Virions associated with progressive multifocal leukoencephalopathy

Schwerdt, P.R.; Schwerdt, Carlton E.; Silverman, Lloyd; Rubinstein, Lucien J.

doi:10.1016/0042-6822(66)90233-9

Cited by 21 publications

(5 citation statements)

References 7 publications

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“…These morphological observations were consistent with the results reported by other investigators [6,10]. Antibody against PML virus had not been detected previously in sera obtained from PML-patients [7,8]. This was understandable since PML usually occurred after a history of a long-standing disease such as Hodgkin's disease or chronic lymphatic leukemia, in which the immunological responses were depressed [3,9].…”

supporting

confidence: 82%

Serological and Morphological Studies on Progressive Multifocal Leucoencephalopathy Virus

Amako

Mori

1972

Japanese Journal of Microbiology

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supporting

confidence: 82%

Serological and Morphological Studies on Progressive Multifocal Leucoencephalopathy Virus

Amako

Mori

1972

Japanese Journal of Microbiology

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“…Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system that was first characterized as a unique clinical and neuropathological entity by Å ström et al in 1958 [1]. The infectious nature of the disease was suggested by electron microscopy studies in the mid-1960s, when polyomalike virions were found within the intranuclear inclusion bodies of oligodendrocytes [2][3][4][5]. In 1971, Padgett et al [6] succeeded in culturing virus from PML brain in human fetal brain spongioblasts and polyomavirus JC, also known as JC virus (JCV), was first isolated and characterized, the name ''JC'' being derived from the initials of the patient with PML.…”

mentioning

confidence: 99%

Pathogenesis of Progressive Multifocal Leukoencephalopathy—Revisited

White

Khalili

2011

The Journal of Infectious Diseases

138

134

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Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system that is rare even though the proven etiological agent of PML, the polyomavirus JC (JC virus), is ubiquitous within the human population. The common feature of PML cases appears to be underlying immunosuppression, and PML has gained clinical visibility because of its association with human immunodeficiency virus and AIDS and its occurrence as a side effect of certain immunomodulatory drugs. A hypothesis has gained general acceptance that JC virus causes a primary infection in childhood and enters a latent state, after which immunosuppression allows viral reactivation leading to PML. Nonetheless, many important aspects of PML pathogenesis remain unclear, including the molecular bases of latency and reactivation, the site(s) of latency, the relationship of archetype and prototype virus and the mode of virus transmission within the body and between individuals. In this review, we will revisit these areas and examine what the available evidence suggests.

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“…PML is a relatively new disease, originally described by Åstrom and Richardson in 1958 (41), who also first suggested the possibility of an infectious organism as the etiological agent (42), theory that was later confirmed with the discovery of small viral particles in the nuclei of infected cells (43,44,45,46). The next step in the characterization of PML as an infectious disease came with the cultivation and isolation of the virus in a fetal glial cell culture of spongioblasts (47).…”

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confidence: 99%

HIV disorders of the brain; pathology and pathogenesis

Valle

Piña‐Oviedo²

2006

Front Biosci

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Infection with HIV-1 has spread exponentially in recent years to reach alarming proportions. It is estimated than more than 33 million adults and 1.3 million children are infected worldwide. Approximately 16,000 new cases are diagnosed every day and almost 3 million people die every year from AIDS, making it the fourth leading cause of death in the world. Since the introduction of highly active anti-retroviral therapy (HAART) in the mid 1990s, the morbidity and mortality associated with HIV-1 infection has significantly decreased and AIDS has become a chronic disorder. However, neuropathological conditions associated with AIDS are still present in approximately 70 to 90% of patients and can be the result of HIV itself or of opportunistic infections. Here we briefly review the pathology and pathophysiology of AIDS-Encephalopathy, of some of the significant opportunistic infections affecting the brain in the context of AIDS, including Progressive Multifocal Leukoencephalopathy (PML) a demyelinating disease caused by the human neurotropic JC virus, Toxoplasmosis, Cryptococcosis and of primary CNS lymphoma, a brain malignancy frequently associated with HIV-1 infection, all of them considered AIDS defining conditions.

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Virions associated with progressive multifocal leukoencephalopathy

Cited by 21 publications

References 7 publications

Serological and Morphological Studies on Progressive Multifocal Leucoencephalopathy Virus

Serological and Morphological Studies on Progressive Multifocal Leucoencephalopathy Virus

Pathogenesis of Progressive Multifocal Leukoencephalopathy—Revisited

HIV disorders of the brain; pathology and pathogenesis

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