Dr Michelle Dickinson: nanotechnologist on what one Covid case taught experts about virus evolution

Most of us have had to take a few days off work or school because of the flu or Covid-19. But imagine being sick with Covid, not for a week or two, but for 750 days! 

That’s exactly what happened to one patient described in a recent paper published in the Lancet (Characterisation of a persistent SARS-CoV-2 infection lasting more than 750 days in a person living with HIV: a genomic analysis - The Lancet Microbe). 

The patient, a 41-year-old man living with HIV, continuously tested positive for Covid-19 for 26 months. Because his HIV was poorly controlled, his immune system was compromised. He had also not been vaccinated against Covid-19 and never received antiviral treatment during his illness. 

While this was an incredibly tough experience for him personally, it offered researchers a rare chance to watch in real time how a virus can evolve inside a single human body. 

Over the course of 750 days, scientists collected eight samples from the patient. From these, they extracted viral RNA and sequenced the virus’s genome. 

They found that: 

• 68 new viral mutations appeared over time. 
• 10 of these mutations were in the spike protein, the part of the virus that helps it enter human cells. 
• Some of these matched the exact changes later seen in the highly transmissible Omicron variant. 

Even more concerning, one alteration made the virus better at evading immune responses. 

The important part of this study in that these mutations showed up in the patient months before they were detected spreading widely in the community. 

This suggests that long-term infections in immunocompromised people can act like mutation incubators, where the virus experiments with new tricks before releasing them into the wider population. 

This case highlights several important lessons: 

• Persistent infections matter: They aren’t just unusual cases. They can directly influence how viruses evolve and have a consequence on the rest of the world. 
• High-risk patients need better support: Improved access to antiretroviral therapy for HIV, vaccination, and Covid-19 treatments can reduce the chances of these prolonged infections. 
• Stopping variant incubation is key: By treating persistent infections early, we may be able to slow down or even prevent the emergence of dangerous new variants. 

This story is a sobering reminder that pandemics don’t just happen on a global stage, they can begin quietly, inside the body of a single individual. For scientists, these unusual cases are windows into viral evolution. For the rest of us, they underscore why protecting vulnerable groups isn’t just compassionate, it’s critical for everyone’s health. 

LISTEN ABOVE

See omnystudio.com/listener for privacy information.

Episode Transcript

Speaker 1 (00:06):
You're listening to the Sunday Session podcast with Francesca Rudkin
from News Talks EDB.

Speaker 2 (00:13):
Joining me now with her science study of the week,
Doctor Michelle Dickinson, Good morning, Anchored morning. Now, this is
really interesting. I mean it's a bit of a bit
of sweet scientific story, this one because we have a patient,
a forty one year old man living with HIV who's
continuously tested positive the COVID nineteen for twenty six months,
which personally, I imagine for him has been pretty tough,

(00:35):
but he has been able to provide researchers and scientists
with just this fascinating opportunity to see what COVID does
in a human body, how it evolves totally.

Speaker 3 (00:48):
And look, you know, anybody who's been sick with the
flu or COVID or the cold and you're out for
a week or even two, you're like, oh, there's like eternity, right,
dred And fifty days this man tested positive for COVID nineteen.
And that's unusual because he did have HIV which was
not well managed, which meant he was immune compromised. And
so if you go back and I know, people might

(01:08):
not want to talk about COVID again. But if you
go back to the time when we were under a pandemic,
there were many variants of COVID that we were exposed to.
We started with the alpha, we went to delta, we
went to omicron, and you most people don't understand what
that meant, but what it meant is the virus changed
to Basically, usually viruses try and change to be better,
to survive, better, to transmit better, to achieve what they

(01:31):
want to achieve, which is to replicate more in people's bodies.
And the question is how do they do that? Because
if we're ever going to experience them, I think we
will another pandemic. Understanding how the virus changes and how
to stop that is going to be how we prevent this.
So this poor man had the COVID for seven hundred

(01:52):
and fifty days, but during that time, actually scientists were
able to take eight different specimens collected from him and
run viral RNA and sequence the virus's genome at different
points in time during his infection. And what they learned
was number one, they found sixty eight new viral mutations
over time. Okay, so we know that the virus is mutating,

(02:13):
and we know that viruses do that. Especially second lot
sixty eight sounds like a lot. It is a lot, Yes,
it's a lot, but it's because they could live that
it could survive in this host, this man for so
long that it could just keep changing things and see
what worked. So because he was immune compromised, his immune
system wasn't able to take out the virus. It was like,
let's try this, let's do this, Let's see if this

(02:34):
means that more of us can replicate or survive more.
What was so interesting is out of these sixty eight,
ten of the mutations were on the spike protein. Now
you may have heard of the spike protein with covid,
but basically that's where the virus attaches to the human
cells and gets into it. So the way that the
virus replicates is it gets into a human cell and

(02:55):
then it forces that cell to produce more of the
virus rather than do what the cell was supposed to
do in your body. So being able to attach and
enter the human cell better means that it's more likely
to replicate.

Speaker 1 (03:06):
What I found.

Speaker 3 (03:07):
Fascinating in the study is some of these changes matched
the exact changes that we later saw in omicron, which
was the highly transmissible variant of COVID. The reason why
this is important is we saw these changes ten months
before omicron was detected in the public, So these changes

(03:28):
that made it more highly transmissible were seen in this
patient and we didn't realize this until much later on,
meaning that these changes in immune compromised people are probably
the reason why the next variant actually happened. So what
that means is, if you're thinking about pandemics, it's not

(03:48):
about maybe stopping the virus from affecting the whole population.
It's about going where is the most risk for this
virus to change and transform and actually be more dangerous potentially,
And it's typically in these immune compromised patients who host
the act as virus incubators. They ho the virus for
long periods of time, so the virus can change and

(04:10):
try some stuff and get better and be more efficient
and then be more transisible, and then that patient spreads
it and that's how it spreads. So really interesting, I mean,
this poor patient, but a really interesting study, and the
first time scientists have been able to study real time
what happened with the COVID nineteen virus, how it changed,
and what type of patients are at risk, which makes

(04:32):
you think that actually, in the longer term, you can
focus on these patients and go, actually, if we only
have a certain amount of resources, the types of people
we need to focus on those who are really immon
compromise that might be harboring and being an incubator for
the virus, because that might be the thing that affects
the world population in the long run.

Speaker 2 (04:50):
Thank you so much, Michelle, appreciate that.

Speaker 1 (04:53):
For more from the Sunday session with Francesca Rudken, listen
live to News Talks it'd be from nine am Sunday,
or follow the podcast on iHeartRadio.