[HN Gopher] From second thoughts on the germ theory to a full-bl...
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       From second thoughts on the germ theory to a full-blown host theory
        
       Author : Hooke
       Score  : 22 points
       Date   : 2023-07-15 15:06 UTC (1 days ago)
        
 (HTM) web link (www.pnas.org)
 (TXT) w3m dump (www.pnas.org)
        
       | throwaway72762 wrote:
       | This is excellent but also galaxy brain level. Not something
       | that's ready for popular digestion, given the levels of basic
       | science denial that have popped up post COVID, even among
       | supposedly empirical communities like tech.
       | 
       | Eventually if this gains more predictive power then it can be
       | merged with germ theory and explained better to the public.
        
         | bawolff wrote:
         | I didn't read the whole thing just the abstract, but isn't this
         | just the modern standard view?
         | 
         | Germs cause disease. Your immune system stops germs. To get a
         | disease the germ must both get into you and either overwhelm or
         | find a way past your immune system.
         | 
         | This hardly seems like something beyond public comprehension.
        
           | nextos wrote:
           | I also found it a bit too philosophical in the sense that we
           | can already explain a lot of the variations in outcomes to
           | infection.
           | 
           | For example, HLA/MHC is a family of genes tasked with the
           | presentation of antigens (e.g. chunks of proteins) from
           | pathogens and your own cells to the immune system. It is a
           | very polymorphic region, i.e. full of genetic variants that
           | lead to lots of differences in the peptides that are
           | presented, to stop spread of infections at population level.
           | 
           | If you have one of the lucky/unlucky alleles, you will have
           | high chances of protection/susceptibility. Some alleles, like
           | HLA-B57, protect against HIV but it's a tradeoff. Carriers
           | are much more susceptible of autoimmunity [1].
           | 
           | From an environmental point of view, if you have dysbiosis,
           | e.g. if your gut microbiome ecology is altered, T cell
           | receptor distributions will be altered and you are more
           | likely to have a bad response to certain infections.
           | 
           | [1] Effects of thymic selection of the T-cell repertoire on
           | HLA class I-associated control of HIV infection.
           | https://www.nature.com/articles/nature08997
        
       | pazimzadeh wrote:
       | In our lab we call it the lock and key hypothesis:
       | 
       | One size doesn't fit all: unraveling the diversity of factors and
       | interactions that drive E. coli urovirulence
       | https://pubmed.ncbi.nlm.nih.gov/28217693/
       | 
       | Bacterial virulence phenotypes of Escherichia coli and host
       | susceptibility determine risk for urinary tract infections
       | https://pubmed.ncbi.nlm.nih.gov/28330863/
       | 
       | It can be useful to look at infections from the perspective of
       | microbes:
       | 
       | The acquired immune system: a vantage from beneath
       | https://pubmed.ncbi.nlm.nih.gov/15539148/
       | 
       | TLDR: Microbes were here long before us and will be here after
       | us. We are living in their world and the more we try to fight
       | them head on, the more they will bother us. Best to adapt and co-
       | opt.
        
         | jvm___ wrote:
         | Microbes love on every square inch of the world, or close
         | enough to it compared to humans.
         | 
         | Humans live like shower fungus at the local gym, we live in the
         | cracks and near the water sources, on the scale of earth we
         | might as well be microscopic.
        
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       (page generated 2023-07-16 23:00 UTC)