Leprosy, Liver Disease, and God’s Goodness

When I was a student at West Virginia State College (now West Virginia State University), I spent afternoons in the weight room and got to know some of our school’s football players, including star running back Hollis Payton. He was cousins with NFL great Walter Payton, arguably one of the best running backs to ever play in the NFL. Payton had an all-star career over 13 seasons that included 9 Pro Bowl appearances and the 1977 MVP award. Hollis would often hold court in the weight room and regale us with behind-the-scenes stories about his cousin.

Sadly, Walter Payton died in 1999 at the age of 46 while waiting for a liver transplant. He had a rare liver disease called primary sclerosing cholangitis. This condition can lead to cirrhosis of the liver, liver cancer, and cancer of the bile duct, which is what ultimately took Payton’s life. The most important facet of Payton’s legacy extends far beyond football. His premature death focused attention on the need for organ donations. Now, strange as it sounds, researchers have discovered that a leprosy-causing bacterium may point to a treatment that may make liver transplants unnecessary altogether.

The Need for Liver Transplants
As of 2021, over 105,000 people were waiting for an organ donation. Seventeen people die each day waiting for organ transplants. Even though 40,000 transplants are performed each year, a new person is added to the transplant waiting list every 10 minutes.

The need for liver transplants is pressing. Just over 10% (11,891) of the current organ transplant waiting list consists of people in need of a liver. Fortunately, 9,236 liver transplants were performed in 2021. Still, a significant gap exists between the need and the availability of suitable livers.

Patients can receive one of two types of liver transplants. One uses livers from deceased donors. The other makes use of a portion of a liver from living donors. This type of donation is possible because of the remarkable ability of the liver to regenerate. Once the patient’s diseased liver is removed, the surgeons replace it with about 50 to 70% of the right lobe of the donor’s liver. Astonishingly, within 4 to 6 weeks the donor’s liver will completely regenerate.

Liver Regeneration
The liver’s capacity to regenerate sets it apart from the other solid organs. Its regenerative abilities allow this organ to function as the body’s detoxification site. The liver experiences chronic exposure to toxins, which damages the liver. But because this organ can regenerate itself, it can overcome the aftereffects of these chemical assaults.

Despite its ability to regenerate, repetitive injury to the liver can still lead to long-term damage. Exposure to toxins, viral infections, and disease can all take their toll. When this level of damage occurs, the liver’s regenerative capacity can’t keep pace and the only recourse is a liver transplant.

Life scientists work to understand the mechanisms involved in liver regeneration. With this understanding, they hope to one day develop techniques to stimulate diseased and damaged livers to regenerate at an accelerated rate, obviating the need for liver transplants. They also hope to apply this insight to stimulate other solid organs to regenerate, thereby alleviating the growing need for organ donors.

Unexpected Insight from Leprosy
The potential to make progress toward these two goals comes from a surprising place—the mechanism that the leprosy-causing bacterium, Mycobacterium leprae, uses to spread in humans once they have been infected by this microbe.  

Leprosy is an infectious disease that isn’t highly contagious and spreads only through extensive contact. Leprosy causes damage to the nerves, skin, eyes, and respiratory tract. Due to the nerve damage, patients lose the ability to feel pain. The loss of pain sensation can result in a loss of extremities because of severe injury or infection (by another microbe) that goes unnoticed and untreated.

Researchers interested in studying M. leprae have long used armadillos (one of the few animals that can harbor M. leprae) as a type of incubator to grow the bacteria so that they can be harvested and studied. Because M. leprae infects liver cells in armadillos, researchers often harvest the bacteria from the armadillos’ livers.

A research team from the University of Edinburgh discovered that M. leprae infections of nine‑banded armadillos cause their livers to become enlarged without any evidence of damage or tumors.1 They wondered if M. leprae might be causing the armadillos’ livers to undergo accelerated regeneration by altering the liver cells in the same way they alter cells called Schwann cells in humans.

The M. leprae Infection Mechanism
M. leprae attacks Schwann cells when this microbe infects humans. Schwann cells are a type of glial cell. In fact, they are the primary glial cell type in the peripheral nervous system (the part of the nervous system that lies outside the brain and spinal cord). As part of the nervous system, glial cells support neurons. They also serve a structural role, a regulative role (for the firing of neurons), and an immune role.

Schwann cells produce the myelin sheath that surrounds the neurons of the peripheral nervous system. They also help maintain the neurons and play a role in the regeneration of peripheral nerves.

The loss of leprosy patients’ ability to feel pain makes sense because M. leprae targets Schwann cells. Harboring M. leprae cells compromises the Schwann cells’ capacity to support the neurons of the peripheral nervous system. 

M. leprae is described as an obligate intracellular parasite. It can survive only inside the host cell it infects. M. leprae has a relatively small genome because it relies on host cell biochemistry to survive. This dependency raises the question of how M. leprae cells disseminate throughout the host.

In 2013, the University of Edinburgh team pursued this question and discovered that when M. leprae infects Schwann cells, the bacteria reprogram the Schwann cells’ genomes so that they revert to a stem-cell/progenitor cell stage.2 M. leprae appears to inactivate genes that lead to cellular differentiation when they are expressed and to activate genes that lead to a dedifferentiated cell state, similar to the state of early-stage embryo cells. 

The Schwann cells in the stem cell/progenitor cell state migrate into other tissues. When these cells find their way into muscles, the dedifferentiated Schwann cells transform into muscle cells, becoming part of the muscle tissue. Because these cells harbor M. leprae cells, the infection spreads.

The Effect of M. leprae on Armadillo Livers
To understand M. leprae behavior in armadillo livers, the investigators infected nine-banded armadillos with M. leprae. After waiting between 10 to 30 months, the researchers removed the livers from the armadillos. They noted that the livers had become enlarged yet appeared to be healthy. The livers displayed normal microanatomical features and showed no evidence of fibrosis, tumors, or other anomalies. 

The team also noted that the liver cells displayed increased cell division. The gene expression profile of these cells displayed similar characteristics to liver progenitor cells.

Potential Biomedical Applications
The researchers hope that by elucidating the molecular mechanisms involved in reprogramming liver cells, they might be able to apply this insight to treat liver disease by coaxing the cells of diseased livers to regenerate at a faster rate. If they can achieve this objective, it may make liver transplant procedures largely unnecessary. They also hope that this newfound understanding will provide the means to stimulate regeneration in solid organs that lack the capacity to regenerate. Perhaps biomedical researchers could one day leverage this understanding to grow organs in the lab from stem cells.

It’s fascinating—and a bit ironic—to think that the very mechanisms that M. leprae uses to spread within the human host are the same mechanisms that biomedical researchers may one day leverage to regenerate livers and, possibly, other organs. As a Christian and a biochemist, I attribute this irony to God’s providence.

God’s Providence
In Christian theology, providence refers to God’s continual role in: (1) preserving his creation, (2) ensuring that everything happens, and (3) guiding the universe. The concept of divine providence also posits that when God created the world, he ordained the laws and natural processes that preserve and sustain his creation. He also built into nature everything humans (and other living organisms) would need. Accordingly, every good thing that people possess has been provided by God, either directly or indirectly, through the world he made.

Because human beings have been made in God’s image, we’re able to develop and use science to characterize the world that God has made, and we possess the wherewithal to use science to develop technologies that benefit humanity (and all life on Earth). As image bearers, we’ve been given the command to subdue Earth and to exercise dominion over the planet and all its life. We’re also commanded to be stewards and caretakers of God’s creation. These commands provide the motivation to pursue science and develop technologies. So, too, does our recognition of God’s providence. 

As Christians we are motivated to pursue science so we can learn about the world and develop technologies that make it possible for humans (and other life-forms) to flourish. Part of these efforts includes working to mitigate human pain and suffering.  

In this vein, scientific and biomedical research has helped us to understand the cause of leprosy and has led to development of treatments for the disease. (Leprosy is treated with a cocktail of antibiotics called a multidrug treatment regime.) Today, leprosy is rare. There are only about 200,000 people worldwide who live with leprosy, and these cases are mostly in resource-poor countries.

If poverty and corruption didn’t complicate things, many experts think that we could eradicate leprosy from the world in short order. 

Of course, this leads to the question: Why would God create M. leprae in the first place? 

I’ve addressed this question in detail elsewhere (see “Did God Create Flesh-Eating Bacteria? A Creation Model for the Origin of Human Disease”), and RTB has developed a creation model for the origin of human infectious diseases. We take the view that God created humans to be free from the threat of human pathogens. Over time, however, some of the microbes that were part of humanity’s natural microbial flora underwent mutations that rendered them pathogenic. We also suggest that microbes that naturally infect other animals could be another source of human pathogens, as these microbes experienced mutations that allowed them to jump from an animal to a human host. This explanation could account for the origin of leprosy in humans, given that there are natural animal hosts (such as armadillos) for leprosy. 

It’s interesting to note that a team of international collaborators discovered that leprosy appears to have originated in East Africa close to the time that modern humans originated.3 In fact, the genetic variability of M. leprae can serve as a proxy for human genetic variability, because its origin and spread closely tracks humanity’s origin and migration around the world.

Without question, leprosy is devastating for those who contract the disease. It has caused significant human pain and suffering. But God’s providential care for humanity is still on full display. Even a disease-causing microbe like M. leprae reflects God’s provision for us in that it holds the key for biomedical researchers to one day regenerate livers and, possibly, other organs.

Indeed, God does work in all things to bring about good.

Maybe one day soon, when we remember people like Walter Payton, it will be for their accomplishments in life and not their tragic deaths while they waited for a liver.



1.  Samuel Hess et al., “In vivo Partial Reprogramming by Bacteria Promotes Adult Liver Organ Growth without Fibrosis and Tumorigenesis,” Cell Reports Medicine 3, no. 11 (November 15, 2022): 100820, doi:10.1016/j.xcrm.2022.100820.

2. Toshihiro Masaki et al., “Reprogramming Adult Schwann Cells to Stem Cell-Like Cells by Leprosy Bacilli Promotes Dissemination of Infection,” Cell 152, no. 1–2 (January 17, 2013): 51–67, doi:10.1016/j.cell.2012.12.014.

3. Marc Monot et al., “On the Origin of Leprosy,” Science 308, no. 5724 (May 13, 2005): 1040–1042, doi:10.1126/science/1109759