BK Virus, JC Virus & Polyomaviruses Explained

Most adults carry at least one polyomavirus and never know it. In a study of Dutch blood donors, essentially everyone had antibodies to BK virus, about two-thirds had them to JC virus, and more than 80% had them to Merkel cell polyomavirus. These viruses are small, ancient, and well adapted: they settle in after childhood and stay for life. For healthy people the arrangement is invisible. For people whose immune systems are suppressed, it can end in kidney transplant damage, a destructive brain disease, or skin cancer.

Educational content, not medical advice. Talk to your doctor before changing any medication, treatment, or routine. Information here reflects current research, but every person's situation differs.

This article explains how polyomaviruses work, how BK virus, JC virus, and Merkel cell polyomavirus differ, why each causes its own disease, and how clinicians currently manage them. It is a general explainer, not guidance for any individual patient.

What polyomaviruses are and how they work

Polyomaviruses belong to the family Polyomaviridae. Among viruses that infect vertebrates they are some of the simplest:

• Genome: a double-stranded circular DNA molecule of roughly 5,000 base pairs, small enough that it encodes only a handful of proteins.
• Capsid: a non-enveloped icosahedral protein shell, roughly 40 to 45 nanometers across. "Non-enveloped" means there is no fatty outer membrane, which generally makes such viruses tougher against disinfectants than enveloped viruses.
• Replication site: the host cell nucleus, where the virus borrows the cell's own DNA-copying machinery.
• Persistence: after the first infection, the virus is not cleared. It lingers at low levels in particular tissues.

The routes of transmission are not fully settled. Respiratory, oral, and fecal-oral routes are all suspected, and the early-childhood timing of infection suggests ordinary close contact within families.

A tiny genome with a big trick

Because the genome is so small, the virus cannot make its own DNA polymerase, the enzyme that copies DNA. A good analogy is a squatter who moves into a vacant factory but has no tools and no electricity. Instead of bringing equipment, the squatter forces the owner to run the machines. The virus does this with its early proteins, called large T antigen and small T antigen. Large T antigen binds and disables cell-cycle brakes, including the tumor suppressor protein Rb, which pushes the cell toward the DNA-copying phase of its cycle. Only then are late proteins made, including the capsid protein VP1, which builds new virus particles. When the cell is full of new virions, it bursts.

That last step explains a lot of disease. In BK nephropathy and in PML, the damage comes from the virus lysing (bursting) the cells it infects. In Merkel cell carcinoma, the opposite happens: the virus DNA ends up integrated into a tumor cell's genome in a damaged form that can no longer make complete virus particles but keeps the part that drives cell growth.

The family is bigger than three

More than a dozen human polyomaviruses have now been identified. A 2018 study in PLoS ONE counted thirteen recognized human polyomavirus species, plus one newer virus (LIPyV, identified in 2017) not yet assigned to a species, and tested blood donors for antibodies to all fourteen. A landmark review by DeCaprio and Garcea in Nature Reviews Microbiology in 2013 described the family expansion, noting that most of the newer viruses were found by sequencing rather than by growing them in culture. The table below lists the best-characterized members and what the 2013 review reported.

Virus	Discovered	Disease association reported in 2013 review	Suspected main site
BK polyomavirus (BKPyV)	1971	Polyomavirus-associated nephropathy, hemorrhagic cystitis	Urinary tract, kidney
JC polyomavirus (JCPyV)	1971	Progressive multifocal leukoencephalopathy (PML)	Kidney, brain in disease
KI polyomavirus (KIPyV)	2007	None identified	Respiratory tract
WU polyomavirus (WUPyV)	2007	None identified	Respiratory tract
Merkel cell polyomavirus (MCPyV)	2008	Merkel cell carcinoma	Skin
HPyV6 and HPyV7	2010	None identified	Skin
Trichodysplasia spinulosa polyomavirus (TSPyV)	2010	Trichodysplasia spinulosa (a rare skin condition in immunosuppressed patients)	Skin
HPyV9	2011	None identified	Skin, blood, urine
MW and STL polyomaviruses	2012	None identified	Gut

Source: DeCaprio and Garcea, 2013. Apart from MCPyV and TSPyV, the review noted no clear clinical syndrome for the newer viruses. This article focuses on the three with established, serious disease: BK, JC, and Merkel cell polyomavirus. To see how viruses in general enter and take over a cell, see our guide to how viruses work from infection to replication.

Silent infections: how common are they?

Serology (testing blood for antibodies) is how researchers estimate how many people have been infected. The numbers vary with the assay, the population, and the age group, so treat them as ranges rather than precise figures.

Virus	2018 Dutch blood-donor study (n = 1,044)	2013 review range
BK virus	about 99%	82 to 92%
JC virus	about 63%	40 to 55%
Merkel cell polyomavirus	about 82%	60 to 65%

Sources: Kamminga et al., PLoS ONE 2018 and DeCaprio and Garcea, 2013. The gap between the two columns shows how much the method matters. Newer, more sensitive antibody tests tend to find higher rates than older ones.

Two patterns stand out in the 2018 study. For BK virus, seropositivity was stable across ages but antibody levels fell in older groups. For JC virus, seropositivity showed no clear age trend, but antibody levels rose with age. These patterns are consistent with BK infection occurring early in life and JC virus continuing to stimulate the immune system over time, though the study alone does not prove why.

Where the viruses hide

After the first infection, an immune system that works properly holds the virus at very low levels. BK virus is associated with the kidney and the lining of the urinary tract, which is why traces can show up in the urine of healthy people. JC virus is also found in the kidney, and reviews describe it as able to reach the brain only in unusual circumstances. A rough analogy is a pilot light: a tiny flame that stays lit without heating the house, and that becomes a problem only if the controls fail.

BK virus: the transplant nephrologist's challenge

Why the kidney is the problem organ

BK virus rarely troubles healthy people. In a kidney transplant, though, two things line up. The graft is a kidney, the virus's favorite long-term home. And the recipient takes drugs to suppress the T cells that would normally control it.

A 2021 review of BK virus-associated nephropathy by Funahashi in the journal Pathogens summarizes the numbers for kidney transplant recipients: BK virus appears in the urine (viruria) in about 30 to 60%, in the blood (viremia) in 10 to 30%, and progresses to BK virus-associated nephropathy in up to 10%. Nephropathy ultimately caused graft loss in 15 to 38% of affected patients, and in about half of those cases the immediate cause was rejection after immunosuppression had been reduced. Source: Funahashi, Pathogens 2021.

The stages of BK nephropathy

The disease usually unfolds in a recognizable order:

1. Viruria. The virus is shed in urine, often detectable weeks to months after transplant.
2. Viremia. Virus appears in the blood, a sign that it has spread beyond the urinary tract and is replicating at higher levels.
3. Nephropathy. Biopsy shows virus-infected tubular cells, inflammation, and later scarring (fibrosis).
4. Graft dysfunction or loss. Persistent injury can destroy kidney function.

Biopsy findings are graded by pattern, and the risk of graft loss rises with the severity of that pattern. The same review cites graft-failure rates of roughly 16%, 31%, and 50% across the Banff 2018 classes 1 to 3.

Screening: finding the virus before it finds the kidney

Because the earliest stages cause no symptoms, transplant centers screen. The American Society of Transplantation's 2019 guideline for BK polyomavirus in solid organ transplantation recommends testing for virus in the blood by quantitative nucleic acid testing monthly until month 9 after kidney transplant, then every three months until two years, with the Funahashi review adding annual checks to year five. Pediatric recipients may need surveillance beyond two years. Source: Funahashi, Pathogens 2021, which summarizes the guideline.

Screening works like a smoke alarm. It does not put out the fire, but it catches smoke while the blaze is still small, when action is far more effective than after the structure is damaged.

The guideline expresses thresholds on a logarithmic scale. Blood levels above 3 log10 copies per milliliter (1,000 copies/mL) on two measurements within three weeks suggest probable disease, and levels above 4 log10 copies/mL (10,000 copies/mL) suggest presumptive disease. The Kidney Disease: Improving Global Outcomes (KDIGO) guidance, as summarized in the same review, suggests reducing immunosuppression when blood levels stay persistently above 4 log10 copies/mL. Different guidelines use different cutoffs, and individual centers adopt their own protocols.

The balancing act: treating by doing less

There is no antiviral drug with proven, BK-specific effectiveness. The main intervention is to reduce immunosuppression so that the patient's own T cells can regain control. This creates a genuine dilemma. Too much immunosuppression feeds the virus. Too little invites rejection of the transplanted kidney. Picture a seesaw where the clinician is trying to find the point of balance, and where each side of the seesaw damages the same organ.

The review describes several accepted approaches, which are judgment calls made by transplant teams:

Approach	What it involves	Evidence note
Reduce the calcineurin inhibitor	Lower the dose of drugs such as tacrolimus by roughly 25 to 50%, then reduce or stop the antimetabolite	Considered largely equivalent to the alternative
Reduce the antimetabolite first	Cut the dose of the second drug by about 50% before touching the calcineurin inhibitor	Reported clearance of virus from blood in about 95% in one series
Switch drugs	Move to a different immunosuppressant class	Used selectively
Add antivirals or immune globulin	Cidofovir, IVIG, fluoroquinolones	The review reports insufficient clinical evidence for routine use; cidofovir is toxic to the kidney

The cost of this strategy is real. In the review, T-cell-mediated rejection occurred in 4.3 to 14.6% of patients during immunosuppression reduction, and 14% developed new donor-specific antibodies within 14 months of diagnosis. Clearance of virus from the blood is high when the problem is caught at the viremia stage (80 to 100% in the review) and lower once nephropathy is established on biopsy. That is the argument for screening.

Hemorrhagic cystitis after bone marrow transplant

BK virus also causes trouble in people who receive hematopoietic stem cell transplants (HSCT, commonly called bone marrow transplants). Here the target is the bladder. The result is hemorrhagic cystitis: painful bladder inflammation with blood in the urine. A 2018 consensus guideline from the European Conference on Infections in Leukaemia (ECIL-6) reports that BK virus hemorrhagic cystitis occurs in 8 to 25% of children and 7 to 54% of adults undergoing allogeneic transplant (using donor cells), with an average of about 13%. Risk is higher after allogeneic than autologous transplant and appears highest after haploidentical transplants that use post-transplant cyclophosphamide, at about 24.5%. Source: ECIL-6 guideline, Journal of Antimicrobial Chemotherapy.

Diagnosis requires a triad: bladder symptoms, significant blood in the urine, and very high urine virus levels (above 7 log10 copies/mL), after other causes are excluded. Treatment is mainly supportive: hydration, transfusion of platelets as needed, and pain control. Intravenous cidofovir has only marginal support from uncontrolled data, and the guideline authors state that no randomized controlled trials are available to guide prevention or treatment. Unlike in kidney transplants, reducing immunosuppression has no clear risk-benefit balance here, because it may worsen graft-versus-host disease. The guideline also does not recommend screening people without symptoms, because no effective preemptive treatment exists.

JC virus: from a quiet kidney resident to a brain disease

What PML is

JC virus is named for the initials of the first patient from whom it was isolated in 1971, a person with a rare brain disease. That disease is progressive multifocal leukoencephalopathy, or PML. "Leukoencephalopathy" means a disorder of the brain's white matter, the insulated wiring that connects regions. "Multifocal" means it appears in several patches. "Progressive" means it gets worse.

In PML, JC virus infects oligodendrocytes, the cells that wrap nerve fibers in myelin insulation. When the virus bursts those cells, patches of white matter lose their insulation. Think of stripping the plastic coating from electrical cables: the wires may still be there, but signals short-circuit. That is different from multiple sclerosis, where the immune system itself attacks myelin. PML results from direct viral destruction, and it tends to occur precisely when the immune system is too weak to respond.

Reviews of the disease describe a pattern in which the virus strains found in PML differ from those circulating harmlessly in the urine. In particular, rearrangements in the virus's noncoding control region, and changes in the VP1 capsid protein, have been linked to the ability to replicate in the brain. The details are still being worked out, and they illustrate a general point about persistent viruses: a pathogen that has lived peacefully for decades can evolve inside a single host.

Who gets PML

PML is rare and almost always occurs in people with profound immune impairment. The table summarizes the main settings, with figures from sources cited in this article.

Setting	Why immunity is impaired	What the sources report
HIV infection before effective therapy	Loss of CD4 T cells	Reported in up to 8% of people with HIV in the pre-combination-therapy era (Cureus 2023 review); other sources cite 2 to 4%
Natalizumab treatment for multiple sclerosis	The drug blocks immune cells from entering the central nervous system	2.1 cases per 1,000 patients across 99,571 treated patients as of February 2012; lowest in antibody-negative patients, highest in antibody-positive patients with prior immunosuppressant use and 25 to 48 months of treatment (Bloomgren et al., NEJM 2012)
Blood cancers and some other immune-targeting drugs	Combined disease and treatment effects	Documented but uncommon
Solid organ and stem cell transplant recipients	Anti-rejection drugs	Documented but rare

The natalizumab figures come from Bloomgren and colleagues' 2012 analysis in the New England Journal of Medicine, as summarized in public abstracts. Natalizumab (brand name Tysabri) carries a boxed warning for PML in the United States. The label names three risk factors: the presence of anti-JC virus antibodies, longer treatment duration, and prior use of immunosuppressants. Later work added an antibody index, a measure of how strongly a patient's blood reacts to the virus, as a fourth factor. Because the drug works by keeping immune cells out of the nervous system, the same mechanism that calms multiple sclerosis can also remove the brain's patrols against a reactivating virus. Doctors can use the risk factors to weigh benefits against risks for each patient, and current estimates live in product information that is updated over time.

The highest estimate in the 2012 analysis was 11.1 per 1,000 patients, for antibody-positive people with prior immunosuppression who had been treated for 25 to 48 months. Because the figure depends on the dataset and the time window, anyone weighing the risk should consult the current product information rather than a single number.

Symptoms and diagnosis

PML develops over weeks to months. Symptoms depend on where lesions form and can include changes in thinking and personality, weakness on one side of the body, loss of vision in part of the visual field, clumsiness, and speech problems. MRI typically shows patchy white-matter lesions. Doctors confirm the diagnosis by testing spinal fluid for JC virus DNA in the right clinical setting, and in uncertain cases by brain biopsy. The American Academy of Neurology published consensus diagnostic criteria in 2013 (Berger et al., Neurology). A negative spinal fluid test does not always rule PML out, so a repeat test or biopsy may be needed when suspicion remains high.

Treatment and outlook

No drug has been established that directly kills JC virus. Treatment is therefore about restoring the immune system. In HIV, that means starting antiretroviral therapy. In drug-induced PML, it means stopping or removing the offending drug.

Outcomes have improved with effective HIV therapy, though they remain serious. A 2023 systematic review in Cureus by Aye and colleagues found that before combination antiretroviral therapy only about 9% of patients with HIV-associated PML survived beyond one year, with median survival around six months. After the introduction of effective therapy, one-year survival reached roughly 60% in the review, and one 25-year cohort reported 73% alive at one year and 22% alive beyond 10 years. A baseline CD4 count below 100 cells per microliter was linked to higher mortality. Source: Aye et al., Cureus 2023. The review's authors conclude that no specific treatment beyond antiretroviral therapy has been established and call for clinical trials. Many survivors are left with lasting neurological deficits.

The paradox of immune recovery

As immune function returns, the immune system may attack JC virus already in the brain, causing a flare of inflammation and temporary worsening called immune reconstitution inflammatory syndrome (IRIS). The Cureus review reports IRIS in 4 to 22% of HIV-related PML cases. It is one of the reasons clinicians monitor patients closely when immune function is being restored. For background on how the HIV mechanism sets the stage, see our HIV explainer. For the broader picture of how immune cells detect infection, see how the human immune system fights viruses.

Merkel cell polyomavirus and cancer

A virus found in a tumor

In 2008, Yuan Chang, Patrick Moore, and colleagues at the University of Pittsburgh, including first author Huichen Feng, reported finding a new polyomavirus in Merkel cell carcinoma (MCC), a rare and aggressive neuroendocrine skin cancer. They used a method called digital transcriptome subtraction, which compares the genetic material in tumor tissue against the human genome to find what does not belong. The paper in Science, titled "Clonal integration of a polyomavirus in human Merkel cell carcinoma," identified the virus now called Merkel cell polyomavirus (MCPyV). It was the first human polyomavirus to be strongly linked to cancer.

How the virus drives the tumor

Studies describe the virus DNA in roughly 80% of Merkel cell carcinomas, integrated into tumor cells' genomes in a clonal pattern, meaning every cell in the tumor descends from one infected cell. In virus-positive tumors, the integrated viral genome typically carries a truncated large T antigen. The truncation removes the part needed to replicate the virus, which stops the cell from bursting, but it keeps the part that binds Rb. The cell keeps dividing, trapped in a growth program meant only to be temporary. Small T antigen contributes further growth signals.

An important caveat is that not all Merkel cell carcinomas are virus-driven. Reviews note that in some regions, notably Australia, most cases are virus-negative and linked instead to heavy ultraviolet exposure. That points to two different routes to the same cancer. Seeing that most adults carry the virus and almost none develop the cancer also shows that infection alone is not enough: the tumor needs the virus, the right mutations, and typically a weakened immune system or sun damage.

How common and how serious

According to the American Cancer Society, about 3,000 people in the United States are diagnosed with Merkel cell carcinoma each year, most of them over 70. The society links rising diagnoses partly to more people living with weakened immune systems. Source: American Cancer Society key statistics.

Five-year relative survival for people diagnosed between 2015 and 2021, based on the National Cancer Institute's SEER data, was 79% for localized disease, 66% for regional disease, 31% for distant disease, and 69% across all stages. Source: American Cancer Society survival rates.

Immunotherapy changed the picture

Because virus-positive tumors display viral proteins, immune checkpoint inhibitors were a natural fit. These drugs release a brake on T cells, letting them attack tumors more effectively; our article on cancer immunotherapy explains the mechanism.

Drug	Target	FDA approval for Merkel cell carcinoma	Key result
Avelumab (Bavencio)	PD-L1	March 2017, accelerated approval; described by the FDA as the first approved treatment for the disease	Overall response rate of 33% in patients whose disease had progressed after chemotherapy, with 86% of responses lasting six months or longer
Pembrolizumab (Keytruda)	PD-1	December 19, 2018, accelerated approval	Overall response rate of 56% and complete response rate of 24% in 50 previously untreated patients (KEYNOTE-017)
Retifanlimab	PD-1	March 22, 2023, accelerated approval	Approved on the basis of response rate and duration in the POD1UM-201 trial

Sources: FDA on pembrolizumab and Merkel Cell Carcinoma advocacy group notice on retifanlimab, supplemented by the FDA's 2017 announcement for avelumab. Avelumab came first, in 2017, and pembrolizumab followed in December 2018. "Accelerated approval" means the FDA approved the drug based on tumor response, with continued approval dependent on confirmatory trials.

The constant presence that makes these viruses dangerous in transplant patients also helps in cancer care. Virus-positive Merkel cell tumors carry viral proteins that the immune system can learn to recognize once checkpoint inhibitors release the brake.

Comparing the three at a glance

Feature	BK virus	JC virus	Merkel cell polyomavirus
First described	1971	1971	2008
Adult seroprevalence (ranges across studies)	About 82 to 99%	About 40 to 63%	About 60 to 82%
Typical tissue association	Kidney, urinary tract	Kidney; brain in disease	Skin
Main disease	BK nephropathy, hemorrhagic cystitis	PML	Merkel cell carcinoma
Who is at risk	Kidney and stem cell transplant recipients	Advanced HIV, natalizumab, other severe immune impairment	Older adults, immunosuppressed people
How the damage happens	Virus bursts infected cells	Virus bursts oligodendrocytes	Integrated viral DNA drives growth
Main management approach	Screen, then reduce immunosuppression	Restore immune function	Surgery, radiation, checkpoint inhibitors

Common confusions

"These are the same as herpes viruses"

They are not. Polyomaviruses have small circular DNA genomes and no envelope. Herpesviruses are much larger, enveloped, and belong to a different family. Both groups establish lifelong latency, which is why they are often grouped in conversation. Our explainer on herpes viruses shows how the two strategies compare, and the cytomegalovirus article covers another virus that reactivates in transplant recipients.

"PML is contagious"

PML is not spread from patient to patient in the way that a cold is. The JC virus involved is generally the patient's own, long-resident virus changing and reactivating under immune suppression. The infection itself, though, is common and acquired early in life.

"A positive antibody test means disease is coming"

Antibodies show past exposure. The majority of adults test positive for BK virus, and most of them will never have a symptom. In natalizumab care, the antibody result is used to estimate risk, not to diagnose disease. A positive result shifts a probability, and for any one person the chance of PML is still low in absolute terms.

"The virus is the whole story"

In every polyomavirus disease, the virus is necessary but not sufficient. The immune system is the second half of the equation. BK nephropathy is largely a disease of the transplant setting. PML requires profound immune impairment. Merkel cell carcinoma requires viral mutations plus other factors. Understanding the immune context is as important as understanding the virus.

What we still do not know

Several questions remain open. How the viruses spread between people is not fully worked out. Why some patients with similar immune suppression develop BK nephropathy and others never do is an active research question. The role of the newer polyomaviruses in human disease, apart from MCPyV and TSPyV, is largely unknown, and the DeCaprio and Garcea review noted that infectious virus had not yet been isolated for any of the newer ones. And no BK-specific or JC-specific antiviral has been proven in controlled trials, which is why the main tools remain immune restoration, careful monitoring, and supportive care. To our knowledge, no vaccine against a human polyomavirus is in routine clinical use. Researchers have discussed vaccines for transplant recipients and for people at high risk of Merkel cell carcinoma, but this is an area where readers should check current sources.

Frequently asked questions

Q: Are BK virus and JC virus the same as the herpes viruses that cause cold sores? A: No. BK and JC viruses belong to the family Polyomaviridae, with small circular DNA genomes and no outer envelope. Herpesviruses are larger, enveloped, and belong to a different family. Both families establish lifelong latency, but their structure, replication, and disease patterns differ.

Q: Can a healthy person pass JC virus to someone with a weakened immune system? A: PML is not considered contagious in the usual sense. The JC virus that causes it is generally the patient's own virus, acquired in childhood and later reactivated or altered under severe immune suppression. The clinical priority is managing the patient's own immune status.

Q: Why does natalizumab increase the risk of PML? A: Natalizumab keeps immune cells from entering the central nervous system, which is how it helps in multiple sclerosis. The same effect reduces immune surveillance in the brain against JC virus. The FDA boxed warning names anti-JC virus antibodies, longer treatment duration, and prior immunosuppressant use as risk factors.

Q: How is BK virus monitored after a kidney transplant? A: According to the American Society of Transplantation guideline summarized in a 2021 review, blood is tested for BK virus monthly until month 9, then every three months until two years, with longer follow-up in some cases. Rising levels prompt doctors to consider reducing immunosuppression. Protocols vary by center.

Q: How is PML diagnosed? A: Diagnosis combines clinical symptoms, brain MRI showing white-matter lesions, and spinal fluid testing for JC virus DNA. Brain biopsy is reserved for uncertain cases. Consensus criteria were published by the American Academy of Neurology in 2013.

Q: Does everyone infected with Merkel cell polyomavirus develop cancer? A: No. In the 2018 blood-donor study, about 82% had antibodies to the virus, yet Merkel cell carcinoma affects about 3,000 people per year in the United States. The cancer needs integration of the virus in a truncated form plus other factors, and some tumors are virus-negative.

Q: Is there a vaccine or a cure? A: To our knowledge, no vaccine against a human polyomavirus is in routine use, and no antiviral specifically for BK or JC virus has proven effective in controlled trials. Management relies on screening, immune restoration, and supportive care. For Merkel cell carcinoma, checkpoint-inhibitor immunotherapy is approved for advanced disease.

The takeaway

Polyomaviruses show how much of health is a negotiation. BK, JC, and Merkel cell polyomaviruses infect most people, cost them nothing for decades, and remain harmless as long as immune surveillance holds. Each disease in this article starts the same way: the surveillance weakens, and a virus that was always present begins to act on its own program. The differences lie in where the virus lives and what damage follows, whether that is the transplanted kidney, the brain's white matter, or a skin tumor.

That framing also explains the treatments. Screening finds BK virus early enough to act. Restoring immunity is the best-supported answer to PML. And for Merkel cell carcinoma, releasing the immune system's brakes turned a poorly treatable cancer into one with real response rates. In each case, the treatment is not a drug aimed at the virus but a recalibration of the immune response that was keeping it quiet.

Sources

1. Kamminga S, et al. "Seroprevalence of fourteen human polyomaviruses determined in blood donors." PLoS ONE. 2018;13(10):e0206273. PMC6198985
2. DeCaprio JA, Garcea RL. "A cornucopia of human polyomaviruses." Nature Reviews Microbiology. 2013;11(4):264-276. PMC3928796
3. Funahashi Y. "BK Virus-Associated Nephropathy after Renal Transplantation." Pathogens. 2021;10(2):150. PMC7913099
4. Hirsch HH, Randhawa PS; AST Infectious Diseases Community of Practice. "BK polyomavirus in solid organ transplantation: guidelines from the American Society of Transplantation Infectious Diseases Community of Practice." Clinical Transplantation. 2019. (Summarized via source 3.)
5. ECIL-6 guidelines for the prevention, diagnosis and treatment of BK polyomavirus-associated hemorrhagic cystitis in hematopoietic stem cell transplant recipients. Journal of Antimicrobial Chemotherapy. 2018;73(1):12-21. Oxford Academic
6. Aye SL, et al. "The Prognosis of Progressive Multifocal Leukoencephalopathy in HIV/AIDS Patients Undergoing Highly Active Antiretroviral Treatment: A Systematic Review." Cureus. 2023;15(9):e45155. PMC10575567
7. Bloomgren G, et al. "Risk of natalizumab-associated progressive multifocal leukoencephalopathy." New England Journal of Medicine. 2012;366(20):1870-1880.
8. Berger JR, et al. "PML diagnostic criteria: consensus statement from the AAN Neuroinfectious Disease Section." Neurology. 2013;80(15):1430-1438.
9. Feng H, et al. "Clonal integration of a polyomavirus in human Merkel cell carcinoma." Science. 2008;319(5866):1096-1100.
10. American Cancer Society. Key statistics for Merkel cell carcinoma and survival rates.
11. U.S. Food and Drug Administration. FDA approves pembrolizumab for Merkel cell carcinoma, December 19, 2018.

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