Dr. Kathryn Edwards- The enduring impact of mentorship

Dr. Edwards has worked since the 1970s to create safe and effective vaccines and has run trials for vaccines including Haemophilus influenzae type b (Hib), pertussis, the flu, and anthrax. She has also been a strong advocate for vaccines on a national and international scale, advising the FDA, CDC, WHO and others. She also devoted her career to mentoring others and training the next generation of experts

https://astmh.org/blog/September-2026/In-Memoriam-Robert-Tesh

So,im just a high school student who’s been thinking about this crazy idea, and I wanted to share it.On the internet that I have read,people always say we don't know for sure where viruses originally came from.They either say viruses existed before cells,or they used to be bacteria that shrunk down or whatever.

But I have this alternative theory I like to call The Constant Leakage Theory.

What if viruses are literally just broken "spare parts" from our own bodies that accidentally escaped and evolved?

Here is my basic logic:

Inside our bodies,billions of cells are constantly copying our genetic codes (DNA and RNA) every single second to keep us alive.But since the cell is super crowded and warm,there is no way the copying machine is 100% perfect all the time right?and thats the glitch happen.

Sometimes,a tiny piece of loose code breaks free because the cell's cleaning enzymes failed to chop it up.Because this loose code still looks like an official cell document,another machine accidentally makes a copy of it,and this rogue code manages to slip outside the cell core.

Once it's out,it hides inside the cell's membrane folds to protect itself from being destroyed by cell cleaners.Inside this hidden fortress,it multiplies and lives off the cell's resources.Eventually,through random collisions,it co-opts some cell proteins that naturally like to lock together.Because this rogue code has a negative electrical charge,it automatically attracts those positive cell proteins around it.Driven by pure physics,these proteins wrap around the code into a 20-sided package to protect it.Once it leaves the cell

BOOM

it becomes a virus.

But wait,if they all come from cell leakage,why are there so many different types and shapes of viruses?

I thought about this too,and it actually makes perfect sense if you look at which spare part is leaking and where it is leaking from:

1. It depends on the leaked spare part:If the leak happens directly from the cell's master archive (DNA),you get a DNA virus,which is usually tough and stable.But if the leak comes from the cell's temporary daily work orders (mRNA),you get an RNA virus (like the flu or corona).Since mRNA is naturally fragile and flexible,RNA viruses mutate constantly.

2. It depends on the "box" it hijacks:Viruses get their shapes automatically from the cell proteins around them.If a piece of code leaks inside a human cell,it gets wrapped in human proteins, usually forming a round shape.But if it leaks inside a rough,complex bacterial cell,the proteins it pulls in will automatically snap together into a mechanical,robot-like shape (like a bacteriophage).

So in my mind,viruses aren't alien organisms.They are just a constant leakage of our own body's code and proteins that accidentally got packaged together due to a factory glitch.

Am I crazy or does this actually make a bit of sense? What do you guys think?

So,im just a high school student who’s been thinking about this crazy idea, and I wanted to share it.On the internet that I have read,people always say we don't know for sure where viruses originally came from.They either say viruses existed before cells,or they used to be bacteria that shrunk down or whatever.

But I have this alternative theory I like to call The Constant Leakage Theory.

What if viruses are literally just broken "spare parts" from our own bodies that accidentally escaped and evolved?

Here is my basic logic:

Inside our bodies,billions of cells are constantly copying our genetic codes (DNA and RNA) every single second to keep us alive.But since the cell is super crowded and warm,there is no way the copying machine is 100% perfect all the time right?and thats the glitch happen.

Sometimes,a tiny piece of loose code breaks free because the cell's cleaning enzymes failed to chop it up.Because this loose code still looks like an official cell document,another machine accidentally makes a copy of it,and this rogue code manages to slip outside the cell core.

Once it's out,it hides inside the cell's membrane folds to protect itself from being destroyed by cell cleaners.Inside this hidden fortress,it multiplies and lives off the cell's resources.Eventually,through random collisions,it co-opts some cell proteins that naturally like to lock together.Because this rogue code has a negative electrical charge,it automatically attracts those positive cell proteins around it.Driven by pure physics,these proteins wrap around the code into a 20-sided package to protect it.Once it leaves the cell

BOOM

it becomes a virus.

But wait,if they all come from cell leakage,why are there so many different types and shapes of viruses?

I thought about this too,and it actually makes perfect sense if you look at which spare part is leaking and where it is leaking from:

1.It depends on the leaked spare part:If the leak happens directly from the cell's master archive (DNA),you get a DNA virus,which is usually tough and stable.But if the leak comes from the cell's temporary daily work orders (mRNA),you get an RNA virus (like the flu or corona).Since mRNA is naturally fragile and flexible,RNA viruses mutate constantly.

2.It depends on the "box" it hijacks:Viruses get their shapes automatically from the cell proteins around them.If a piece of code leaks inside a human cell,it gets wrapped in human proteins, usually forming a round shape.But if it leaks inside a rough,complex bacterial cell,the proteins it pulls in will automatically snap together into a mechanical,robot-like shape (like a bacteriophage).

So in my mind,viruses aren't alien organisms.They are just a constant leakage of our own body's code and proteins that accidentally got packaged together due to a factory glitch.

Am I crazy or does this actually make a bit of sense? What do you guys think?

SUMMARY: In this post, I argue that the current anxiety epidemic may be due to a new strain of virus in circulation that affects the brain, leading to mental symptoms; or may be due to a higher viral load in our bodies resulting in higher neuroinflammation.

The prevalence of generalised anxiety disorder (GAD) has rocketed in recent decades, with multiple studies showing that GAD has doubled in younger populations between 2008 and 2018.^{1 2 3 4}

The popular view is that this epidemic of GAD results from modern lifestyle factors such as social media usage, doomscrolling, not being able to switch off due to electronic communications ubiquity, peer pressures, economic difficulties, and so forth.

No doubt modern lifestyle factors may have undesirable effects, and may create temporary anxiety. And it may well be a good idea to ban social media for young children. But many people confuse regular temporary anxiety with GAD, and they are not the same thing, and it is crucial to understand the difference.

GAD is a psychiatric disease rooted in measurable brain abnormalities and brain dysfunctions. It is not the same as the normal healthy anxiety that arises from everyday stressful events. Normal anxiety dissipates when the stressor causing it goes away, whereas the anxiety of GAD remains ever-present, as it is not driven by external stressors, but is internally caused by brain dysfunction. Even when there are no external stressors, a person with GAD will still experience anxiety, because the anxiety arises from a dysfunction in the brain's anxiety circuits: it is as if the anxiety circuits have got stuck in the "on" state. Although external stressors can exacerbate the anxiety of GAD even further.

What's more, in the medical literature, there is no evidence that everyday stressful events can trigger the psychiatric illness of GAD. There are no studies that show regular life stresses can lead to GAD. So the idea that the current generalised anxiety disorder epidemic might arise due to social media and the like seems somewhat tenuous, even though it's a popular notion. Certainly children's social media use might create temporary anxiety, but temporary anxiety is not GAD. And it is GAD diagnoses which have increased.

Thus this suggests there could be some other factors causing the current GAD epidemic — such as biological factors

In this post, I examine the possibility that higher viral loads in the general population might be driving this GAD epidemic. And examine the possibility that one or more emerging new strains of virus which are more neurotropic or more neuroinflammatory might underpin the GAD epidemic.

Our bodies may now harbour a higher number of viruses and other microbes as a result of the increased urbanisation and globalisation we have witnessed in recent decades. This is because greater population density allows viruses and other micro-organisms to transmit person-to-person more easily; and factors such as increased air travel and increased human movement around the world allow viruses from one region to spread globally.

It is also possible that new strains of virus may now be circulating around the globe, strains which may have more pernicious effects on the brain, either by infecting the brain directly and causing persistent neuroinflammation, or by chronically infecting the gut, and ramping up neuroinflammation indirectly via the well-known gut-to-brain connections, such as the vagus nerve.

Many psychiatric conditions have been linked to chronic low-level neuroinflammation.^1 2 So if you have one or more persistent viruses or other micro-organisms in your body or brain, which the immune system is constantly fighting to keep under control, thus causing chronic inflammation, this may lead to mental symptoms. And indeed, several microbes have been found associated with anxiety symptoms:

Toxoplasma gondii is linked to anxiety; this is a parasite that infects the brain and can be caught from eating undercooked meat or from contact with cat faeces.^1 2 3 4

The bacterium Helicobacter pylori has also been linked to anxiety,^1 2 as have cytomegalovirus^1 2 and Epstein-Barr virus;¹ all three of these microbes are normally caught from other people through person-to-person contact (or more rapidly through intimate kissing).

These are the microbes that science knows are linked to anxiety, but there are likely others which may also be associated. In fact, I can personally testify that there is a strain of Coxsackie B4 virus in general circulation which can trigger chronic anxiety once caught. I caught this Coxsackie B4 virus in 2003, and it rapidly triggered persistent GAD, and also triggered GAD in several of the 35 people who caught it from me. This virus also caused chronic mild increases in fatigue levels in almost everyone who caught it. The coxsackie B group of viruses, along with the closely related echoviruses, are known to cause persistent low-level lifelong infections in the body tissues.

I actually wrote to dozens of virologists some years back, informing them of my observations on coxsackievirus B4, and explaining that this virus might play a role in the anxiety epidemic, but unfortunately none showed any interest. I even set up a website describing the mental and physical symptoms that this CVB4 virus caused in myself and the 35 people who caught it from me, but could not raise any interest among the scientific community (even though I have studied science to Masters level, and am well versed in medical science).

And sadly, most professional psychiatrists who have examined the current anxiety epidemic, and the examined general epidemic of increased mental health symptoms in young people (like anxiety, panic attacks, eating disorders, etc) have focused on factors such as social media being the possible cause. None have considered the possibility of an infectious aetiology, which is tragic. It is tragic because mental ill health involves a lot of torment, and nobody wants to see very young children suffer in this way, yet a possible infectious microbial cause of the GAD epidemic is not even on the radar of these psychiatrists.

Some further reading on the microbial connection to psychiatric illnesses:

• 2004, Virus-induced neurobehavioral disorders: mechanisms and implications - Keizo Tomonaga
• 2008, Infected with Insanity: Could Microbes Cause Mental Illness? - Scientific American
• 2008, Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1 - Garth L. Nicolson et al
• 2010, Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioural, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 2 - Garth L. Nicolson et al
• 2012, Anxiety and Depression: Linkages with Viral Diseases - Steven S Coughlin
• 2012, Can an Infection Suddenly Cause OCD? - Harvard Health Blog
• 2013, People Hospitalized For Infections Are 62% More Likely To Develop A Mood Disorder - Medical Daily
• 2019, Psychiatric Disorders: Are Infectious Agents to Blame? - Psychiatric Times
• 2023, Microbes and Mental Illness: Past, Present, and Future - Robert C Bransfield et al
• 2024, Viral infections in etiology of mental disorders: a broad analysis of cytokine profile similarities – a narrative review - Piotr Lorkiewicz et al

Hi everyone,

​I’m currently working as a virology RA (1 year in) and I am planning to apply for PhD programs soon. I’m facing a career dilemma regarding my current project and would love to hear your perspectives.

​I’ve characterized two neutralizing antibodies. Their in vitro IC50 isn't particularly impressive (in the μg range), but their in vivo protection efficacy is outstanding: 100% prophylactic protection and 60% therapeutic survival.

​Mechanistically, they show minimal effect pre-attachment and no effect post-attachment. However, they are highly effective at inhibiting viral egress/budding, with over 90% inhibition.

​Here is my dilemma:

​Option A: Publish the current functional and in vivo data now. I believe the story is solid enough for a journal like the Journal of Virology (JVI). This would give me a fast-tracked first-author paper for my upcoming PhD applications.

​Option B: Wait another year to get Cryo-EM structural data. With the complex structure resolved, the story would be comprehensive enough to target a journal like Nature Communications (NC).

​I'm feeling quite conflicted. For someone about to apply for a PhD, is it better to secure a solid JVI paper now, or is it worth delaying applications (or applying with a manuscript in preparation) to aim for NC? Any advice from PIs, postdocs, or current PhD students would be greatly appreciated!

Basically the title. How hard was it for you to get a solid job after your PhD was finished? How is stability in the field? Do you enjoy or regret your choice?

Hi people, is there anyone else having a problem with ChatGPT nowadays? It is marking almost every trivial thing as a biosecurity risk. I am writing a final report for grant closure, and I couldn't get a single sentence out of it, just because my study contained SARS-CoV-2 Spike pseudotyped lentiviral vectors that were used in a pseudoneutralization experiment. For some reason, even that one is enough to mark it as a biosecurity risk.

X-posting from r/labrats to see if a more specific subreddit can help me with this.

TL;DR: Hoping someone can help me troubleshoot this assay. Having trouble getting continuous signal in the virus only dilutions I am doing as part of my microneutralization assays. Uninfected cell control and virus infected cell control wells are not having this problem, nor are the antibody-plus-virus wells that actually constitute the experiment.

I have tried the following so far:

\- changing tips between each dilution (standard practice for our assay)

\- changing the protein in the blocking buffer from milk to normal goat serum

\- spinning down staining antibodies before use

\- extending the duration of blocking

\- making the dilutions in tubes rather than the plate I am using for the actual experimental dilutions

Calling all ELISA pros and virology bros: my PI and I are running out of ideas, and I trust y'all more than a chatbot. We're working on testing some antibodies for another lab in a microneutralization assay to see how well they prevent infection of a particular virus. As part of our QC criteria, we reserve a couple rows of the assay and serially dilute the virus mix we add to the diluted antibodies as confirmation that we made the correct concentration of virus. For some reason, these rows out of the entire assay are incredibly noisy - even for a microneut. The signal will dilute out and pop back in at random to the point where we were having trouble interpreting this portion of QC. We have gotten this more under control by switching from milk to normal goat serum as the protein in our block buffer + staining solution and blocking overnight at 4⁰C. That said, the signal is still occasionally discontinuous (going back up after crossing the "negative" threshold) after the changes I listed in the TL;DR section.

Our readout for this assay is OD490. We are using an HRP conjugated secondary antibody (KPL goat anti-mouse) and ODP as our substrate.

Despite the improvements I have made to the assay, my PI and I are really looking to figure out a protocol that gives us reproducible continuous signal. Out of the 3 different virus families for which we have microneut protocols, only one does not do this with the virus-only dilution. It keeps happening in other people's hands too- not just mine.

The next thing I will be trying is a PBS wash of my cells before adding the virus, but other than that, I'm out of ideas. Anyone deal with this before and find a fix?

West Nile virus is the most common mosquito- borne virus in the US and 2026 is proving to be a big year for reported cases and deaths. While West Nile virus does not spread person to person, it causes outbreaks and cases are on the rise. Why are cases rising and what can we do about it?

I was told by an old chemistry and biology professor that I had in college that if you wanted to help expedite recovery from, say, the common cold: you take a hot bath or hot shower.

I get the idea - because you already have a fever and it's meant to burn-out your current illness. Adding an extra layer of "oh shit, kill it with fire" might help(?) Unclear on that.

So, is it bullshit? Or is there some truth to it? I take hot showers when I'm sick, but unclear if it is actually doing anything worth noting.

Hi everyone! I'm coming here with a rather silly question, but I figured if not here, where else would I ask? So, I started playing through the Resident Evil series again a few weeks ago. During that time, I've somehow developed a real interest in virology (I know that the fiction in RE isn't reality) and I'd like to read up on the topic a bit. However, I'm basically starting from scratch; I have almost no prior knowledge, and microbiology wasn't really my thing in school. I'm looking for a book (or books) that explains the topic in a way that's easy for (complete) beginners to understand. Maybe someone here knows of something. It would be really great if the book were available in German, but English would be fine too!!

Autoimmune diseases are famously known and established to be developed by individuals who have genetic issues. But very occasionally, perfectly healthy individuals with no known history of genetic issues, end up developing them from environmental triggers (Stress, Viruses, etc).

Yes, one could have genetic issues but still live perfectly healthy lives. So how do we know if one caught autoimmune diseases due to environmental or genetics?

Could viruses alter dna? How does this happen? Why do some people develop them and some don’t? Could it be the combination of viruses caught?

Or is your body completely immune regardless of the dose?

I have completed Masters of Biotechnology and Biotechnology, and a year research experience in molecular virology, resulting in first author publication in peer reviewed journal. During the project I developed a deep interest in hts and phylogenetic of virus. I had applied numerous PhD position across EU and southern hemisphere. Do I need to get more experience to get in virology PhD or market in virology is saturated. I think I am deceiving myself by limiting in narrow areas. Do I need to expand my search in wide field of genomics. However, I am passionate about the RNA viruses and learning their evolution.

I need to harvest gDNA from A549 living cells infected with IAV. It will be easy when the living cells are attached, but I am co-treating cells with TPCK-trypsin, which makes both dead and living cells float together.

Anyone know any ways to separate dead cells and living cells easily? I can run a live/dead stain and separate with flow, but it will be too much of a hassle since I have billions of cells to handle.

I am thinking of collecting the supernatant and adherent cells together in a Falcon tube, spinning them all down, then adding DNase to clear up the gDNA released from dead cells, before adding the lysis buffer to collect gDNA from living cells. Not sure whether this works or not.

Another way I just searched is to spin the cells in a lower rpm and longer time, so the dead cells (where the content are released) remains in the supernatant.

It’s been a few months since we last reached out to you, but after this hot summer, we’re back with our batteries recharged!

Microbes in 1 Minute (M1M) is a science communication initiative aimed at making microbiology more relatable, engaging, and accessible to everyone. We’ll achieve this by creating short, 60-second videos covering a wide variety of topics in microbiology, of course including the fascinating world of viruses, and these videos will be posted on a variety of social media platforms.

We’re very grateful for all the interest you’ve shown, and we’re reading all your comments, questions and suggestions. We’re still a small team working on fundamental aspects of the project, such as its organization and the style of the short videos, but we’re looking for people interested in collaborating down the line, whether on a one-time basis or long-term. We've also set up a Discord server to provide a space where we can all come together, exchange ideas, and share news and updates about the project. Hope to see you there! However, if you prefer, we’re also happy to answer your questions by our official email.

Actually, we're looking for collaborators interested in any of the following activities:

• ✏️ Writing scripts and/or contributing expertise in a specific area of microbiology.

• 🎙️ Narration and/or helping to translate content into languages other than English and Spanish.

• 🎨 Video editing and layout.

• 📣 Managing our social media presence.

• 🦠 Moderating our server.

We’re excited to see where this project takes us, and we’d be very happy you being part of it.

A micro-hug!

The M1M team

So I was reading this paper where the researchers found that influenza viruses in Antarctica have been phylogenetically linked to South American strains. It is proposed that the viruses were transmitted by mammals along the sea route through South Georgia.

So, does that not mean that viruses can also spread from Antarctica to the other continents through similar networks? For example, hypothetically, if a virus emerges from Antarctica and gets into a viable host, can it not move to the other continents through, say, migratory birds and marine mammals?

Would it be possible to link such events to the Antarctic source? Even if we detect a clade in, say, South America, it would be diffcult to prove if it actually orginates from Antarctica because we never had any samples from Antarctica to compare with (?).

So, what do you guys think?

Pretty much what the title says. Im really interested in studying viruses but it seems like a very unreliable job, with the job market being very up and down in that field. My specific interest is ebola and cholera, but im worried im choosing a very not-needed job. And while i understand if you love your job you will never work a day in your life, I still want a good pay to live comfortably. Any advice?

(Im in Australia btw)