Related Experiment Video

Updated: May 11, 2026

Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry
11:54

Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry

Published on: July 13, 2019

New insights on human polyomavirus JC and pathogenesis of progressive multifocal leukoencephalopathy

Anna Bellizzi1, Elena Anzivino, Donatella Maria Rodio

  • 1Department of Public Health and Infectious Diseases, Sapienza University of Rome, P.le Aldo Moro, 5-00185 Rome, Italy.

Clinical & Developmental Immunology
|May 22, 2013
PubMed

Insights

John Cunningham virus (JCV) causes progressive multifocal leukoencephalopathy (PML). Research now explores JCV infection, its link to immune status, and PML pathogenesis, especially with new therapies.

Area of Science:

  • Virology
  • Immunology
  • Neurology

Background:

  • John Cunningham virus (JCV), a polyomavirus, is the causative agent of progressive multifocal leukoencephalopathy (PML).
  • PML was historically rare but became more prevalent with the human immunodeficiency virus (HIV) pandemic, with HIV-induced immunodeficiency being the primary risk factor.
  • Recent observations link PML to treatments involving monoclonal antibodies for autoimmune diseases, highlighting the role of host immunity.

Purpose of the Study:

  • To comprehensively review current understanding of JCV infection.
  • To examine new findings on PML pathogenesis.
  • To focus on molecular interactions in JCV infection and immune surveillance's role in viral reactivation.

Main Methods:

  • Literature review of JCV infection and PML pathogenesis.
  • Analysis of epidemiological and clinic-pathologic data.
  • Focus on cellular and viral molecular pathways and host immune modulation.

Main Results:

  • JCV is the etiological agent of PML.
  • HIV-induced immunodeficiency is the most common predisposing factor for PML.
  • Monoclonal antibody therapies for autoimmune diseases are associated with increased PML cases.

Conclusions:

  • Host immunity plays a critical role in PML pathogenesis.
  • Understanding the interplay between cellular pathways, viral factors, and immune surveillance is key to managing JCV infection and PML.
  • Further research is needed to elucidate the mechanisms of viral reactivation and disease development.

More Related Videos

Merkel Cell Polyomavirus Infection and Detection13:45

Merkel Cell Polyomavirus Infection and Detection

Published on: February 7, 2019

Isolation of Brain-infiltrating Leukocytes06:44

Isolation of Brain-infiltrating Leukocytes

Published on: June 13, 2011

Related Concept Videos

Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Cytomegalovirus Disease01:27

Cytomegalovirus Disease

Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...