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Detection of Polyfunctional T Cells in Children Vaccinated with Japanese Encephalitis Vaccine via the Flow Cytometry Technique
Published on: September 23, 2022
Immune surveillance and response to JC virus infection and PML
Sarah Beltrami1, Jennifer Gordon
1Department of Neuroscience and Center for Neurovirology, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA, 19140, USA.
Abstract:
The ubiquitous human polyomavirus JC virus (JCV) is the established etiological agent of the debilitating and often fatal demyelinating disease, progressive multifocal leukoencephalopathy (PML). Most healthy individuals have been infected with JCV and generate an immune response to the virus, yet remain persistently infected at subclinical levels. The onset of PML is rare in the general population, but has become an increasing concern in immunocompromised patients, where reactivation of JCV leads to uncontrolled replication in the CNS. Understanding viral persistence and the normal immune response to JCV provides insight into the circumstances which could lead to viral resurgence. Further, clues on the potential mechanisms of reactivation may be gleaned from the crosstalk among JCV and HIV-1, as well as the impact of monoclonal antibody therapies used for the treatment of autoimmune disorders, including multiple sclerosis, on the development of PML. In this review, we will discuss what is known about viral persistence and the immune response to JCV replication in immunocompromised individuals to elucidate the deficiencies in viral containment that permit viral reactivation and spread.
Insights
JC virus (JCV) causes progressive multifocal leukoencephalopathy (PML) in immunocompromised individuals. This review explores JCV persistence and immune responses to understand viral reactivation and spread in conditions like HIV-1 infection and after monoclonal antibody therapy.
Area of Science:
- Neurovirology
- Immunology
- Infectious Diseases
Background:
- Human polyomavirus JC virus (JCV) is the cause of progressive multifocal leukoencephalopathy (PML), a severe demyelinating disease.
- Most individuals are infected with JCV but remain asymptomatic due to immune control.
- PML incidence is rising in immunocompromised populations due to JCV reactivation.
Purpose of the Study:
- To review the mechanisms of JCV persistence and immune responses.
- To elucidate factors contributing to JCV reactivation in immunocompromised states.
- To explore the role of HIV-1 coinfection and monoclonal antibody therapies in PML pathogenesis.
Main Methods:
- Literature review of studies on JCV persistence, immune response, and PML.
- Analysis of viral interactions with host immunity in immunocompromised individuals.
- Examination of clinical data regarding PML development in specific patient groups.
Main Results:
- JCV establishes lifelong, subclinical infections in most hosts.
- Immunocompromise disrupts viral containment, leading to JCV replication and PML.
- HIV-1 and certain immunomodulatory therapies are associated with increased PML risk.
Conclusions:
- Understanding JCV persistence and immune evasion is crucial for preventing PML.
- Identifying deficiencies in viral containment can guide therapeutic strategies.
- Further research into JCV-host interactions is needed to combat PML.
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