cossu, i hope you can jump in if someone in diabetology asks how the microbiota could actually trigger autoimmunity, i tried to summarize what you said but couldnt do it justice!
https://www.researchgate.net/topic/Diabetology3/post/Could_the_viral_trigger_for_type_1_diabetes_be_a_bacteriophage_that_attacks_gut_microbiota#
Viral pathogens enter the host thereby encountering an immune system which is shaped by the symbiotic microflora. So, it can be said that the interplay between the host as well as viral pathogens is important. Bacteriophages are classical examples which stimulate the host defense factors and are regarded as beneficial to the patient.
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