Ultrastructural studies in the lytic phase of progressive multifocal leukoencephalopathy in AIDS patients.
ABSTRACT Brain fragments from eight cases (four autopsies and four biopsies) of patients with acquired immune deficiency syndrome (AIDS) with JC virus (JCV) lytic infections were examined ultrastructurally. Particular efforts were made to look for virions and their subcellular distribution in cells not usually involved by papovavirus infection. The cellular and subcellular distribution of virions was investigated with emphasis on cell types not normally associated with papovavirus infection. The pattern of JCV infection was as follows: 1) oligodendrocytes; nucleus only, 7 cases; cytoplasm only, no cases; 2) astrocytes (normal and "bizarre"); nucleus and cytoplasm, two cases; cytoplasm only, four cases; 3) macrophages; nucleus and cytoplasm, one case; cytoplasm only, four cases; and 4) neurons; nucleus and cytoplasm, two cases; cytoplasm only, three cases. Perivascular, endothelial, ependymal, and microglial cells were never infected. Our ultrastructural data indicate that cell types other than oligodendrocytes can be involved productively by JCV in the lytic phase of progressive multifocal leukoencephalopathy (PML) in AIDS patients. Neuronal cells, especially, can be infected productively by the JCV, and this should be considered in clinical interpretation of cortical symptoms and signs in suspected or proven cases of PML.
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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.Journal of NeuroVirology 12/2013; · 2.85 Impact Factor
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