The Slow Infection Caused by Visna Virus

Haase, Ashley T.

doi:10.1007/978-3-642-66289-8_4

Cited by 111 publications

(53 citation statements)

References 199 publications

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“…In some cases, CNS disorders may be the only manifestation of HIV infection (672,838). In animal model systems (e.g., visna virus and caprine arthritis-encephalitis virus infection), CNS disease usually results from direct infection of the brain parenchyma, particularly glial cells, astrocytes, and possibly microglia (418). These latter cells, as noted above, form the macrophage counterpart in the brain compartment.…”

Section: F Anti-lymphocyte Antibodiesmentioning

confidence: 99%

Pathogenesis of Human Immunodeficiency Virus Infection

Levy¹

1989

Annals of the New York Academy of Sciences

222

290

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Section: F Anti-lymphocyte Antibodiesmentioning

confidence: 99%

Pathogenesis of Human Immunodeficiency Virus Infection

Levy¹

1989

Annals of the New York Academy of Sciences

222

290

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“…Visna disease is a slow persistent infection of sheep caused by a retrovirus (2,3). During our investigation of the molecular pathogenesis of this disease, we showed that virus persistence is a consequence of restricted gene expression in vivo (4).…”

Section: Surementioning

confidence: 99%

Detection of viral sequences of low reiteration frequency by in situ hybridization.

Brahic¹,

Haase²

1978

Proc. Natl. Acad. Sci. U.S.A.

386

131

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The sensitivity of in situ hybridization has been increased at least 10-fold by hybridizing in cDNA excess, by increasing the diffusion of the cDNA through the cells, by hybridizing at optimum temperature, and by stabilizing hybrids during autoradiography. Saturation of intracellular RNA with l cDNA has been achieved. The assay is quantitative. In situ ybridization has been used to detect and quantitate visna virus RNA in infected cells. By using [3HlcDNA with specific activity of 2 X 108 dpm/,ug and conditions that reduce background to negligible levels, 10-20 copies of viral RNA per cell can be detected and quantitated after 2 days of autoradiographic exposure.In situ hybridization is potentially a very powerful technique for localizing specific genes on chromosomes, following their expression in cells, and detecting and quantitating viral genes in infected cells. Unfortunately, until now the lack of sensitivity of the technique has restricted its use to the study of highly repeated genetic sequences such as the tandemly repeated genes coding for rRNA (1). Visna disease is a slow persistent infection of sheep caused by a retrovirus (2, 3). During our investigation of the molecular pathogenesis of this disease, we showed that virus persistence is a consequence of restricted gene expression in vivo (4). Although proviral DNA is present in the tissues of infected animals, no viral proteins can be detected and the amount of infectious virus synthesized is minimal. In order to analyze this phenomenon further and, in particular, to determine the level at which the restriction is imposed, we have improved the sensitivity of in situ hybridization approximately 10-fold. This enables us to detect 1-10 copies of viral genome per cell with radioautographic exposures of a few days. It should now be possible, with this technique, to address a number of important issues in gene regulation by using radioactive cDNA transcribed in vitro from purified mRNA. MATERIALS AND METHODSPreparation of [3HlcDNA.[3H]DNA complementary to the visna virus genome was prepared in an endogenous reaction in which purified visna virus was used as a source of both RNA-dependent DNA polymerase and viral 70S RNA. The reaction mixture contained 50 mM Tris-HCI (pH 7.4), 8 mM MgCI2, 1 mM dATP, dGTP, and dCTP, 0.1 mM [3H]dTTP at a specific activity of 90 Ci/mmol or greater, 10 mM dithiothreitol, 100,ug of actinomycin D per ml, 0.02% (vol/vol) Triton X-100, and 250 ;g of purified visna virus per ml. The total reaction volume was usually 4 ml. The reaction mixture was incubated at 450C for 2 hr. and the reaction was terminated by addition of EDTA and Sarkosyl to final concentrations of The publication costs of this article were defrayed in part by page charge payment. This article must therefore by hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact. 6125 10 mM and 0.5% (wt/vol), respectively. The mixture was incubated for 10 min at 370C; nonradioactive dTTP (in 20-to 100-fold excess) and 200,gg of ye...

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“…Visna is a chronic encephalomyelitis with occasional focal demyelinating lesions caused by a persistent infection by a naturally transmitted retrovirus of sheep (Gudnadottir 1974;Haase 1975;Narayan et al 1977;Petursson et al 1978;Nathanson et al 1980). We have underhaken a series of studies (Georgsson et al 1977(Georgsson et al , 1978Petursson et al 1976Petursson et al , 1978Petursson et al , 1980Nathanson et al 1979Nathanson et al ,, 1980 of the pathogenesis of visna following irtracerebral virus injection of Icelandic sheep, which are particularly susceptible to thi:, disease.…”

Section: Introductionmentioning

confidence: 99%

Cerebrospinal fluid immunoglobulins in sheep with visna, a slow virus infection of the central nervous system☆

Martin¹,

Goudswaard²,

Pálsson³

et al. 1982

Journal of Neuroimmunology

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SummaryIcelandic sheep were injected intracerebrally with visna viru,% wh/ch produces a persistent infection of the CNS accompanied by encephalomyelitis and focal demydinating lesions. Studies were conducted on two groups of sheep, with short-total infections (25 sheep sampled 1-3 months after infection) and long-term ivtcctions (14 sheep sampled 5-6 years after infection). Quantitative determination of CSF immnogiobulin levels 5 years after hafeetion indicated that IgM concentration wa~; usually elevated, IgG2 was occasionally elevated and lgGl was rarely elevated. CSF ofigoclonal bands were seen in about half the sheep examined 5 years after ;~nfection. T~,er¢ was a correlation between high titers of CSF antiviral antibody and both elevated CSF lgM concentration and CSF oligoclonal bands. Serum/CSF IgG1 ratios indicated that the blood-brain barrier was apparently intact in long-term visna infection, consistent with intrath~w.al synthesis of IgM and of antiviral antibody. The alterations in CSF immunoglobulins in visna re, scmble those found in other" persistent CNS virus infections and in multiple sclerosis.

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The Slow Infection Caused by Visna Virus

Cited by 111 publications

References 199 publications

Pathogenesis of Human Immunodeficiency Virus Infection

Pathogenesis of Human Immunodeficiency Virus Infection

Detection of viral sequences of low reiteration frequency by in situ hybridization.

Cerebrospinal fluid immunoglobulins in sheep with visna, a slow virus infection of the central nervous system☆

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