Could Aging be an Infectious Disease?

Sidny

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This may be of interest to those on here who’s illness was triggered by an infection.

Making the case that aging could be primarily driven by infections, told from the perspective of a future “Mick and Rorty” episode … for kicks
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https://blog.infino.me/could-aging-be-an-infectious-disease/


“12 viral strains, so far (I’ll likely find more!), are dependent on this critical mitochondria and complement cascade modulating protein for survival. Why? Some work indicates that this may be relevant for export from the nucleus. Another possibility is exploiting p32’s ability to bind and sequester complement c1q to inhibit the immune response.

Many infectious agents appear to accelerate atherosclerosis in mouse models, particularly when APOE(the top Alzheimer’s gene)is knocked out. This tells us something very important about the role of cholesterol in the repair of infections in both alzheimer’s and cardiovascular disease.

This right here is quite fascinating, for it directly links a lot of plausible causal mechanisms of viral-mediated development of two major diseases. It also seems to link the aging gene expression data (complement cascades) with the top genetic causes of Cardiovascular and Alzheimer’s disease (Complement receptor, APOE, and p14/p16).”


As it turns out, viruses have been found to interfere with this cell cycle in many ways. Some accelerate it, and others freeze it at specific locations. Many viruses freeze the cell cycle at this precise location to maximize viral replication. Its precisely at this state that the cell is producing abundant energy, and it is ready to copy the human genome, but it has not committed to doing so just yet. This is the perfect time to copy a viruses code instead.
There exists abundant evidence that this is happening :

Most interestingly of all, cells in the senescent state are what we traditionally think of as a primary marker of aging. Senescence is specifically characterized by cells arrested in the G1/S state. These cells produce high levels of reactive oxygen species. These hallmarks of aging MATCH the hallmarks of viral replication, hijacking our cells to become factories for malicious code we do not want.”
 
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