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PubMed2002

Central nervous system infections in individuals with HIV-1 infection.

Opportunistic infections of the central nervous system (CNS) are common complications of advanced immunodeficiency in individuals with human immunodeficiency virus type 1 (HIV-1) infection. Neurological disease is the first manifestation of acquired immunodeficiency syndrome (AIDS) in 10% to 20% of symptomatic HIV-1 infection. Prompt diagnosis and treatment of such disorders is critical. Also, in the era of highly active antiretroviral therapy (HAART), these disease states have changed in presentation and epidemiology. Therefore, we review the epidemiology, pathogenesis, clinical features, diagnosis, and management of five common central nervous system disorders in individuals with HIV-1 infection: toxoplasma encephalitis, primary central nervous system lymphoma, cryptococcal meningitis, cytomegalovirus encephalitis, and progressive multifocal leukoencephalopathy.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

CT assessment of CNS complications of AIDS.

Although acquired immunodeficiency syndrome (AIDS) is not directly fatal, individuals with the disease are susceptible to a host of life-threatening opportunistic infections and complications. This article focuses on the central nervous system (CNS) complications of HIV/AIDS and computed tomography's role in diagnosing these conditions. After completing the article, readers will know the signs and symptoms, causes or proposed causes and computed tomographic (CT) appearance of 4 important CNS complications of HIV/AIDS: Progressive multifocal leukoencephalopathy (PML). Toxoplasmosis. CNS lymphoma. AIDS dementia complex (ADC).

AIDS Dementia Complex↗
PubMed1980

Experimental glioma in primates: a computed tomography model.

Owl and squirrel monkeys inoculated intracerebrally with human polyomavirus obtained from the brain of patient with progressive multifocal leukoencephalopathy developed cerebral gliomas. Among these tumors, three out of five were detected and accurately localized by contrast enhanced computed tomography (CT) when the animals were still clinically normal. Various CT features of these tumors corresponded to specific pathologic changes, such as histologic type and presence of hemorrhage and necrosis. Also, tumor progression was clearly demonstrated in repeat scans of one animal. The CT sensitivity and the capability of distinguishing various pathologic features are encouraging. It appears that a much needed, suitable model of experimental cerebral tumors in primates is now available for CT studies.

Animals↗
PubMed1997

Clinical and biologic features of the AIDS dementia complex.

Human immunodeficiency virus type 1 infection is frequently associated with complications of the nervous system, involving all levels of the neuraxis. Many of these represent focal disorders, such as toxoplasmosis, lymphoma, and progressive multifocal leukoencephalopathy. This article reviews the salient clinical and biological features of these disorders.

AIDS Dementia Complex↗
PubMed2003

Productive infection of cerebellar granule cell neurons by JC virus in an HIV+ individual.

BACKGROUND: In the setting of severe immunosuppression, the polyomavirus JC (JCV) can cause a lytic infection of oligodendrocytes. This demyelinating disease of the CNS white matter (WM) is called progressive multifocal leukoencephalopathy (PML). JCV has a very narrow host-cell range and productive infection of neurons has never been demonstrated. Patient, methods, and results: An HIV-1-infected patient presented with signs of pyramidal tract and cerebellar dysfunction. Brain MRI revealed T2 hyperintensities in the WM of both frontal lobes and cerebellar atrophy. His disease progressed despite therapy and he died 6 months later. In addition to classic PML findings in the frontal lobe WM, autopsy revealed scattered foci of tissue destruction in the internal granule cell layer (IGCL) of the cerebellum. In these foci, enlarged granule cell neurons identified by the neuronal markers MAP-2 and NeuN reacted with antibodies specific for the polyomavirus VP1 capsid protein. Electron microscopy showed 40 nm viral particles, consistent with polyomaviruses, in these granule cell neurons. In addition, JCV DNA was detected by PCR after laser capture microdissection of cells from the areas of focal cell loss. Finally, in situ hybridization studies demonstrated that many granule cell neurons were infected with JCV but did not contain viral proteins. Sequence analysis of the JCV regulatory region from cerebellar virions showed a tandem repeat pattern also found in PML lesions of the frontal lobe WM. CONCLUSION: JCV can productively infect granule cell neurons of the IGCL of the cerebellum. This suggests a role for JCV infection of neurons in cerebellar atrophy occurring in HIV-infected individuals.

Acquired Immunodeficiency Syndrome↗
PubMed1978

Virus infection in demyelinating diseases.

Several animal and human demyelinating diseases of the central nervous system (CNS) are associated with RNA or DNA viruses. These viruses infect CNS cells lytically or persistently. They mainly belong to the group of envelope viruses which derive their envelope partly from the host cell membrane. The process of virus release may result in the appearance of new antigens of virus-infected cells or the incorporation of cell membrane material into the viral envelope. These changes may lead to an immune response which selectively injures the CNS. These alterations of host cell membranes and host cell functions, together with the immune mechanism, are central to many of the hypotheses regarding virus-induced demyelination. The role of virus infection in progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis, visna and mouse hepatitis virus infections, is discussed in relation to the demyelinating process of these diseases.

Animals↗
PubMed1988

Neuroepidemiology of acquired immunodeficiency syndrome.

Data from the Centers for Disease Control (CDC) and from the hospitals affiliated with the University of California, San Francisco show a significant incidence of neurological complications in AIDS patients and suggest that patients from different risk groups and geographic regions are at different relative risk for specific neurological complications. CDC national surveillance data show that Haitian-born AIDS patients are 3.7 times more likely to have neurological complications than are patients in other risk groups; neurological illness is also reported more often in intravenous drug abusers and black AIDS patients. Cryptococcal meningitis is most prevalent among intravenous drug abusers, Haitians, and blacks, and is most commonly reported in New Jersey, a state with a large proportion of AIDS patients in these three groups. Cerebral toxoplasmosis is reported much more often in Haitians than in other risk groups and is most prevalent in Florida among both Haitians and non-Haitians, probably because of greater exposure to Toxoplasma gondii organisms in the semitropical climate of Florida. The prevalence rates for progressive multifocal leukoencephalopathy (PML) and primary central nervous system lymphoma are similar throughout various risk groups and regions of the United States.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Opportunistic infections of the central nervous system in patients with AIDS].

Between August 1985 and March 1989 we had evaluated 70 AIDS patients. We had identified 7 opportunistic Central Nervous System infections, others toxoplasmosis and tuberculosis: A case of progressive multifocal leukoencephalopathy presented with aphasia as their initial manifestation, a probable herpesvirus type 1 polyradiculoneuropathy, four cryptococcal meningitis and syphilitic neuroretinitis.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Prevalence of long-term BK and JC excretion in HIV-infected adults and lack of correlation with serological markers.

The natural history of polyomavirus infection, and sensitivity of diagnostic assays remain unclear. A stratified group of 94 human immunodeficiency virus (HIV)-infected patients was studied for both virological and serological markers of active infection with both JC virus and BK virus. JC DNA was detected in the urine of 18 of 81 (22%) patients and BK DNA in 30 (37%) patients. Whilst patients with a low CD(4) cell count (P =.009), CD(4)/CD(8) ratio (P =.031) and beta2M concentration (P =.042) were significantly more likely to be excreting BK, JC excretion did not correlate with any of the immunological markers measured. Furthermore, when all the immunological factors were taken into account, there was no association between either BK or JC excretion and age of the patient (P =.149 for BK, P = 0.891 for JC). BK IgM antibody was detected in only 3 of 30 (10%) BK excretors. JC IgM was detected in 5 of 18 (27. 7%) JC excretors but also in 11 of 63 (17.5%) patients without demonstrable JC excretion. Therefore IgM was a very poor indicator of viruria. One year follow-up on a subset of patients showed that both DNA detection in urine and IgM antibody remain stable over many months despite falling CD(4) cell counts, and would indicate that events leading to enhanced viral production probably occur early after HIV infection. Replication of JC virus in the brain leading to the onset of progressive multifocal leukoencephalopathy (PML) could not be predicted using any of the markers studied.

Adult↗
PubMed1989

[Development of acute myelocytic leukemia in the course of Sjögren's syndrome].

A 53-year-old female, who had been having xerostomia and xerophthalmia for two years, was admitted in November 1984, because of subfever and malaise. Laboratory examination revealed pancytopenia with appearance of blasts, mild hypergammaglobulinemia, and elevated titers of ANA, anti SS-A and anti SS-B. Bone marrow aspirate showed increased myeloblasts. Schirmer's test and Rose Bengal's test were both positive, and sialography showed apple tree like appearance. Pathological findings of biopsied lip mucosa showed remarkable infiltration of lymphocytes. The patient was diagnosed acute myelocytic leukemia and Sjögren's syndrome. In spite of recovery of peripheral blood after combination chemotherapy (BHAC-DMP), a disturbance of consciousness appeared and she died of its progression. It was suspected clinically that she was suffered from progressive multifocal leukoencephalopathy (PML). It is sometimes reported that patients with Sjögren's syndrome develop malignant lymphoma, but it is very rare that Sjögren syndrome develop AML.

Female↗
PubMed1980

[Slow virus infections of the central nervous system].

The major slow viral infections discovered in man manifest themselves in chronic neurological disease. Studies of these diseases have allowed a better understanding of the mechanisms of virus persistence in the central nervous system. Findings are summarized from recent investigations on such slow viral infections as subacute sclerosing panencephalitis, progressive multifocal leukoencephalopathy and the spongiform encephalopathies. From the examples presented it is evident that there is a great diversity of virus-host interactions in slow viral infections of the central nervous system.

Adult↗
PubMed1998

HIV rounds at Cornell: selected neurologic complications of HIV disease.

Neurological disorders are among the most frequent and devastating complications of HIV infection and AIDS. As patients survive longer with the availability of highly active anti-retrovital therapy, it is likely that the frequency of some of these disorders will increase, since patients will survive long enough to develop them. The central and peripheral nervous system may be affected by numerous primary and secondary complications. These neurological disorders include HIV dementia, primary CNS lymphoma, toxoplasmosis, progressive multifocal leukoencephalopathy, vacuolar myelopathy, peripheral neuropathies, and myopathy. In this review we discuss current thoughts on clinical features, pathogenesis, diagnostic evaluation, treatment and clinical trials in several of these HIV-associated neurologic disorders.

AIDS Dementia Complex↗
PubMed2003

Polyomavirus JCV excretion and genotype analysis in HIV-infected patients receiving highly active antiretroviral therapy.

OBJECTIVE: To assess the frequency of shedding of polyomavirus JC virus (JCV) genotypes in urine of HIV-infected patients receiving highly active antiretroviral therapy (HAART). METHODS: Single samples of urine and blood were collected prospectively from 70 adult HIV-infected patients and 68 uninfected volunteers. Inclusion criteria for HIV-infected patients included an HIV RNA viral load < 1000 copies, CD4 cell count of 200-700 x 106 cells/l, and stable HAART regimen. PCR assays and sequence analysis were carried out using JCV-specific primers against different regions of the virus genome. RESULTS: JCV excretion in urine was more common in HIV-positive patients but not significantly different from that of the HIV-negative group [22/70 (31%) versus 13/68 (19%); P = 0.09]. HIV-positive patients lost the age-related pattern of JCV shedding (P = 0.13) displayed by uninfected subjects (P = 0.01). Among HIV-infected patients significant differences in JCV shedding were related to CD4 cell counts (P = 0.03). Sequence analysis of the JCV regulatory region from both HIV-infected patients and uninfected volunteers revealed all to be JCV archetypal strains. JCV genotypes 1 (36%) and 4 (36%) were the most common among HIV-infected patients, whereas type 2 (77%) was the most frequently detected among HIV-uninfected volunteers. CONCLUSION: These results suggest that JCV shedding is enhanced by modest depressions in immune function during HIV infection. JCV shedding occurred in younger HIV-positive persons than in the healthy controls. As the common types of JCV excreted varied among ethnic groups, JCV genotypes associated with progressive multifocal leukoencephalopathy may reflect demographics of those infected patient populations.

Adult↗
PubMed1988

[New human papovaviruses: JC and BK].

BK and JC viruses are human papovaviruses widespread in human population. Primary infection with those viruses are generally asymptomatic and reactivation occur upon immunodepression. JC virus found to be associated with Progressive Multifocal Leukoencephalopathy. In the other hand BK virus mostly reactivated after immunosuppression. Both viruses have oncogenic potential when inoculated subcutaneously or intracerebrally to experimental animals. However, there is no direct relation has been shown yet for association of those new human papovaviruses with human malignancies.

BK Virus↗
PubMed1998

[Stereotaxic brain biopsy in AIDS patients with neurological manifestations].

Prospective series showing the importance of computerized stereotactic brain biopsy in the management of AIDS patients neurologically symptomatic and confirmed by images. Patients undergone an algorithm step by step done by their own doctors and referred to us for stereotactic biopsy. Our protocol was opened in August 1995 and closed in December 1996. Twenty patients were biopsied. This protocol is similar to the Levy's one (Chicago IL, USA). We have got diagnosis in all cases. Lymphoma was predominant and followed by toxoplasmosis, progressive multifocal leukoencephalopathy and HIV encephalopathy. We included one patient with diploic giant cells lymphoma. Our mortality and morbidity was zero. By these results we conclude that stereotactic biopsy in AIDS patients is safe and effective.

AIDS Dementia Complex↗
PubMedDate not supplied

Opportunistic infections of the central nervous system in children with HIV infection: report of 9 autopsy cases and review of literature.

Central nervous system (CNS) abnormalities attributed to direct effects of HIV infection are seen in most of children with acquired immunodeficiency syndrome (AIDS). Secondary CNS infections with opportunistic and common pathogens are infrequent in this age group. We report 9 cases of opportunistic infection of the CNS found among 65 autopsy cases of pediatric AIDS. These included 4 cases of cytomegalovirus (CMV) infection, 1 of which was associated with aspergillosis, and 2 cases of candidiasis, 1 of which coexisted with Mycobacterium avium intracellulare (MAI) infection. There were also 2 cases of leptomeningitis, 1 due to Mycobacterium tuberculosis (MTB) and the other to Cryptococcus neoformans. In 1 child progressive multifocal leukoencephalopathy (PML) coexisted with mycotic encephalitis caused by an Aspergillus sp.

AIDS-Related Opportunistic Infections↗
PubMed1999

ERK/MAP kinase is chronically activated in human reactive astrocytes.

Reactive astrogliosis is the most prominent macroglial response to diverse forms of CNS injury. We assessed a potential role for the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathway because it represents a common effector for several major families of transmembrane receptors implicated in astrogliosis. Immunohistochemical detection of activated ERK/MAPK in a series of human neurosurgical specimens utilizing phosphorylation state-dependent antibodies consistently revealed intense immunoreactivity in reactive astrocytes in both subacute and chronic lesions, including infarct, mechanical trauma, chronic epilepsy, and progressive multifocal leukoencephalopathy. Neurons, oligodendroglia, and most inflammatory cells showed little or no detectable activation. These observations suggest a testable hypothesis: activation of the ERK/MAPK pathway is an obligatory step for the triggering and/or persistence of reactive astrogliosis.

Adult↗