Speaker 1: I want you to close your eyes for a second.
Picture a warm, humid evening in rural Bangladesh. It's quiet,
the air smells like, you know, wet earth and vegetation.
You're standing in a grove of date palm trees. It
feels peaceful, maybe even a little romantic in that sort
of rustic way. Right and high up on the trunk
of one of these trees, somebody has shaved away the
bark and hung a clay pot.
Speaker 2: It's a scene that's played out for I mean centuries. Yeah,
that pot is there to collect the sap.
Speaker 1: Right. It drips down, drop by sweet drop all night long.
It's the sugary, refreshing nectar that the locals absolutely love.
It's a tradition.
Speaker 2: It is.
Speaker 1: You wake up in the morning, you walk up to
the grove, you take the pot down, and you drink
it fresh. It's raw, it's cool, it's delicious.
Speaker 2: It sounds like the definition of farm to table or
a tree to table.
Speaker 1: It does. But now I want to ruin that image
for you, okay, because while the village is sleeping, there's
a visitor. A silhouette glides through the moonlight. It's big,
a wingspan of maybe four five feet a fruit bat,
specifically a flying fox, and it is thirsty.
Speaker 2: And this is where the idyllic scene turns into a well,
a biological crime scene.
Speaker 1: That's the perfect way to put it. The bat lambs
on the tree right above that clay pot. It hangs there,
maybe upside down, and it starts licking the sap stream.
Speaker 2: It's just having a drink, just having a drink.
Speaker 1: But bats are messy eaters. Maybe it dribbles saliva into
the pot. Maybe because it's perched right there, it urinates
into the collection jar who then it flies off into the.
Speaker 2: Dark, leaving absolutely no trace that it was ever there exactly.
Speaker 1: The sap looks the same, it smells the same. The
next morning a villager drinks it, and a week later
that person isn't just sick. They are fighting a pathogen
that is so aggressive, so efficient at dismantling the human
central nervous system, that their chance of dying isn't one
in one hundred like the flu. No, it's somewhere between
forty percent.
Speaker 2: And those are numbers that epidemia generally only seeing their nightmares.
To put that in perspective for everyone listening, COVID nineteen
had a case fatality rate that was generally speaking, well
under one percent for the general population.
Speaker 1: So less than one percent.
Speaker 2: Right, we are talking about a coin toss with death
or in some outbreaks, much much worse than a coin toss.
Speaker 1: Welcome to thrilling Threads. I'm your host, and today we
are absolutely not talking about the common cold. We are
unpacking a stack of sources, research papers, who surveillance reports,
and some really dense epidemiological studies that span from the
late nineties all the way to the vaccine trials happening
right now in January twenty twenty six.
Speaker 2: And it is a stack that tells a very specific
and I think very terrifying story.
Speaker 1: We are diving into the Nepa virus nev. Even the
name sound sharp, doesn't it Nepa.
Speaker 2: It does sound a bit unassuming, but it's named after
the village in Malaysia where it was first isolated. Compun
sing Guy Nepa.
Speaker 1: The Neper River village exactly.
Speaker 2: But make nomus. This virus is a beast. It's paramixovirus.
Speaker 1: Paramixovirus. That's a mouthful. Is that the same family as
the flu no no.
Speaker 2: Flu is orthomixivity paramix viruses are a different breed. They
include things like measles and mumps, things we're familiar with.
But NEPA is special. It has this dual attack mechanism
that makes it incredibly dangerous. Most viruses, you know, they
pick a lane. They either attack your lungs like a
respiratory virus, or they attack your nervous system. NEPA says, why.
Speaker 1: Not both, So it's a double agent in a way.
Speaker 2: Yeah, it causes severe respiratory distress think pneumonia on steroids.
But it also causes encephalitis.
Speaker 1: Which is brain swelling.
Speaker 2: Inflammation of the brain tissues. Yes, your brain essentially swells
inside your skull. It is on the World Health Organization's
Priority pathogen list for potential pandemics, and it has been
for years now.
Speaker 1: A priority pathogen. That doesn't sound good.
Speaker 2: No, it means it's on their watch list of things
that could cause the next big one. And looking at
the documents we have in front of us, covering the
initial nineteen ninety eight discovery up to the clinical data
from twenty twenty five, this is what researchers call a
paradigmatic challenge.
Speaker 1: A paradigmatic challenge that sounds like polite scientists speak for,
we are in big trouble.
Speaker 2: It basically means it breaks the rules we're used to.
It doesn't behave like other viruses.
Speaker 1: Well, let's break down those rules, because this isn't just
a medical story. As I was reading through these files,
it felt like a detective story.
Speaker 2: It really is.
Speaker 1: It starts with a mystery in Malaysia, moves to a
tragedy in Bangladesh, and ends with a race against time
and laboratories happening.
Speaker 2: Right now, and that race is actually heating up. The
landscape in twenty twenty six is very different than it
was even five years ago.
Speaker 1: So let's rewind the clock. Take us back to the
origin story. We were in Malaysia. It's nineteen ninety eight.
The village is Campum Sungey Nipa. What was happening on
the ground.
Speaker 2: It was absolute chaos. You have to imagine the confusion.
Pig farmers started collapsing, and I don't mean just feeling
a bit under the weather. Yeah, they had high fevers,
they were deliri, they were having seizures. A cluster of men,
all with the same job, all coming down with this
severe neurological illness.
Speaker 1: And when you see people with seizures and fevers in
a tropical country like Malaysia, what's the first thing a
doctor thinks of mosquitos?
Speaker 2: Always mosquitos. It's just reflex at that point, you think malaria,
you think danngay or us case. They thought it was
Japanese encephalitis.
Speaker 1: Which is a mosquito born disease, right, and it's endemic
in that region.
Speaker 2: So the Malaysian health officials and the government did exactly
what the text books says you should do for a
mosquito outbreak. They rolled out the fogging trucks.
Speaker 1: I've seen those.
Speaker 2: Yeah, they started spraying insecticide everywhere to kill the mosquitos.
They focused entirely on vector control.
Speaker 1: But it didn't work.
Speaker 2: It didn't make a dent. Yeah, the cases kept rising,
people were dying, and critically, the epidemiologist on the ground
started noticing something that just didn't fit the mosquito narrative.
Speaker 1: What was the glitch in the matrix?
Speaker 2: It was the pigs.
Speaker 1: The pigs.
Speaker 2: Japanese encephalitis can infect pigs, but it doesn't usually cause
massive visible illness in the animals. They act as a reservoir,
a silent one, but they don't drop dead in droves, okay.
But in Kampung Sunga Nipa, the pigs were sick, very
very sick, sick.
Speaker 1: How what were the symptoms.
Speaker 2: They had this distinctive, loud, barking cough. Farmers called it
the one mile cough because you could hear it from
a distance. It was clearly a respiratory infection tearing through
the pigstyes. And when the investigators looked at the human data,
they realized that the people getting sick were almost exclusively
the pig farmers.
Speaker 1: So not the random villagers down the road, just the
people handling the pigs.
Speaker 2: Correct. If it were mosquitoes, everyone would be getting bitten
mosquitoes don't check your job title before they bite you.
But here it was the people working the abatoirs, the
people cleaning the pens. The contact was the key.
Speaker 1: So it wasn't the insects buzzing in the air. It
was the animals they were wrestling with every day.
Speaker 2: That was the breakthrough. They realized this was a zoonotic spillover,
a disease jumping from animals to humans, but the transmission
route was specific. In Malaysia, the route was bats to
pigs to humans.
Speaker 1: Okay, let's parse that bats to pigs. How does a
pig catch a virus from a bat? Do they like
hang out together?
Speaker 2: Not socially no, But the farms were often planted with
fruit trees, mangoes, durians to provide shade or extra income.
Speaker 1: Oh, I see where this is going.
Speaker 2: Fruit bats love mangoes. So a bat comes in at night,
eats half a mango, drops the rest into the pig pen.
That mango is covered in bat's.
Speaker 1: Saliva, and pigs are basically biological vacuum cleaners.
Speaker 2: They will eat anything. So the pig eats the contaminated fruit.
Now here's the crucial concept from our source material. The
pig acted as an amplifying host.
Speaker 1: An amplifier like a guitar amp. It makes the signal louder.
Speaker 2: That's a perfect analogy. The bat is the musician playing
a very quiet note. The virus in the bat is present,
but at a low level. When that virus it's into
the pig, it finds a biological environment that is absolutely
perfect for replication. It reproduces massively.
Speaker 1: This goes crazy.
Speaker 2: The viral load, The amount of virus in the body
becomes enormous. The pig is a much better host for
this virus than the bad is in terms of replication.
Speaker 1: So the pig becomes a virus factory factory.
Speaker 2: With a cough, a very loud cough. Because pigs in
these commercial farms are kept in very close quarters, the
virus tears through the herd like wildfire. The pigs are coughing, sneezing,
spring respiratory droplets everywhere. Oh man, the farmers are working
right in this cloud of virus.
Speaker 1: That is a terrifying image. You're standing in a shed
with a thousand coughing pigs breathing an air that is
thick with a deadly pathogen.
Speaker 2: And once they realize this, once they identified the virus
of the vector, the solution was brutal. To stop the outbreak,
they had to destroy the amplifier.
Speaker 1: I remember reading the numbers on this. It's staggering.
Speaker 2: They caulled over one million pigs. One million. Imagine the
logistics of that. The army was brought in. It was
a massive, desperate operation. It completely devastated the Malaysian pork industry.
It was an economic catastrophe for those farmers. Many lost
their livelihoods overnight. But and this is the hard truth
of epidemiology. It arguably saved countless human lives because it
broke the chain of transmissions. It stopped the amplifier, it
pulled the plug. And here is the key difference between
what happened then and what we see now, which I
know we're going to get to. In Malaysia, human to
human transmission was very rare. It was almost entirely animal
to human. If you didn't work with pigs, you were
generally safe. The virus wasn't adapted well enough to jump
from person to person efficiently.
Speaker 1: Right, So the outbreak thens, the pigs are gone, the
virus fades away, and for a minute the world thought, Okay,
that was a freak event, a one off.
Speaker 2: That's what everyone hoped, a contained zoonotic blip.
Speaker 1: But the virus didn't disappear. It just moved, or rather
we found it behaving differently somewhere else. Yes, this brings
us to the second part of our story, the shift.
We're moving the map from Malaysia to Bangladesh and India.
Speaker 2: Specifically West Bengal and the state of Kerala in India.
Speaker 1: Now, I feel like I've seen Kerala in the news
a lot regarding this, it keeps popping up.
Speaker 2: You have it's become a hotspot. There was a major
outbreak in twenty eighteen, another flare up in twenty twenty one,
and again just a couple of years ago in twenty
twenty three. The twenty twenty three outbreak was particularly alarming
because it happened while the world was still exhausted and
on edge from COVID nineteen.
Speaker 1: I remember that there was a tragic case involving a
young boy, right, yes.
Speaker 2: A fourteen year old boy. The details are heartbreaking. He
didn't work on a farm, he wasn't pig farmer. He's
just a kid.
Speaker 1: So how did he get it.
Speaker 2: It's believed he may have eaten fruit that was contaminated
by a bat. He tested positive and despite the best
efforts of the doctors, he passed away. It sent shock
waves through the region because it reminded everyone that this
threat hadn't gone away. He can just appear out of nowhere.
Speaker 1: But here's the puzzle that confuses me. In Malaysia, you
have these massive industrial pig farms, millions of pigs amplifying.
Speaker 2: The virus right the virus factories in.
Speaker 1: These villages in Bangladesh and Kerala. There aren't massive pig farms.
Speaker 2: No, the agricultural landscape is completely different. The cultural context
is different.
Speaker 1: So if the amplifier is gone, how is the virus
getting from the bat to the human.
Speaker 2: That is the question that kept scientists up at night
for years. If there are no pigs, what is the bridge.
Speaker 1: The answer brings us back to that clay pot we
talked about in the intro, the date palm route, the
raw sap.
Speaker 2: It turns out, in these regions the virus doesn't need
an amplifier, It just needs a vehicle, a sweet, delicious vehicle.
The terrapist bats, the flying foxes love the sugar in
that sap.
Speaker 1: So we have evidence of this.
Speaker 2: It's not just a hunch, Oh, it's definitive. There is
a brilliant study. Our notes referred to it as the
Bamfi evidence, named after a lead researcher. They set up
infrared night vision cameras pointed at these date palm.
Speaker 1: Pots spy cameras for bats.
Speaker 2: Essentially, and the footage is undeniable. You see these massive
bats landing on the cut in the tree, licking the
sap stream as it flows down. You see them climbing over.
Speaker 1: The pots, so they're right there at the source.
Speaker 2: Right there. And bats, to put it delicately, urinate frequently
to reduce body weight for flight.
Speaker 1: So they are peeing in the drink.
Speaker 2: You're peeing in the drink, or their saliva, which is
loaded with virus, drips into the pot. Now, usually a
virus outside the body is fragile. Sunlight kills it, heat
kills it. But sugar nepa is surprisingly stable in sugar
rich solutions, especially if they are kept cool, like in
a clay pot overnight. So the bat visits at three am,
a human drinks the SAP at seven am. The virus
is still viable. Wow, it has a direct highway into
the human digestive system.
Speaker 1: That is incredibly disturbing. You're drinking a viral cocktail. But
there's something else in the Bangladesh data that scares me
even more than the SAP. In Malaysia, you said you
had to touch a pig to get sick. Human to
human spread was almost nonexistent.
Speaker 2: Right, It was a dead end for the virus mostly,
But looking at the.
Speaker 1: Reports from Bangladesh and India, that rule doesn't seem to
apply anymore.
Speaker 2: No, it doesn't. And this is the shift we're talking about.
This is what puts NIPA on the pandemic potential list.
In these outbreaks, we see distinct confirmed chains of human
to human transmission.
Speaker 1: There is a statistic here in the source deck that
I circled in reading. It says ninety one percent of
the index patients the first people to get sick developed
symptoms during the SAP collection season.
Speaker 2: Right, that makes sense. That's the bat connection, that's the
spillover event.
Speaker 1: But then it says seven percent of patients were responsible
for infecting fifty percent of secondary cases.
Speaker 2: That is the classic definition of a super spreader.
Speaker 1: What makes someone a super spreader is their virus different.
Speaker 2: It can be a few things. It can be that
their individual viral load is exceptionally high for whatever biological reason,
but often it's about their symptoms and their social context.
The bangladex strain of NEPA causes massive respiratory.
Speaker 1: Issues, more so than the Malaysian one, much more so.
Speaker 2: So. If a patient is coughing violently, they are projecting
aerosols containing the virus. They become a little fog machine
of death.
Speaker 1: And who is getting infected.
Speaker 2: It's tragic. It's the caregivers. It's the family members wiping
the sweat off their brow. It's the nurses changing their
ivy lines. It's the people who love them and are
trying to care for them.
Speaker 1: That's that's heavy. It targets compassion.
Speaker 2: It really does. It exploits our most basic human instinct
to care for the sick. And there is another cultural
aspect mentioned in the sources too, which is just heartbreaking.
Corpse to human transmission.
Speaker 1: Transmission from the deceased.
Speaker 2: Yes, in many traditions in this region, the family washes
the body of the deceased before burial. It's a final
act of intimacy and respect, of course, But if that
person died of NEPA, their fluids, saliva, respiratory secretions are
still teeming with live virus. We have verified clusters where
the virus move from a deceased patient to the warning
family during these rituals.
Speaker 1: God, so the funeral becomes the start of the next outbreak.
Speaker 2: Exactly, and this changes the containment strategy entirely. In Malaysia,
you could solve the problem with bulldozers and rifles. You
call the pigs. In Bangladesh, you can't call the humans.
You have the change behavior. You have to tell a
mother she can't hug her dying child. You have to
tell a son he can't wash his father's body in
the traditional way.
Speaker 1: Which is infinitely harder than managing livestock.
Speaker 2: Infinitely is asking people to go against generations of culture
at the most emotionally devastating moment of their lives.
Speaker 1: So we have the pigs, we have the sap, and
we have the heartbreaking human element. But let's look at
the landlord of this virus, the source segment three, the reservoir.
Speaker 2: The flying fox, the debis genus.
Speaker 1: These aren't the little bats that flutter around your porch
light eating mosquitoes.
Speaker 2: No, No, these are old world fruit bats. They are big, beautiful,
magnificent creatures. And I want to be clear, they are
ecologically essential. They pollen flowers, they disperse seeds. Without them,
the rainforests basically collapse.
Speaker 1: But they are also the natural bunker for hennepaviruses, this
family of viruses.
Speaker 2: Yes, they are the reservoir host. The virus lives in
them without causing them any harm.
Speaker 1: What I don't get is if this virus kills ninety
percent of the humans it touches, and it kills pigs.
Why isn't the forest floor littered with dead bats? Why
are they immune?
Speaker 2: That is one of the hottest topics in immunology right now.
The bad immune system is a marvel of evolution. How so, Well,
think about what a bat does. It flies. Flight is
incredibly metabolically expensive. It's like running a marathon. Constantly generates
a huge amount of heat. Okay, when you or I
get a fever, our body temperature goes up a few
degrees to help kill a virus. Bats generate that kind
of heat naturally just by flying.
Speaker 1: So they are constantly running a low grade fever in
a sense.
Speaker 2: In a way, yes, and their immune systems have evolved
to be in a constant state of high alert but
dampened inflammation. They tolerate the virus, they keep it suppressed,
They carry it, but they don't get sick. It's a
symbiotic relationship that has evolved over millions of years.
Speaker 1: Okay, so the bat is a carrier, but they don't
shed the virus all the time. Right, It's not like
every bat is a flying biological weapon twenty four to seven.
Speaker 2: No, and that's a crucial point for predicting outbreaks. Viral shedding.
When the bat actually releases the virus in its urine
or saliva isn't constant. It pulses, and the evidence suggests
it correlates with stress.
Speaker 1: Stress like bad anxiety. Are they worried about their taxes?
Speaker 2: Physiological stress Pregnancy is a big one. The strain on
the body can cause them to shed more virus, but
increasingly the sources point to nutritional stress starvation.
Speaker 1: Which brings us to the environmental angle.
Speaker 2: It does when we cut down the rainforests, when we
replace wild fruit trees with pummel plantations or cities, the
bats don't just vanish.
Speaker 1: They get hungry, and a hungry bat goes looking for food.
Speaker 2: Exactly, it forces a foraging change. They leave the deep
forest and come to the orchards. They come to the
mango trees in our backyards, they come to the date
palms in the villages. We are destroying their homes, so
they are moving into ours, and.
Speaker 1: Because they are stressed and starving, their immune systems are
a bit weaker and they're shedding more virus.
Speaker 2: Precisely, it's a feedback loop. We stress the environment, the
environment stresses the bat. The bat sheds the virus the
virus hits us. This is the core of the one
health concept.
Speaker 1: One health. I've heard that term thrown around.
Speaker 2: It's the idea that you cannot separate human health from
animal health or environmental health. They're all interconnected. You can't
solve NEPA just by looking at the virus in a
test tube. You have to look at the chainsaw cutting
down the forest half a world.
Speaker 1: Away, because they're the same problem.
Speaker 2: They are the same problem, just with a long and
complicated fuse.
Speaker 1: That makes sense. But let's say the chainsaw has done
its work, the bat has shed the virus, and it's
inside a human. I want to see men way, let's
talk about the mechanics of this killer. Segment four virology,
How the key fits the lock.
Speaker 2: Where the science gets really elegant in a horrifying way.
NEPA is an RNA virus. Yeah, but to understand why
it kills so effectively, you have to look at the
surface of the virus particle. It has two main weapons,
two proteins sticking out of his shell, the G protein
and the F protein. G and F sounds like a
bad report card. What do they do think of a
G protein that's for glycoprotein as a grappling hook. Its
job is to find a specific spot on one of
your cells and latch on.
Speaker 1: Does it just grab any cell.
Speaker 2: No, it's very specific. It's a specialist. It hunts for
a receptor on your cells called frin B two.
Speaker 1: F n B two. That's the lock.
Speaker 2: That's the lock. And this is the AHA moment for
why NEPA symptoms are so weird and so widespread in
the body. We have to ask where is fn B
two located in the human body.
Speaker 1: I'm guessing not just in one place.
Speaker 2: No, it's a highly conserved protein, which means it's really important,
So it's everywhere. Yeah, But it's found in two main
areas relevant to NEPA. First, it's in the endothelial cells,
the lining of your blood vessels and arteries, all of
them pretty much. And second is found in neurons.
Speaker 1: Blood vessels, and brain cells exactly.
Speaker 2: And think about your lungs. Your lungs are basically a
giant sponge of blood vessels for gas exchange. So the
virus gets breathed in hits, the lungs attacks the blood
vessels there, causing the respiratory distress, the bleeding. Then it
enters the bloodstream, rides that highway all over your body,
and because it targets neurons, it crosses the blood brain barrier.
Speaker 1: And attacks the brain, hence encephalitis.
Speaker 2: It's a roadmap written in our own biology. It uses
our own infrastructure, getst us, but it gets worse. There
is a secondary receptor. It can also use frin B three.
Speaker 1: Where is that one?
Speaker 2: The brain stem?
Speaker 1: The brainstem, that's the lizard brain, right, the part that
keeps the lights on.
Speaker 2: It controls your autonomic functions, breathing, heart rate, swallowing, the
most basic critical life support systems. If the virus hits
EFRONB three heavily, it basically unplugs the computer. This is
why patients can deteriorate so fast.
Speaker 1: So the G protein hooks on. What does the F
protein do?
Speaker 2: F stands for fusion. Once the grappling hook is secure,
the F protein activates like a spring loaded spike. It
harpoons the cell membrane and fuses the viral skin to
your cell skin, opening a door so the virus can
dump its genetic material inside. Were fine, but the F
protein is messy. It's really aggressive. It doesn't just fuse
the virus. To the cell. It's so sticky that it
causes your infected cell to fuse with its.
Speaker 1: Neighbors like melting together.
Speaker 2: Yes, it creates these giant, multinucleated monster cells. We call
them sincitia sinsidia. It's from the Greek four together. Imagine
a microscopic horror movie where fifty cells melt into one giant,
dysfunctional blob. This leads to massive cell death and vasculitis
inflammation of the blood vessels. The walls of your artery
start to die and leak.
Speaker 1: That is visceral and where is our immune system? While
all this is happening, usually, if a virus enters, we
send in the swat team. The alarms go off.
Speaker 2: MIPE has thought of that. It has a suite of proteins.
They have names like PEVWW and C encoded in its
genetic script. These are antagonists.
Speaker 1: What are they antagonize?
Speaker 2: Interferon Interferon is your body's air raid siren. When a
cell gets infected, it releases interferon to tell the neighboring
cells shields up, we are under attack.
Speaker 1: Prepared defenses right the alarm system.
Speaker 2: Nepus proteins actively hunt down the signaling molecules that make
the alarm work. They're called STAT one and STET two,
and they block them, they disable them.
Speaker 1: So it cuts the phone lines.
Speaker 2: It cuts the phone lines, kills the guard dog, and
disables the alarm system before it can even make a sound.
By the time the immune systems heavy hitters finally realize
what's happening, the virus has already replicated a billion times.
Speaker 1: That explains the speed, That explains the fatality rate. So
let's talk about what that feels like for the victim.
Segment five, the clinical nightmare.
Speaker 2: It is in nightmare, and it's unpredictable. The incubation period,
the time from the drink of SAP to the first symptoms,
is usually four to fourteen days, but there are documented
cases where it has been as long as forty five days.
Speaker 1: Forty five days, so I could go on a to Bangladesh,
come home to New York, go back to work, see
my family, feel perfectly fine for a month and a half,
and then drop.
Speaker 2: Theoretically, yes, and that long silent incubation period is a
huge risk for global spread. Someone could get on a
plane feeling fine and be a ticking time bomb.
Speaker 1: What does the onset look like.
Speaker 2: It starts deceptively. It mimics a dozen other things. Fever, headache,
muscle pain, myyalgia. You think you have a bad flu,
maybe a sore throat.
Speaker 1: Okay, so you take some asper and you go to bed.
Speaker 2: Right, But then fast dizziness we call it altered sensorium.
You get confused, you don't know where you are, Your
personality might change.
Speaker 1: The brain swelling is starting exactly.
Speaker 2: Mean cephalitis is kicking in. Then come the seizures and
eventually coma. In the Bangladesh strain, which we need to remember,
is the more lethal one. Acute respiratory distress syndrome or
ARDS is very common. Sixty to seventy five percent of
patients get it, and ARDS is it's where your lungs
fill with fluid. Drowning in your own flu is while
your brain is shutting down is an absolutely brutal way
to go.
Speaker 1: We mentioned the two strains, Malaysia and Bangladesh. Is there
a big difference in survival rates?
Speaker 2: Significant? The Malaysian strain was predominantly neurological. It had a
mortality rate of about forty percent, still.
Speaker 1: Terrible that the Bangladesh strain.
Speaker 2: It hits the lungs and the brain harder. The mortality
rate hovers around seventy five percent, but in some small
outbreaks it is hit ninety percent or even one. Yes,
small clusters where everyone who got it died, it is
much much deadlier.
Speaker 1: There is one more feature in these notes that sounds
like pure psychological torture, relapsed encephalitis.
Speaker 2: This is the thing that really scares infectious disease doctors.
A patient survives NEPA, they beat the odds, they're one
of the lucky few. They recover, they go home, They
live their life for months, maybe even a year or more.
And then and then the virus, which has been hiding
in a dormant state somewhere in the central nervous system,
maybe in the eye or deep in the brain tissue
where the immune system can't easily see it, reactivates. It
comes back, It comes back, and the patient develops encephalitis
all over again, sometimes with no warning. We call it
late onset NEPA.
Speaker 1: That is incredibly cruel. You think you've won, but the
war isn't over.
Speaker 2: It's rare, but it happens. And even for those who
survive and don't relapse, the cicila, the after effects are harsh.
Survivors often have persistent convulsions, personality changes, cognitive deficits. The
damage the virus does to the neurons doesn't always heal.
Speaker 1: Okay, that is the heavy stuff, that is the monster.
But we are recording this in January twenty twenty six.
Science moves fast. Let's look for the silver lining segment
six countermeasures.
Speaker 2: The landscape is definitely changing. It's much more hopeful now.
Speaker 1: If I am in Kerala today and I get diagnosed
with NEPA, what is the treatment? Is there a pill?
Is there something they can give me?
Speaker 2: If you walk into a hospital today, the reality is stark.
The standard of care supportive, which means we keep you hydrated,
we put you on a ventilator. If you can't breathe,
we give you anti seizure meds. We try to keep
your body alive long enough for your immunes system to
hopefully figure it out. There are no fully licensed, globally
available drugs specifically approved for NEPA yet yet.
Speaker 1: But I know there are trials. I've seen the reports.
Speaker 2: There is a lot of movement in the experimental space. Historically,
they tried drug called ribevierin during the Malaysia outbreak. It's
a broad spectrum anti viral. Did it work The data
is a messy. One study suggested it reduced mortality by
thirty six percent, which sounds great, but later studies in
animal models couldn't replicate that success. The consensus now is
that it's probably not very effective.
Speaker 1: What about antibodies. We heard so much about monoclonal antibodies
during COVID Yes, there.
Speaker 2: Is a specific one called M one O two point four.
Speaker 1: M one O two point four, catchy name. How does
it work?
Speaker 2: Remember the G protein the grappling hook.
Speaker 1: Right, the one that grabs onto ourselves.
Speaker 2: This antibody is designed to stick to the G protein.
It basically covers the hook and glue. If the hook
is covered, it can't grab the Effrin B two receptor.
The virus just bounces off the cell. It's a shield,
it's a neutralizer. It is completed phase one safety trials
in humans, and it has been used on a compassionate
use basis in a few cases. It shows real promise
if you give it early. But once the virus is
inside the brain, it's harder for big antibody molecules to
get across the blood brain barrier.
Speaker 1: So timing is everything. What about simple anti virals? I
seem desivere.
Speaker 2: Ah rem de sivere.
Speaker 1: Yeah.
Speaker 2: The African green monkey study, this was a very compelling
piece of research from a few years back. They exposed
monkeys to a lethal dose of NEPA, then gave them
rims survival.
Speaker 1: Wow.
Speaker 2: But and there is always a butt. It was given
as post exposure prophylaxis. That means they gave the drug
very shortly after infection, before symptoms got severe. So it
proves the drug works mechanically against the virus, but whether
it saves a patient who is already in a coma
is a different and much harder question.
Speaker 1: And then there's a holy grail vaccines. I see notes
here about Oxford University. This is the big news right now.
Speaker 2: Yes, this is the big news for twenty twenty five
and twenty twenty six. The vaccine race has finally, finally accelerated.
Oxford launched the world's first Phase two trial for their
NEPA vaccine chad ox one neve ChAdOx one.
Speaker 1: I know that code. That's the astrazenica COVID vaccine technology,
isn't it? The chimpanzee adenovirus spector.
Speaker 2: It is the exact same platform. It's a viral vector.
They take a harmless chimp cold virus, strip out its insides,
and put in the genetic code for the neperg protein.
Speaker 1: So they use a harmless virus to deliver a picture
of the bad virus to your immune system.
Speaker 2: Exactly. It trains your immune system to recognize the grappling
hook without ever exposing you to the actual dangerous NEPA virus.
It's a proven platform. We know it worked for other diseases,
and early data is very promising.
Speaker 1: And there's an m RNA one two.
Speaker 2: Oh of course, yeah, Medorna have a candidate mRNA twelve
fifteen in clinical trials. Concept of the covid shots. You
inject the instruction manual, your body builds the G protein,
your immune system learns to fight it.
Speaker 1: So why has it taken so long? NPA was found
in nineteen ninety eight, it's twenty twenty six. That's nearly
thirty years. Why are we just doing phase two trials now?
Speaker 2: That is the tragedy of economics. It's what we call
a market failure. NEPA outbreaks are sporadic, they're unpredictable. They
happen in poor rural areas of Bangladesh.
Speaker 1: In India, so not a big market.
Speaker 2: There isn't a billion dollar market for a NIPA vaccine
like there is for the flu, or for a global
pandemic that's already started. Big pharma didn't prioritize it because
it wasn't profitable.
Speaker 1: Until they realized it could become a global pandemic.
Speaker 2: Right. That's why groups like CEPI, the Coalition for Empidemic
Preparedness Innovations, stepped in. They were formed after Ebola to
address this very problem. They use donor money to fund
these trials because they know it's not about profit, it's
about insurance.
Speaker 1: They're buying us insurance against the apocalypse.
Speaker 2: That's a dramatic way to put it.
Speaker 1: But yes, so until we have that shot in every arm,
which could still be years away, we are left with
prevention segment seven the future, and weirdly, the best prevention
might be low tech.
Speaker 2: Surprisingly, so we could talk about mRNA and monoclonals all day,
but in Bangladesh, the most effective tool they found costs pennies.
It's a bamboo skirt.
Speaker 1: A bamboo skirt for the tree.
Speaker 2: For the tree you weave a barrier of bamboo strips,
or even use a polyepolene sheet and you wrap it
around the shaved part of the tree where.
Speaker 1: The pot hangs like a lambshade.
Speaker 2: Basically, it physically stops the bat from getting to the
flowing sap. If the bat can't lick the stream, the
virus doesn't get in the pot. It's that simple scarecrow.
It's a physical firewall.
Speaker 1: Yeah.
Speaker 2: And another simple solution boil the sap. If you boil
it to make molasses, which they call gurr, the heat
kills the virus instantly. It becomes completely safe to eat.
Speaker 1: But people like it raw. It's a delicacy you do.
Speaker 2: It's like telling a Frenchman he can't have unpasteurized cheese
or Japanese poosts and they can't have sushi. Yeah, it's
a cultural practic.
Speaker 1: So it's a classic clash between tradition and biosecurity.
Speaker 2: It is, and that is the hardest battle to win.
Public health isn't just about science. It's about anthropology. It's
about communication.
Speaker 1: On the high tech side, what are we doing to
stop the big one? To see it coming?
Speaker 2: Surveillance, genomic surveillance specifically We are sequencing the virus from
every outbreak. We are watching its genetic code like a hawk.
Speaker 1: What are you looking for?
Speaker 2: We know, for example, that the Bangladesh strain is six
nucleotides longer than the Malaysian one. That helps us track
the lineage. But mostly we are watching for mutations. NEPA
is an RNA virus. It mutates, It makes mistakes when
it copies itself, and.
Speaker 1: One of those mistakes could be a terrible.
Speaker 2: Upgrade, exactly the nightmare scenario. The next pandemic risk that
keeps the WHO up at night is that it picks
up a mutation that allows it to spread more easily
through the air more efficiently from person to person.
Speaker 1: Like COVID or measles.
Speaker 2: If NEPA evolved to spread as efficiently as measles but
kept its seventy percent mortality.
Speaker 1: Rate, that's civilization ending stuff. I don't even want to
think about that.
Speaker 2: It would be catastrophic. That is why the WHO is
so worried. That is why we are tracking it. We're
also developing better faster diagnostics. ELIZA tests r TPCR. So yeah,
when a case appears, we can know instantly if it's NEPA.
And not Japanese encephalaitis or malaria. Speed is everything.
Speaker 1: So what does this all mean. We've gone from the
pig farms of Malaysia to the date palms of Bangladesh.
We've looked at the molecular grappling hooks, the zombie cells,
and the bamboo skirts.
Speaker 2: I think the summary is that NEPA is a thrilling
thread because it exposes the fragility of our relationship with nature.
We have a virus that is perfectly happy in a bat.
It does no harm there. But when we force that
bat into our world, when we push into its world,
that virus becomes a weapon of mass destruction.
Speaker 1: And the trigger is almost always us.
Speaker 2: That is the final thought I want to leave you with.
We often talk about fighting the virus, we use war metaphors,
but the recurrence of NIFA isn't an act exodent of nature.
It's a symptom of human encroachment. Right as we cut
down forests, as we change the climate, we aren't just
losing trees. We are removing the buffer zone between us
and the animal kingdom. We are inviting the reservoir hosts
into our living rooms.
Speaker 1: We are tearing down the fence and then acting surprise
when the wolf comes in.
Speaker 2: Exactly, The question isn't just how do we treat Nepa?
The real question is how do we restore the ecological
balance so the bats stay in the forest where they belong.
Because if we don't solve the ecological spillover problem, we
will just be fighting the next virus and the next
one after that forever.
Speaker 1: That is a heavy but necessary perspective. It's not just biology,
it's ecology, and I want to turn that to you,
the listener. We talked about the bamboo skirts. We know
that a simple piece of bamboo can stop a ugly outbreak,
but it requires people to change a tradition that goes
back centuries, drinking that raw morning sap.
Speaker 2: It asks a community to give up a piece of
their joy, their culture for safety.
Speaker 1: Exactly. So where do you stand on that? How much
should we or the global health community interfere with local
traditions to prevent a global threat. Is it ethical to
demand that culture change to stop a virus.
Speaker 2: It's a question with no easy answer. There's no right answer.
Speaker 1: We'd love to hear your take, leave a comment on
whatever platform you're listening on, and let us know your thoughts.
Speaker 2: And if you see a bat, maybe appreciated from a distance.
Speaker 1: They're important, very safe distance. This has been thrilling Threads.
Thanks for diving in with us, Stay curious, d S.
Speaker 2: Goodbye,