[bawolff]

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]

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

[throwaway72762]

The article doesn't contest that view but instead considers how germs are an orthogonal dimension and that we are starting to understand better that the host and all of its cells, not just some ill defined subset called immune cells, are responsible for host health and that when functioning properly can coexist with germs without letting them cause disease.

I wonder whether this perspective aligns well with research into bat viral reservoirs as they exemplify this model.