# Viruses and Chronic Aging: Building a Research Community by Amy Proal | Devcon SEA

- Speakers: [Amy Proal](https://streameth.org/speakers/amy-proal)
- Channel: [Devcon](https://streameth.org/devcon)
- Date: 2025-10-09
- Duration: 16:36
- Topics: Science & Technology
- Watch: https://streameth.org/watch/yt-OcwxbzqP8Jc
- YouTube: https://www.youtube.com/watch?v=OcwxbzqP8Jc

## Description

Did you know that mitochondrial dysfunction, inflammation, and cognitive decline are directly accelerated by viruses? In fact, the viruses that infect us over a lifetime are technically not even alive, and therefore must “hack” our human cellular metabolism machinery to do anything at all. This talk will overview the first-ever global collaborative network studying & treating chronic viruses as drivers of aging, including how certain lifespan-promoting drugs may help combat viral activity.

Speaker(s): Amy Proal
Skill level: Intermediate
Track: [CLS] d/acc Discovery Day: Building Towards a Resilient Utopia

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## Transcript

[Music] hi I'm Amy proall I'm the president and research director of poly bio Research Foundation and today I'm truly excited to talk to you about viruses and chronic aging building a research community so where am I going with this first what I want to talk about is viruses as drivers of Aging processes this is really not discussed and as understood as it should be and there's so many compelling examples of how viruses can contribute to Chronic aging processes this is really important for the longevity community and for people who are just dealing with many forms of chronic disease if we understand these interactions we can better figure out how to combat them and how to best uh create strategies to mitigate uh viral effects on Aging so let me give you some examples of viruses and how they contribute to aging process so there's definitely many drivers of human aging but here are some of the three main factors mitochondrial dysfunction these are the Just Energy powerhouses of ourselves and they become dysfunctional as we age often inflammaging which is basically just the fact that over time as people get older tend to have more chronic inflammation more immune cells that are just activated in an unproductive way that's called inflam Aging and cognitive decline obviously people who are getting older and aging have memory problems they have brain you know dementia even post Alzheimer's type phenomenon even sometimes so one thing to understand is that as we age and in fact as we are born um and across the Scopes of Our Lives we inherit um viruses from our parents chronic viruses sometimes um they passed in some cases in the womb plus we also over the course of our lives and this happens with exposures with other people it happens from our environment and sometimes the foods and other things that we consume we accumulate different viruses and they become part of what is known as our human viral the viruses in us and there are many viruses that become a burden in our systems as we just live these are the herpes viruses the papiloma viruses um and increasingly a growing number of RNA viruses are also understood to be um persistent viruses that are with us for our life now what does this virum then do to aging well consider are just some of these virum components this is you know sometimes when people are let's say in college they gave mono and people understand that people get sick they get a sore throat they don't feel well they're feverish they try to avoid people for a while what really means uh when you get mono is that you get the abstain bar virus it's a herpes virus and that virus stays with you again this is a persistent virus once you have it it does not clear your system it stays with you for the rest of your life this is the thing if someone's immune system is robust if it's in a good shape if it's active what the immune system does technically is keep these chronic viruses like the Epstein bar virus if you get it and over 90% of people in the world by the way Harbor Epstein bar virus keeps these viruses in check it keeps them in a dormant form the immune system keeps them in a latent form and that way they technically cannot activate and create more proteins or things that can actually drive disease or potentially aging processes now however if viruses do become active if they are moving out of a state of dormy because something happens to the immune system and this could be many things it could be another infection it could be just exposure to pollutants to chemicals to many things that wear down our immune systems over time viruses can become more active and one of the things that viruses do when they activate is that they affect our mitochondria directly in fact this is one of the key things to understand about viruses our health and aging is that viruses are actually obligate intracellular pathogens and what that means is by definition they are not even alive they must in order to replicate and create new versions of their cell they must pull the substrates the backbones to do that to create new versions of themselves from our human cells from our mitochondria so they do this every single virus hijacks our mitochondria in order to create new versions of itself and do basically anything that it does this is a paper that I wrote about this phenomenon with my colleague neuroscientist at Poly bio Mike Van oer who also is a neuroscientist at Harvard we wrote about how pathogens bacterial viral fungal parasite pathogens even hijack the metabolism or the mitochondria of the host cells they in fact to just gain those basic substrates again to just create new versions of themselves this is core to what they do this is a diagram from our paper this is basically a human mitochondria in the diagram at the intermediate of that paper of the figure you can see the TCA cycle that's a very important part of just gaining substrates for our own energy metabolism so that we can function burn glucose you know burn other fuels that allow our mitochondria to make us a energy producers in a in a good way the blue boxes contain different human viruses that are part or can be part part of the human virum persistent chronic viruses and those are just the different parts of metabolic pathways that they hack or hijack as part of their ability to just create new versions of themselves or replicate okay so I mentioned before that inflammaging just chronic inflammation often accelerating over time is also strongly associated with human aging and issues with longevity for example in this paper now what inflammation often results from is the activation of immune cells including cyto which become active and question one of the questions is why but we certainly know that especially cyto amans cells become active now I 11 is an example of a cyto so it's an inflammatory molecule in the human body that can become more active When Things become inflamed now this doesn't make you know seem too surprising then in this paper this team showed that inhibiting this INF inflammatory molecule the cyto uh I 11 extended Mamon Health span lifespan suggesting that inhibition of some forms of inflammation is helpful for in that regard now what though in the first place was causing that cygine I 11 or interlan 11 to be active to be more active than it should be well one of the biggest driving factors again that so many viruses and other bacteria or pathogens or parasites do is they activate immune cells as part of their persistence what happens is the immune system recognizes them tries to Target them or to keep them in check and in the process becomes more active perpetually more perpetually active so here is a study showing that that cyto um il1 or Incan 11 is actually stimulated both in animals and in the lab by viruses including respiratory viruses so these are drivers of inflammaging most pathogens can be direct drivers of inflammaging okay now we just have the ability the viruses and bacteria but I'm going to focus on and viruses here can basically just hack the signaling Pathways that are the heart of our longevity health networks for example there are Pathways in the human body that control processes associated with cellular inessence for example that's the ability of a cell to correctly divide to correctly grow not overdo that not sort of underdo that process but to do it robustly there are networks in the human body that scientists have calculated as mattering in terms of human signaling associated with longevity well this team did network-based analysis and they uncovered dozens of viruses that encode proteins experimentally demonstrated to interact with proteins associated with these human aging networks including cence so so just dozens of viruses and and thousands of interactions between these viral proteins to the point where they ended up calling dozens of viruses in the study that they identified age disorders because of the fact that their proteins could have such detrimental or modulator effects on these aging networks in other words their reproduction and their ability to replicate benefits from directly from interference with their host aging processes and here on this chart are just some of the top viruses that were basically shown to have proteins that interfered with human cellular inessence Pathways there are the herpes viruses which most of us acquire over the course of Our Lives the papiloma viruses interestingly influenza A virus was one of the top drivers of aging and we never even think about the flu type viruses which is influenza in an aging capacity um but we probably should a little bit more so with that in mind then this is a final takea away from that paper this is what the team concluded owing to the considerable number of human viruses this evolutionary minded view encourages a reconceptualization of the Locust of Aging no longer exclusively focused on our own genetic material but expanded towards a larger set of genetic entities interacting with our species such as viruses so Boom the heart of Aging all right now what about cognitive decline what about just direct mechanisms by which viruses or other pathogens can drive cognitive decline here is one this is the team that we work with at Harvard Medical School they're really cool they've been using models of a brain in a dish where they actually recreate the neuron structures of a brain in a model or just experiments in mice to show that the Alzheimer's plaque the ameloid beta plaque that is the the Flack that forms in the brains of patients with Alzheimer's disease that defines the disease actually acts as an antimicrobial peptide or part of the immune response that forms in response to pathogens directly in order to combat them so basically what happens is there's a virus that gets into the brain tissue model and then the plaque forms around it as part of the response to the virus that's what they were showing in this study in response to the herpes viruses but the te is also sewn the same Phenomenon with bacterial pathogens and with fungal pathogens this places infection at the heart of the driving of amalo plaque in the Alzheimer's brain here's another example of a team who's working on the same phenomenon Ben re heads group at Arizona State University this is an image of cytomegalo virus which is another herpes viruses that many of us just carry with us for life it's look in the image here it's concentrated in the micral immune cells of the brain around the plaques of these cells along with the axin and dendroides of neurons again that are inflamed and directly part of the Alzheimer's disease process so there are growing number of teams connecting viruses directly to to neurod degeneration now this is an interesting study okay what do we do well there's some really low hanging fruit no one's even doing anything about this and this is an example of just easy measures we could take to control the impact of viruses on Aging if we made it a priority this is the team in Taiwan and what they did is they tracked people over time some of whom were given just aordable herpes virus existing generic medications so for example let's say someone gives genital herpes they're given Val checks it's just an over-the-counter herpes anti- herpes virus drug so some of the people in the study were given more of those anti- herpes virus drugs and some weren't when they looked at the group that was given these anti-herpetic medications they had a much lower risk of dementia than the people who didn't in fact up to a 10 times lower risk of dementia so really it's extremely low hanging fruit to maybe start to use some of the drugs that we have to inhibit viral activity in the context of human aging now what about in covid Long covid now I know we're all a little burned out on covid but really like part of what our group does is studies still The Chronic consequences of SARS Co 2 we have to it's because it's one more virus that is one of these players that could contribute to chronic disease and fortunately aging processes and you'll hear about long Co and it sounds like a vague phenomenon when you hear about it in the news often really it's not though a lot of us that are directly studying long covid realize that the Persistence of the SARS Co 2 virus in tissue in the human body over time in other words SARS code 2 potentially becoming just another member of the human viron is happening in at least a decent number of people with long covid and here's a paper that a group of us of long Co researchers wrote about SARS Co to persistence as a driver of postco symptoms here's an example of a team that we work with this is in the bottom right gut tissue from the lining of the gut collected from someone almost in one case over two years after they got covid and in this case the person did have symptoms they had chronic symptoms but still this that what you're seeing there in the purple that that pink part is the SARS cooku virus still there in the gut tissue after over two years sort of embedded there with immune cells around it clustered preventing it potentially from being cleared so it's there in a persistent capacity which means that at least in some people SARS cve 2 may be acting or seems to be acting as a persistent virus that can also contribute to chronic disease and aging processes in fact this is a table from one of our papers that just this is just some there are some of the studies that have shown persistent SARS cope 2 up to again then over two years or more after initial infection and at least a sub set of people okay so then what do we do about this well one of the drugs we're actually looking about in the long covid world is rap ayin which I know that some of you will be familiar with in the context of mitigating aging or or extending life span so we are actually running at Mount Sinai um in New York where I serve as the scientific director of a clinic called core um which is a treating people with conditions initiated or exacerbated by infection is we're running a trial of Romy in patients with long covid rapamycin is an mour inhibitor that has you know different properties on the immune system now one of the things that's really interesting about Ramy is that in some studies at least rapalogues or analoges of vamy and drugs similar to it have been shown to in a low once a week dose not in a high dose in a lower dose to enhance parts of the immune response that can better control viral infection so for example that TR that I showed you gave patients two rapalogs over the course of six weeks and a couple things happened first they showed the people taking Romy and an increase and interferon induced antiviral gene expression with interferons being one of the primary molecules or parts of the human response that combats viruses and keeps them down also the people in rap the ramyon group everyone in the trial was given the influenza vaccine but those who took Ramy had a more robust response to the vaccine in other words their immune system seem to activate more and create more antibodies in response to that vaccine also the participants on Ramy even though they just took the drugs for six weeks reported a lower rate of infection for a full year after being on the rapy this includes respiratory infections UTI though all a multiple types of infection suggesting again that rapamycin was helping to control viral activity and in a related study the team found that rapamycin in some patients um improved t- cell exhaustion and again when viruses persist they tend to knock down te- cells uh and their activity which are parts of our immune system making them literally exhausted and rapamycin was shown to potentially improve that again so rap ayin we're triing now to see if it might help patients who have a persistent SARS C2 or other virus problems in Long covid better control those infections and with this means is there's you know a use of Romy in terms of potential viral control that is also probably relevant to human aging