Cultivation of visna virus in tissue culture

Sigurðsson, Björn; Thormar, Halldór; Pálsson, Páll A.

doi:10.1007/bf01250682

Cited by 148 publications

(40 citation statements)

References 5 publications

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“…Sheep choroid plexus (SCP) cells were established as described previously (37,46). Monocyte-derived macrophages were isolated from peripheral blood samples from healthy sheep as previously described (48).…”

Section: Cellsmentioning

confidence: 99%

Duplicated Sequence Motif in the Long Terminal Repeat of Maedi-Visna Virus Extends Cell Tropism and Is Associated with Neurovirulence

Oskarsson

Hreggvidsdóttir

Agnarsdóttir

et al. 2007

J Virol

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Maedi-visna virus (MVV) is a lentivirus of sheep causing chronic inflammatory disease of the lungs (maedi)and the nervous system (visna). We have previously shown that a duplicated sequence in the long terminal repeat (LTR) of MVV is a determinant of cell tropism. Here, we demonstrate that deletion of a CAAAT sequence from either one of the repeats resulted in poor virus growth in sheep choroid plexus cells. A duplication in the LTR encompassing the CAAAT sequence was found in four neurological field cases that were sequenced, but no duplication was present in the LTRs from seven maedi cases; one maedi isolate was mixed. These results indicate that the duplication in the LTR is associated with neurovirulence.

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Section: Cellsmentioning

confidence: 99%

Duplicated Sequence Motif in the Long Terminal Repeat of Maedi-Visna Virus Extends Cell Tropism and Is Associated with Neurovirulence

Oskarsson

Hreggvidsdóttir

Agnarsdóttir

et al. 2007

J Virol

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“…Viral cytopathology, first described for the effects of poliovirus on cultured cells (22), is a characteristic feature of infection by many viruses (23). Several retroviruses, including avian reticuloendotheliosis virus (24,25), certain subgroups of avian leukosis viruses (26), and visna virus (27,28) Virus Detection. Production of infectious virus by transfected HuT 78 cells was measured by the presence of particle-associated reverse transcriptase activity in the culture supernatant (38), the detection of viral antigens in the cells by indirect immunofluorescence, and by direct cytopathic effects (3,33).…”

mentioning

confidence: 99%

Mutational analysis of the human immunodeficiency virus: the orf-B region down-regulates virus replication.

Luciw¹,

Cheng‐Mayer²,

Levy³

1987

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

278

152

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Mutations were made by recombinant DNA techniques in an infectious molecular clone of the human immunodeficiency virus San Francisco isolate 2 (HIVs ) [formerly the prototype isolate of the acquired immunodeficiency syndrome-associated retrovirus (ARV-2)]. The effect of these changes on the replicative and cytopathologic properties of the virus was studied by transfecting modified virus clones into cultured human cells. Mutations in the gag, pol, env, and tat regions precluded virus replication and cytopathology in lymphoid cells. A mutation in orfA dramatically reduced but did not abolish virus replication. Mutant viruses with deletions in the orf-B region were highly cytopathic and replicated to n5-fold higher levels than wild-type virus.They also produced n5-fold more viral DNA in infected lymphoid cells than did wild-type virus. Thus, the of-B region may function to down-regulate virus replication. This mutational analysis of the HIVSF2 genome is a means of assessing genes regulating viral replication and cytopathology.

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“…The molecularly cloned viruses KV1772 (formerly KV1772kv72/67) and KS1 (formerly LV1-1KS1) have been described previously (2,29,30). SCP cells established as described previously (7,28) were grown at 37°C in a humidified atmosphere of 5% CO 2 in Dulbecco's modified Eagle medium (Gibco) supplemented with 2 mM glutamine, 100 IU of penicillin per ml, 100 IU of streptomycin per ml, and either 10% lamb serum (growth medium) or 1% lamb serum (maintenance medium). Macrophage cultures were established as described previously (29).…”

Section: Methodsmentioning

confidence: 99%

Simultaneous Mutations in CA and Vif of Maedi-Visna Virus Cause Attenuated Replication in Macrophages and Reduced Infectivity In Vivo

Gudmundsson

Jónsson

Ólafsson

et al. 2005

J Virol

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Maedi-visna virus (MVV) is a lentivirus of sheep sharing several key features with the primate lentiviruses.The virus causes slowly progressive diseases, mainly in the lungs and the central nervous system of sheep. Here, we investigate the molecular basis for the differential growth phenotypes of two MVV isolates. One of the isolates, KV1772, replicates well in a number of cell lines and is highly pathogenic in sheep. The second isolate, KS1, no longer grows on macrophages or causes disease. The two virus isolates differ by 129 nucleotide substitutions and two deletions of 3 and 15 nucleotides in the env gene. To determine the molecular nature of the lesions responsible for the restrictive growth phenotype, chimeric viruses were constructed and used to map the phenotype. An L120R mutation in the CA domain, together with a P205S mutation in Vif (but neither alone), could fully convert KV1772 to the restrictive growth phenotype. These results suggest a functional interaction between CA and Vif in MVV replication, a property that may relate to the innate antiretroviral defense mechanisms in sheep.

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Cultivation of visna virus in tissue culture

Cited by 148 publications

References 5 publications

Duplicated Sequence Motif in the Long Terminal Repeat of Maedi-Visna Virus Extends Cell Tropism and Is Associated with Neurovirulence

Duplicated Sequence Motif in the Long Terminal Repeat of Maedi-Visna Virus Extends Cell Tropism and Is Associated with Neurovirulence

Mutational analysis of the human immunodeficiency virus: the orf-B region down-regulates virus replication.

Simultaneous Mutations in CA and Vif of Maedi-Visna Virus Cause Attenuated Replication in Macrophages and Reduced Infectivity In Vivo

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