Emma Hilton Profile picture
May 7 17 tweets 3 min read Read on X
On Hantavirus: a (non-technical) thread.

Disclaimer: I am a biology PhD, but not virology/epidemiology. Husbandman is a virology PhD. But I’m told I’m good at communicating science, so here’s my take.

#Hantavirus
Humans get hantavirus from rodents who carry it.

Some people went to Argentina birdwatching in a landfill, and were exposed to hantavirus because rodents like landfills.

Looks like one - if not two - people brought the virus onto their cruise boat.
So now we have an isolated boat with an index case: someone who is infected.

That’s not good for the index case. Hantavirus has a high fatality rate, and that’s scary.
But fatality rate alone does not determine outbreak risk.

A virus that kills 30 % of the people who contract it but barely spreads to anyone else is less dangerous to society than one that kills 0.1 % but infects everyone.

See: COVID.
All viruses work in basically the same way:
They enter your cells>
They hijack the cellular machinery to copy themselves>
They burst out of your cells, often destroying the cell in the process.

In the meantime, your immune system is working to keep you healthy.
But: a virus replicating inside your cells is only a potential danger to you. It’s crap if the virus has a high fatality rate, obvs.

But it becomes a danger to others when it starts leaving your body: sneezing, breathing, secreting, bleeding it out.
This is called shedding. This is the virus going forth and finding a new host.

But different viruses do all this stuff differently.

Some are Door Dash - live fast or die young, sorry about all the sneezing but who needs nose cells anyway.

Some are snipers - they take their time, don’t raise eyebrows, wait for their chance.
People are worrying about long incubation periods - the time between getting infected and having symptoms.

The length isn’t the issue.

What matters is whether a person is shedding during incubation.
COVID shedded before you felt ill.

That’s why it spread so efficiently. You’re infectious before you know you’re sick.

Hantavirus doesn’t appear to shed before you have symptoms. Even if they are 2 weeks or 8 weeks after exposure.
With hantavirus, it t seems to be the case that you incubate for weeks feeling fine, and not infectious.

Then you deteriorate rapidly. And go to bed, or to hospital, or whatever.

But not to birthday parties (see later).
R0 is the average number of people one infected person passes a virus to in a susceptible population.

It’s a predictor of pandemic potential.

Measles is 12–18.
COVID v 1.0 was 2–3.
Flu is like 1.2.

For Andes hantavirus, R0 estimates from the 2018 Argentina (human-to-human) outbreak was between 1 and 2.

Above 1 means it can sustain transmission, but only just.
So now to why boats aren’t really a great indicator of what happens outside a boat.

The R0 of COVID-on-boat was much higher than COVID-on-land.

Loads of people, packed into shared buffets and cramped living spaces.

Petri dish, pressure cooker etc.
If you wanted to maximise transmission of a tricky-to-transmit virus, boats are ideal.

Maybe also all-in hotels in Cape Verde, where I shall be visiting in ten days. I’m more worried about food poisoning than floating Hanta.
Human-to-human transmission of Hanta requires close and/or prolonged contact.

You aren’t catching it walking behind an asymptomatic person in the street, or handling a symptomatic patient who is bagged up.
There’s a paper doing the rounds about ‘superspreaders’. It has beautiful figure, that should be reassuring.

The lessons from the paper is: even if you go to birthday parties while symptomatic, the virus struggles to infect others.

The same situation with COVID might have looked very different.
If the flight attendant dealing with an incredibly sick passenger spent a lot of time around the passenger, including face-to-face assessments around managing a flight - face holding, look at me, let me get you a sick bag - that’s close and/or prolonged contact with a symptomatic patient.
I know the boat didn’t really recognise they were dealing with hantavirus, and made some decisions that look poor *In hindsight*.

But this is not COVID.

Still: just don’t get on flights or go to birthday parties if you feel ill. Sometimes it’s good not to share 🤣

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More from @FondOfBeetles

Apr 8
A cell layer that has developed to protect your body from the outside doesn’t work like a cell layer that has developed to protect your body from the inside.

The cells lining my vagina are not the same cells, and they don’t have the same function, as the ones wrapping your penis.

There’s a name for what happens when you subject dry-adapted “outside skin” to wet-adapted “inside conditions”.

Further reading: trench foot.
My vagina - “inside skin” - hothouses a healthy microbiome that promotes health and healing, and imparts immune function onto small humans that happen to come out of it.

Yours? Less so.
My vagina is a muscular organ, adapted to my healthy female function of receipt of peen, expelling menstrual products and pushing out small humans.

An inside out penis? Less so.
Read 8 tweets
Apr 3
Let’s move the discussion from available techniques for sex screening and to matters of process.

Ross @Scienceofsport has described the need for detailed technical documents that inform sports federations in robust implementation of a sex screening policy. I’ll link to his video next.

But here, I’m going to take a wander through running an assay, highlighting standards and procedures.
First, this is Ross’ video of the overall process, highlighting the need for coherent implementation practices. He - correctly - evokes the reams of technical documents used by WADA in their anti-doping programmes.

Even the simplest of lab assays can have pages of instructions associated with it.
So, the assay for sex screening will be detection of the SRY gene. This is the ‘make male’ gene that is the master switch for testes-not-ovaries.

The assays out there are very sensitive and specific. That means they can detect SRY when it’s present, and they don’t give a signal when it’s absent. They aren’t 100% on either metric, but near as dammit.

This itself may be a problem…
Read 18 tweets
Mar 26
In 2025, Jon Pike and I argued that exclusion of athletes with androgenising XY DSDs from female athletics is justified, because these athletes are male, not female.

@runthinkwrite

tandfonline.com/doi/full/10.10…Image
@runthinkwrite This followed a 2024 paper where we, along with Ross Tucker, Tommy Lundberg, Cathy Devine and many others, argued for a return to sex screening to secure eligibility for female sport.

@Scienceofsport @TLexercise @cathydevine56

onlinelibrary.wiley.com/doi/epdf/10.11…Image
@runthinkwrite @Scienceofsport @TLexercise @cathydevine56 This followed another 2024 paper where we critiqued the (now former) IOC policy on inclusion of trans-identifying males in female sports.

onlinelibrary.wiley.com/doi/epdf/10.11…Image
Read 5 tweets
Feb 6
I am starting to pull out details of this "meta" review that says trans-identifying males don't have advantage over women in sports.

I need a sanity check, because I'm only at Figure 1 and already there's an issue.

bjsm.bmj.com/content/early/…
So this is Figure 1A: fat mass (kg).

Alvares 2025, n=7, fat mass is higher in females as both absolute and relative values. This is logged as "favours cisgender", which is kinda odd because high fat mass isn't usually considered favourable for sports, but whatever.

TIMS: 16.2 kg (24%). F: 19.5 kg (26%).Image
But Ceolin 2024 is also logged as "favours cisgender" when their values are:

TIM: 18.2 kg (24%). F: 15 kg (25%). Their n = 47.
Read 7 tweets
Feb 4
What an insane bunch of cherry-picked metrics, cobbled together to try and argue that trans-identifying males should be in female sport.

bjsm.bmj.com/content/early/…
There are little-to-no controls for physical fitness in the individual studies.

Yet they conclude: “transgender women do not exhibit significant differences in upper-body strength, lower-body strength or maximal oxygen consumption relative to cisgender women after 1–3 years of GAHT.”

You haven’t controlled for fitness!!!
Their "performance" data. Can you see one study that really sticks out as an outlier? Image
Read 10 tweets
Nov 4, 2025
The claim that won't die: trans-identifying males are "underpowered" and therefore "disadvantaged" in sport.

"One can imagine a large car with a small engine competing against a small car with a small engine, and that summarizes the playing field." Joanna Harper, Huff Post, 2016.

"You have a bigger body, and you have a smaller engine to move that vehicle around." Yannis Pitsiladis, BBC, 2019.

"giving trans women the disadvantage of having to power larger skeletal frames with reduced strength and aerobic capacity." Jamie Agapoff, 2025.
What happens when a trans-identifying male suppresses testosterone?

They lose a bit of muscle mass.
Their haemoglobin drops to female-typical levels.

The claim that won't die rests on the idea that trans-identifying males retain their skeletal frame and most of their muscle mass, but become unable to move it around a sports fields, rendering them "disadvantaged".
The words "underpowered" and therefore "disadvantaged" are carefully chosen, and typically leave the reader to infer that this means "underpowered" and therefore "disadvantaged" compared to females.

So it's fair to have them in female sport, right?

Wrong.
Read 10 tweets

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