This is Tupou Neiufu. She is a NZ paralympic swimmer. At two years old, she was injured in a hit a run, and left with a permanent brain injury causing hemiplegia.
She won her first Olympic gold medal at Tokyo 2020.
This is Lisa Adams. She is a NZ paralympic shotputter. She has left hemiplegia.
In 2020, she won her first Olympic gold medal and, in separate competition, set the world record for her event.
This is Sophie Pascoe. She is a NZ paralympic swimmer. At 2 yrs old, she suffered severe leg injuries, resulting in left amputation below the knee, in an accident.
She did not win her first gold medal at Tokyo 2020.
She joined an elite club of 40 athletes with 10 Olympic golds.
This is Anna Grimaldi. She is a NZ paralympic sprinter and longjumper. She was born without a functional right forearm/hand.
She jumped her way to her second Olympic gold at Tokyo 2020.
This is Holly Robinson. She is a NZ paralympic javelin thrower. She was born without a left forearm/hand.
She won her first Olympic gold at Tokyo 2020.
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I think the Andes hantavirus data is being misread right now.
Claims are circulating that the evidence doesn’t seem to support.
I want to walk through them carefully.
The 40% fatality figure: an artefact of who gets counted.
The 40% case fatality rate (CFR) figure comes specifically from hantavirus pulmonary syndrome (HPS), an outcome in a subset of hanta infections.
This is the severe cardiopulmonary presentation. It excludes subclinical infections that resolved without anyone noticing more than “a touch of flu”.
In Jujuy Province, Argentina, the seroprevalence (rate at which people have antibodies due to hanta infection) is 6.5%. Hospitalised HPS cases had a CFR of 13.3%, but most patients were described as having a mild clinical course.
Disclaimer: although an Argentine outbreak, this has not been confirmed as ANDV.
The 40% is the fatality rate among people sick enough to be diagnosed and hospitalised.
It is not the infection fatality rate.
These are not the same thing, and conflating them is causing significant confusion.
The true attack rate: barely any data.
The Boat had approximately 180 exposed individuals, and around ten cases have been detected. Three - soon to be four, I predict - have died.
Without antibody analysis of the full cohort, we don’t know how many mild or subclinical infections were missed entirely.
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.
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”.
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.
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.
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 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.
@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.
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%).
But Ceolin 2024 is also logged as "favours cisgender" when their values are: