Isolation of Aids-Associated Retroviruses From Cerebrospinal Fluid and Brain of Patients With Neurological Symptoms

Lévy, J; Hollander, Harry; Shimabukuro, Joni; Mills, John; Kaminsky, Lawrence S.

doi:10.1016/s0140-6736(85)90587-2

Cited by 164 publications

(66 citation statements)

References 7 publications

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“…Evidence to suggest direct HIV infection of neural cells has been reported. HIV DNA and RNA have been detected in brains of AIDS patients and infectious HIV has been isolated from brain tissue and cerebrospinal fluid (3)(4)(5)(6). These data coupled with the neurologic symptoms experienced by 60% of patients with AIDS (7) strongly suggest that HIV is neurotropic.…”

Section: Introductionmentioning

confidence: 99%

Human immunodeficiency virus-infected macrophages produce soluble factors that cause histological and neurochemical alterations in cultured human brains.

Pulliam

Herndier²,

Tang³

et al. 1991

J. Clin. Invest.

276

122

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We wanted to establish an in vitro human model for AIDS-associated dementia and pursue the hypothesis that this disease process may be a result of soluble factors produced by HIV-infected macrophages. Human brain aggregates were prepared from nine different brain specimens, and were treated with supernatants from in vitro HIV-infected macrophages (SI), uninfected macrophages (SU), infected T cells, or macrophage-conditioned media from four AIDS patients.Seven of nine treated brains exposed to SI showed periph-

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Section: Introductionmentioning

confidence: 99%

Human immunodeficiency virus-infected macrophages produce soluble factors that cause histological and neurochemical alterations in cultured human brains.

Pulliam

Herndier²,

Tang³

et al. 1991

J. Clin. Invest.

276

122

View full text Add to dashboard Cite

show abstract

“…Central nervous system (CNS) infection by retroviruses has become a topic of great concern due to the recognition of severe neurological sequelae from infection with the human immunodeficiency virus (HIV) (Carne et al, 1985;Ho et al, 1985 ;Levy et al, 1985;Petito et al, 1985;Price et al, 1988;Resnick et al, 1985;Shaw et al, 1985;Vazeux et al, 1988). Encephalopathy and dementia occur frequently in association with HIV infection of the brain (Ho et al, 1987;Price et al, 1988) in children and in adults but many questions remain unanswered about the pathogenesis of this CNS infection in humans.…”

Section: Introductionmentioning

confidence: 99%

Asymptomatic Infection of the Central Nervous System by the Macaque Immunosuppressive Type D Retrovirus, SRV-1

Lackner¹,

Marx

Lerche

et al. 1989

Journal of General Virology

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SUMMARYThe aetiological agent of spontaneously occurring simian acquired immune deficiency syndrome (SAIDS) in rhesus monkeys (Macaca mulatta) at the California Primate Research Center is a type D retrovirus designated SAIDS retrovirus serotype 1 (SRV-1). SRV-1 DNA and RNA have previously been detected in the brains of rhesus monkeys with SAIDS in the absence of viral antigen or neuropathological lesions. In this study we further define the relationship between SRV-1 and the central nervous system (CNS) in rhesus monkeys by examining the CNS for infectious SRV-1, viral antigen and anti-SRV-1 antibodies. In addition, cerebrospinal fluid (CSF) was assayed for alterations in IgG and albumin levels, IgG/albumin ratios and cell count in comparison to uninfected control animals. No differences in CSF parameters were detected between infected and uninfected animals except for the presence of infectious SRV-1 which was isolated from the CSF from 13 out of 19 (68%) viraemic rhesus monkeys. The probable source of this virus was the choroid plexus, where approximately 1 in 1000 surface epithelial cells were found to contain viral antigen by immunohistochemistry. Antibodies against SRV-1 were not detected in the CSF even when present in the serum. Neither infectious virus nor viral antigen were found in the brain parenchyma of any animal examined. Thus infection of the CNS by SRV-1 appears to be subclinical without an intrathecal immune response. This may be related to the apparent restriction of productive infection in the CNS to cells of the choroid plexus.

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“…The primate lentiviruses human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infect CD4 ϩ T lymphocytes and macrophages as major target cells (4,8,21,23,31,32,36,39,54). The gene for the viral envelope (Env) proteins determines the capability of virus to infect these cells (24,43,45,61).…”

mentioning

confidence: 99%

Mechanisms for Adaptation of Simian Immunodeficiency Virus to Replication in Alveolar Macrophages

Mori

Rosenzweig

Desrosiers

2000

J Virol

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In contrast to the simian immunodeficiency virus SIVmac239, which replicates poorly in rhesus monkey alveolar macrophages, a variant with nine amino acid changes in envelope (SIVmac239/316E) replicates efficiently and to high titer in these same cells. We examined levels of viral DNA, RNA, antigen, and infectious virus to identify the nature of the block to SIVmac239 replication in these cells. Low levels of viral antigen (0.1 to 1.0 ng of p27 per ml) and infectious virus (100 to 1,000 infectious units per ml) were produced in the supernatant 1 to 4 days after SIVmac239 infection, but these levels did not increase subsequently. SIVmac239 DNA was synthesized in these macrophage cultures during the initial 24 h after infection, but the levels did not increase subsequently. Quantitation of the numbers of infectious cells in cultures over time and the results of experiments in which cells were reexposed to SIVmac239 after the initial exposure indicated that only a small proportion of cells were susceptible to SIVmac239 infection in these alveolar macrophage cultures and that the vast majority (>95%) of cells were refractory to SIVmac239 infection. In contrast to the results with SIVmac239, the levels of viral antigen, infectious virus, and viral DNA increased exponentially 2 to 7 days after infection by SIVmac239/316E, reaching levels greater than 100 ng of p27 per ml and 100,000 infectious units per ml. Since SIVmac239/316E has previously been described as a virus capable of infecting cells in a relatively CD4-independent fashion, we examined the levels of CD4 expression on the surface of fresh and cultured alveolar macrophages from rhesus monkeys. The levels of CD4 expression were extremely low, below the limit of detection by flow cytometry, on greater than 99% of the macrophages. CCR5؉ cells were profoundly depleted only from alveolar macrophage cultures infected with SIVmac239/316E. High concentrations of an antibody to CD4 delayed but did not block replication of SIVmac239/316E. The results suggest that the adaptation of SIVmac316 to efficient replication in alveolar macrophages results from its ability to infect these cells in a CD4-independent fashion or in a CD4-dependent fashion even at extremely low levels of surface CD4 expression. Since resident macrophages in brains and lungs of humans also express little or no CD4, our findings predict the presence of human immunodeficiency virus type 1 that is relatively CD4 independent in the lung and brain compartments of infected people.

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Isolation of Aids-Associated Retroviruses From Cerebrospinal Fluid and Brain of Patients With Neurological Symptoms

Cited by 164 publications

References 7 publications

Human immunodeficiency virus-infected macrophages produce soluble factors that cause histological and neurochemical alterations in cultured human brains.

Human immunodeficiency virus-infected macrophages produce soluble factors that cause histological and neurochemical alterations in cultured human brains.

Asymptomatic Infection of the Central Nervous System by the Macaque Immunosuppressive Type D Retrovirus, SRV-1

Mechanisms for Adaptation of Simian Immunodeficiency Virus to Replication in Alveolar Macrophages

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