Imagine feeling completely well. You go to work. You play with your children. You make plans for next year. And all the while, quietly and without a single symptom, something is going badly wrong inside you.
That is what chronic hepatitis does. Picture a man in his late forties, a farmer in a village a few hours from the city. He has never felt ill a day in his life. He does not know he has carried the hepatitis B virus since infancy, passed to him at birth. By the time he notices a dull ache
under his right ribs and finally sees a doctor, the scan shows liver cancer too advanced to operate on. (He is a composite, drawn from cases familiar to doctors across the region, not a specific patient.) That sequence is not rare. It is an ordinary Tuesday in any hospital in this part of the world.
The World Health Organization’s latest figures, published this July, are sobering. About 240 million people worldwide live with chronic hepatitis B, and 47 million with hepatitis C. Together the two viruses killed roughly 1.3 million people in 2024 — more than malaria — almost all through cirrhosis and liver cancer.
Asia carries most of that weight. WHO’s Western Pacific Region — which includes Malaysia, the Philippines, Vietnam, Singapore and China — accounts for 102 million hepatitis B infections, the largest of any region on earth. Its South-East Asia Region, which covers India,
Indonesia, Bangladesh, Myanmar and Thailand, accounts for a further 43 million, along with more than 200,000 hepatitis-related deaths every year. Between them, the two regions hold six in every ten hepatitis B infections on the planet.
Liver cancer is now the third biggest cancer killer in the world, behind lung and bowel cancer, responsible for roughly one in every thirteen cancer deaths. Nearly half of those deaths — 48 per cent — occur in Eastern Asia alone. And Southeast Asia has the second-highest liver cancer death rate of any region on earth, behind only North Africa.
Malaysia has done better than most. Universal infant hepatitis B vaccination began here in 1989, and it worked. A screening study of 190,077 Malaysian schoolchildren tracked the effect directly: among those born in 1985, before the programme, 2.5 per cent carried the
virus. Among those born in 1996, it was 0.4 per cent — a six-fold fall. That is one of the clearest public health wins in our history.
But two problems remain. Malaysians born before 1989 never had that protection, and many have never been tested. And a second driver has arrived while we were focused on the first. A national survey conducted in 2023 found fatty liver disease linked to metabolic problems —
obesity, diabetes, high cholesterol — in 28 per cent of Malaysian adults. More than one in four. That condition can also end in cirrhosis and liver cancer, and it is climbing.
And liver cancer is climbing our own rankings. In the Malaysia National Cancer Registry’s 2012–2016 report it was the country’s eighth most common cancer. In the 2017–2021 report it is fifth overall, and fourth among Malaysian men. Five-year survival sits at around 13 percent — among the worst of any cancer we track — overwhelmingly because it is found late.
The liver is unusually stoic. Its inner tissue carries no pain-sensing nerves at all; only the thin capsule wrapped around the outside does. That is why pain arrives so late — something has to grow large enough to stretch that outer skin before you feel anything. The liver also has
enormous spare capacity, and can lose a great deal of working tissue while you continue to feel entirely normal.
So the damage accumulates in silence. When someone carries hepatitis B or C for years, the immune system attacks the infected liver over and over. Each round kills liver cells, and the body patches the gaps with scar tissue. Decades of patching turn a soft, springy organ into
something stiff and knotted — cirrhosis. Cells living in that stressed, scarred neighbourhood are far more likely to turn cancerous.
Two different failures are at work here, and it is worth keeping them apart. Finding the infection is not the hard part. A hepatitis B or C test is cheap, quick and accurate, and the reason so many infections go undetected is simply that the test is never done. That is a problem of access and awareness, not of technology.
Finding the cancer early is the hard part. Patients known to be at high risk are already offered scans every six months — and even in that closely watched group, ultrasound detects only around 45 per cent of early-stage liver tumours. Adding a blood marker lifts it to about
63 per cent. Put plainly: in the people we are watching most carefully, something close to half of early cancers are still missed. That is the gap worth attacking. Part of the reason lies in what our tests can and cannot see.
A pathologist reading a liver biopsy under the microscope sees the architecture beautifully — the scarring, the nodules, where the inflammation is worst. What the microscope cannot show is molecular identity: which individual cell has switched on which genes, and which has quietly begun behaving abnormally. For that we use molecular tests, and those work the other way round. The tissue is dissolved and the signal averaged across millions of cells at once. You gain the molecular detail and lose the map.
For decades the choice has been: see where things are or see what they are doing. Single-cell and spatial technology exists to stop making that choice.
Picture a basket of fruit, some of it starting to spoil. Looking at the basket tells you where every piece sits, but not which ones are going off.
Blend it into a smoothie and taste it, and you learn the mix is mostly sweet — but the moment you blend, you can no longer tell which piece came from where. The new methods let you check each piece individually and record exactly where in the basket it was sitting.
It helps to stop thinking of the liver as a lump of tissue and start thinking of it as a city. A healthy liver is built from around a million tiny six-sided districts. Blood arrives through vessels at the outskirts carrying oxygen and nutrients, and drains out through a vein at the centre. That flow creates a gradient — oxygen-rich at the edge, thinner towards the middle — and cells take on different jobs depending on where along it they sit. Cells at the outskirts handle one set of tasks; cells near the centre handle another. It is a division of labour based entirely on address.
Chronic disease wrecks that layout. Scar tissue cuts across the streets and blocks the vessels. The gradients collapse. Cells start doing jobs they were never meant to do, in the wrong place. Regions form where stressed cells sit hidden, and where immune cells — the body’s
own police — cannot easily reach them. That is the neighbourhood in which cancer begins.
Reference maps of human tissue at this resolution already exist. The problem is whose tissue they were built from.
A diversity audit published in July this year examined the major single-cell reference collections. In the Human Cell Atlas, seven out of ten samples had no ancestry recorded at all; among those that did, European donors outnumbered their share of the world population
roughly sixfold. The Human Tumor Atlas Network, a United States collection, was more skewed still — 78 per cent European overall, against the 23 per cent that America’s own cancer statistics would predict, and 88.9 per cent European among its liver tumour samples. Asian donors were the most underrepresented group in every tissue the auditors looked at.
This matters more than it sounds. These atlases are increasingly used to train the artificial intelligence tools that will interpret tomorrow’s diagnostic tests. A reference built mostly from one population, applied to another, does not simply become slightly less accurate — it can be wrong in ways nobody notices until patients are harmed. Our dominant viruses, our genetic backgrounds and our diets are not identical to those of the donors in those datasets.
This is the gap HEPATO-SEE was formed to close. The lead partners are five universities across the region — Sunway University in Malaysia, Mahidol University and the University of Phayao in Thailand, i3L in Indonesia and Mapúa University in the Philippines — working
alongside further universities in the region and beyond, together with health ministries and government agencies, non-governmental organisations, hospitals and community clinics in each country. That breadth is not decoration. A map of this kind is only as good as the range of people it draws on, and reaching patients outside major urban centres depends entirely on the clinics that already serve them.
What the consortium is building is a detailed record of what happens inside the liver as hepatitis and metabolic disease turn into scarring and then into cancer — one cell at a time, with each cell’s location preserved. It is a deliberately regional effort, because the populations it needs to represent are ours.
The realistic goal is not to spot a handful of rogue cells hiding somewhere in the organ; a needle biopsy samples too little tissue for that, however good the technology. It is to identify the tissue-wide signatures of a liver heading for trouble — the collapse of that district
structure, the exhaustion of local immune cells, the stress states that appear years before a tumour does. Those changes are spread throughout the tissue, which is precisely why a small sample can catch them.
And if you know which signatures matter, you can start hunting for them in something far simpler. The end point is not a more expensive scanner. It is ideally a cheap blood test that works in a district clinic, not a machine that exists in three hospitals in the capital.
Honesty matters here. Doctors cannot currently explain why two people with the same infection end up in completely different places — one developing cirrhosis and cancer within fifteen years, the other remaining stable for forty. Something determines which path a patient takes. We do not yet know what. Finding out is much of the point.
Liver disease is a quiet emergency in this region. Our tests can show us where damage sits or what cells are doing, but not both at once — and the reference data behind emerging diagnostic tools barely includes people like us. Mapping the liver cell by cell, in Southeast Asian patients, could reveal the earliest warning signs of cancer and turn them into tests cheap enough to use everywhere.
None of this changes what you can do today, which is far simpler and already available. Hepatitis B has a safe, effective vaccine. Both hepatitis B and C are found with a straightforward blood test, and both can be treated — hepatitis C is now cured in more than 95 per cent of patients with a course of tablets.
And yet. Of the 240 million people worldwide living with hepatitis B, only 65 million — about one in four — know they have it. Just 10 million are on treatment. The gap between what medicine can already do and what is actually reaching people is enormous, and almost all of
it comes down to diagnosis.
If you were born before 1989, if a parent or sibling has hepatitis B, or if you have simply never been tested, ask your doctor. It is one blood test. And if you carry extra weight around the middle, or have diabetes or high cholesterol, ask about your liver too — that conversation
is not happening often enough.
The most dangerous thing about this disease is how well it hides. The simplest way to beat it is to go looking.
