Cytomegalovirus multifocal neuropathy in AIDS

Roullet, E; Assuerus, V.; Gozlan, Joël; Ropert, Alain; Saïd, G; Baudrimont, M.; Amrani, Mohamed; Jacomet, Christine; Duvivier, Claudine; Gonzales-Canali, G.; Kirstetter, M.; Meyohas, Marie-Caroline; Picard, O; Rozenbaum, Willy

doi:10.1212/wnl.44.11.2174

Cited by 78 publications

(47 citation statements)

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“…Al- though ß 2 M(-/-) mice may occasionally retain a very small number of functional CD8+ lymphocytes [33], ß 2 M(-/-) mice have been useful for studies of viral pathogenesis. For example, ß 2 M(-/-) mice exhibited delayed clearance and increased mortality following influenza virus challenge [34].…”

Section: Discussionmentioning

confidence: 99%

Cellular Reservoirs for Coronavirus Infection of the Brain in β<sub>2</sub>-Microglobulin Knockout Mice

Lavi¹,

Sarma²,

Weiss

1999

Pathobiology

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Mouse hepatitis virus (MHV) A59 infection which causes acute encephalitis, hepatitis, and chronic demyelination, is one of the experimental models for multiple sclerosis. Previous studies showed that lethal infection of β₂-microglobulin ‘knockout’ (β₂M(–/–)) mice required 500-fold less virus and viral clearance was delayed as compared to infection of immunocompetent C57Bl/6 (B6) mice. To investigate the mechanism of the increased susceptibility of β₂M(–/–) mice to MHV-A59, we studied organ pathology and the distribution of viral antigen and RNA during acute and chronic infection. A59-infected β₂M(–/–) mice were more susceptible to acute encephalitis and hepatitis, but did not have increased susceptibility to demyelination. Viral antigen and RNA distribution in the brain was increased in microglia, lymphocytes, and small vessel endothelial cells while the distribution in neurons and glia was similar in β₂M(–/–) mice and B6 mice. Acute hepatitis and thymus cortical hypoplasia in β₂M(–/–) mice were delayed in onset but pathologic changes in these organs were similar to those in B6 mice. The low rate of demyelination in β₂M(–/–) mice was consistent with the low dose of the virus given. A less neurotropic virus MHV-2, caused increased parenchymal inflammation in β₂M(–/–) mice, but without demyelination. Thus, CD8+ cells were important for viral clearance from endothelial cells, microglia and inflammatory cells, but not from neuronal and glial cells. In addition, CD8+ cells played a role in preventing the spread of encephalitis.

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Section: Discussionmentioning

confidence: 99%

Cellular Reservoirs for Coronavirus Infection of the Brain in β<sub>2</sub>-Microglobulin Knockout Mice

Lavi¹,

Sarma²,

Weiss

1999

Pathobiology

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“…Nine patients (1 with MGNE, Concomitant peripheral nerve syndromes. Two CMV-related peripheral nerve syndromes are recognized in patients 8 with VE) began treatment before neurological onset, and the remaining 6 (4 with MGNE, 2 with VE) began treatment after with AIDS: multifocal neuropathy [15] and radiculopathy, including subacute ascending lumbosacral polyradiculomyelopaneurological onset. Seven patients (4 with MGNE, 2 with VE) were receiving therapy with zidovudine at neurological onset, thy (PRAM), also known as cauda equina syndrome [12].…”

Section: Extraneurological CMV Infectionmentioning

confidence: 99%

“…Seven patients (4 with MGNE, 2 with VE) were receiving therapy with zidovudine at neurological onset, thy (PRAM), also known as cauda equina syndrome [12]. In the former syndrome, CMV is present in peripheral nerves which continued at a dosage of 507.14 mg/d (SD, 271.46 mg/d) for an average of 13 weeks (SD, 8.96 weeks), but in no [15]; in the latter, there is a direct root and spinal cord involvement [10,12]. case was neurological improvement noted.…”

Section: Extraneurological CMV Infectionmentioning

confidence: 99%

Microglial Nodular Encephalitis and Ventriculoencephalitis Due to Cytomegalovirus Infection in Patients with AIDS: Two Distinct Clinical Patterns

Grassi¹,

Clerici²,

Perin³

et al. 1998

Clinical Infectious Diseases

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In patients with AIDS, cerebral infection due to cytomegalovirus (CMV) results in two distinct neuropathological patterns: microglial nodular encephalitis (MGNE) and ventriculoencephalitis (VE). In order to identify clinical features to facilitate the differential diagnosis of these two forms of CMV encephalopathy in living patients, we retrospectively reviewed the clinical records of 18 patients with MGNE or VE diagnosed at autopsy. We identified the following clinical features as distinguishing the two encephalopathies: (1) MGNE manifests earlier than VE; (2) the onset of MGNE is acute, whereas the onset of VE is insidious; (3) the onset of MGNE is marked by confusion and delirium, which do not occur in VE; (4) VE is frequently associated with radiculopathy, which is absent in MGNE; and (5) VE is associated with more marked alterations in cerebrospinal fluid (high protein levels and pleocytosis). The early neurological manifestations of MGNE should prompt a search for systemic CMV infection, which may lead to earlier treatment. Brain infection caused by cytomegalovirus (CMV) occurswent neurological examination by a specialist were considered primarily in newborns as a result of congenital infection, as well for review. The autopsy findings of those selected included as in immunocompromised adults, particularly organ transplant histologic evidence of MGNE or VE, according to established recipients and patients with AIDS [1, 2]. The morphological criteria [5]. Exclusion criteria were (1) presence of HIV encorrelate of congenital CMV infection is ventriculoencephalitis cephalopathy, opportunistic CNS infection, or cerebral neo-(VE), while in organ transplant recipients CMV infection replasm; (2) history of neurological or psychiatric illness; (3) sults in the pathological pattern known as microglial nodular therapy with drugs able to alter the mental state; and (4) eviencephalitis (MGNE) [3].dence of severe metabolic disorder, as revealed by extensive Two routes of dissemination of CMV infection to the nerblood and urine tests. vous system are known [3]: via the CSF (through ependymal cells) and via the blood (through endothelial cells). In AIDS patients, both modes of CMV dissemination to the brain are encountered. Hematic dissemination results in MGNE with Histopathologic Examination pathological characteristics closely resembling those seen in recipients of organ transplants; dissemination in the CSF results Brain tissues were fixed in 10% buffered formalin and emin VE.bedded in paraffin. Sections from the frontal, parietal, and temAlthough the clinical characteristics of VE are known [4], poral cortex, basal ganglia, cerebellum, and spinal cord and those of MGNE have not been defined. Furthermore, differenfrom each macroscopic lesion were stained with hematoxylin tial-diagnosis studies are lacking, so MGNE and VE are curand eosin for histologic examination. Other stains, including rently distinguishable only at autopsy. We reviewed the clinical periodic acid -Schiff, Ziehl-Neelsen, and Giemsa preparations, re...

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“…Two other peripheral nervous system disorders, mononeuritis multiplex and painful pe ripheral neuropathy, have also been described in HIVinfected patients in association with HCMV infection. Moreover, HCMV has also been demonstrated in the nerves of subjects without any clinical symptoms [53][54][55].…”

Section: Cytomegalovirus Infections Of the Nervous Systemmentioning

confidence: 98%

“…Its asymmetrical and mul tifocal nature can be demonstrated by means of electro myographic and neurographic examinations. The form due to HCMV should be distinguished from a less severe mononeuritis occurring in HIV-infected patients with a less pronounced immunodeficiency [52,53,55], Painful peripheral neuropathy has been considered a distinct variant of the more common distal symmetrical peripheral neuropathy, and has been described in 7.5% of AIDS patients. This syndrome has been associated with HCMV because it is frequently found in AIDS patients with systemic HCMV disease [54].…”

Section: Cytomegalovirus Infections Of the Nervous Systemmentioning

confidence: 99%

Cytomegalovirus Infections of the Nervous System

Cinque

Marenzi

Ceresa³

1997

Intervirology

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Experimental evidence and pathological observation indicate that human cytomegalovirus (HCMV) has a tropism for cells of the nervous system, including both neuronal and glial cells. As demonstrated in animal models, after a viremic phase, the virus may reach the brain, where it may cause mild infection or severe encephalitis. The nervous system is one of the principal target organs in congenital HCMV infections and in HCMV-infected AIDS patients. In the former case, mortality is high and neurological sequelae, such as mental retardation, are frequent; in the latter it may lead to a progressively wasting encephalopathy and death within a few weeks. The diagnosis of the nervous system manifestations due to HCMV can now rely upon the detection of HCMV DNA in cerebrospinal fluid by means of polymerase chain reaction. However, the current antiviral treatments of these complications are of limited effect.

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Cytomegalovirus multifocal neuropathy in AIDS

Cited by 78 publications

References 0 publications

Cellular Reservoirs for Coronavirus Infection of the Brain in β<sub>2</sub>-Microglobulin Knockout Mice

Cellular Reservoirs for Coronavirus Infection of the Brain in β<sub>2</sub>-Microglobulin Knockout Mice

Microglial Nodular Encephalitis and Ventriculoencephalitis Due to Cytomegalovirus Infection in Patients with AIDS: Two Distinct Clinical Patterns

Cytomegalovirus Infections of the Nervous System

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