Human polyomavirus 2: Difference between revisions
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{{DISPLAYTITLE:Human Polyomavirus 2}} | |||
== | == Overview == | ||
[[File:Human_polyomavirus_2_Wharton_plosone_2016.png|thumb|right|Electron micrograph of Human Polyomavirus 2]] | |||
'''Human Polyomavirus 2''', also known as '''JC virus''', is a type of [[polyomavirus]] that infects humans. It is a member of the [[Polyomaviridae]] family and is known for its ability to cause [[progressive multifocal leukoencephalopathy]] (PML), a rare and often fatal demyelinating disease of the central nervous system. | |||
Human | == Discovery and Classification == | ||
Human Polyomavirus 2 was first isolated in 1971 from the brain of a patient with PML. It is classified under the genus ''[[Betapolyomavirus]]'' within the family Polyomaviridae. The virus is named "JC" after the initials of the patient from whom it was first isolated. | |||
== | == Structure == | ||
The virus is a small, non-enveloped virus with a circular double-stranded [[DNA]] genome. The capsid is icosahedral in shape and composed of 72 capsomers. The genome encodes for several proteins, including the [[T-antigen]]s, which are crucial for viral replication and transformation. | |||
== Epidemiology == | |||
Human Polyomavirus 2 is widespread in the human population, with seroprevalence rates ranging from 50% to 80% in adults. Primary infection typically occurs in childhood and is usually asymptomatic. The virus remains latent in the kidneys and other tissues. | |||
== | == Pathogenesis == | ||
In immunocompromised individuals, such as those with [[HIV/AIDS]] or those undergoing immunosuppressive therapy, the virus can reactivate and cause PML. The reactivation leads to the destruction of [[oligodendrocytes]], resulting in demyelination and neurological symptoms. | |||
== Clinical Manifestations == | |||
The primary disease associated with Human Polyomavirus 2 is progressive multifocal leukoencephalopathy. Symptoms of PML include: | |||
* Weakness or paralysis | |||
* Vision problems | |||
* Cognitive impairment | |||
* Speech difficulties | |||
== | == Diagnosis == | ||
Diagnosis of Human Polyomavirus 2 infection is typically made through detection of viral DNA in the [[cerebrospinal fluid]] using [[polymerase chain reaction]] (PCR). Brain imaging, such as [[MRI]], can also support the diagnosis by revealing characteristic lesions. | |||
== Treatment == | |||
There is currently no specific antiviral treatment for Human Polyomavirus 2. Management of PML involves restoring immune function, such as through antiretroviral therapy in HIV-positive patients. Experimental treatments are being investigated, but none have been conclusively proven effective. | |||
== | == Prevention == | ||
Preventive measures focus on maintaining immune function to prevent reactivation of the virus. This includes careful management of immunosuppressive therapies and monitoring of at-risk patients. | |||
== Related Pages == | |||
* [[Polyomavirus]] | |||
* [[Progressive multifocal leukoencephalopathy]] | |||
* [[Immunocompromised host]] | |||
[[Category: | [[Category:Polyomaviruses]] | ||
[[Category: | [[Category:Viral diseases]] | ||
Revision as of 05:15, 16 February 2025
Overview
Human Polyomavirus 2, also known as JC virus, is a type of polyomavirus that infects humans. It is a member of the Polyomaviridae family and is known for its ability to cause progressive multifocal leukoencephalopathy (PML), a rare and often fatal demyelinating disease of the central nervous system.
Discovery and Classification
Human Polyomavirus 2 was first isolated in 1971 from the brain of a patient with PML. It is classified under the genus Betapolyomavirus within the family Polyomaviridae. The virus is named "JC" after the initials of the patient from whom it was first isolated.
Structure
The virus is a small, non-enveloped virus with a circular double-stranded DNA genome. The capsid is icosahedral in shape and composed of 72 capsomers. The genome encodes for several proteins, including the T-antigens, which are crucial for viral replication and transformation.
Epidemiology
Human Polyomavirus 2 is widespread in the human population, with seroprevalence rates ranging from 50% to 80% in adults. Primary infection typically occurs in childhood and is usually asymptomatic. The virus remains latent in the kidneys and other tissues.
Pathogenesis
In immunocompromised individuals, such as those with HIV/AIDS or those undergoing immunosuppressive therapy, the virus can reactivate and cause PML. The reactivation leads to the destruction of oligodendrocytes, resulting in demyelination and neurological symptoms.
Clinical Manifestations
The primary disease associated with Human Polyomavirus 2 is progressive multifocal leukoencephalopathy. Symptoms of PML include:
- Weakness or paralysis
- Vision problems
- Cognitive impairment
- Speech difficulties
Diagnosis
Diagnosis of Human Polyomavirus 2 infection is typically made through detection of viral DNA in the cerebrospinal fluid using polymerase chain reaction (PCR). Brain imaging, such as MRI, can also support the diagnosis by revealing characteristic lesions.
Treatment
There is currently no specific antiviral treatment for Human Polyomavirus 2. Management of PML involves restoring immune function, such as through antiretroviral therapy in HIV-positive patients. Experimental treatments are being investigated, but none have been conclusively proven effective.
Prevention
Preventive measures focus on maintaining immune function to prevent reactivation of the virus. This includes careful management of immunosuppressive therapies and monitoring of at-risk patients.
