Pathogenesis of central nervous system lesions in visna: Cell-mediated immunity and lymphocyte subsets in blood, brain and cerebrospinal fluid

Torsteinsdóttir, Sigurbjörg; Georgsson, Guðmundur; Gísladóttir, E.; Rafnar, Björg; Pálsson, Páll A.; Pétursson, Gudmundur

doi:10.1016/0165-5728(92)90065-s

Cited by 40 publications

(20 citation statements)

References 29 publications

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“…The pronounced inhibitory effect of the drug on viral infection was also demonstrated by the lower grade of inflammatory lesions in the brains of PMEA-treated lambs. Thus, the PMEA-treated lambs had either no or only minimal brain lesions, whereas the untreated control lambs had brain lesions of similar character and severity as in an earlier experiment with the same visna virus clone (24). This reflects an inhibition of viral replication since the early inflammation in visna virus infection is caused by an immune response to virus replication in the brain (27,28 …”

Section: Resultsmentioning

confidence: 79%

“…), and at sacrifice. Peripheral blood mononuclear cells (PBMCs) were separated from heparinized blood by sedimentation on Histopaque-1077 (Sigma) (24). The PBMCs were tested for virus by inoculation of 3-12 x 106 cells onto monolayers of SCPC in 50-ml tissue culture flasks (Nunc).…”

Section: Methodsmentioning

confidence: 99%

“…ELISA was performed as described earlier (24 Histology. Specimens from several organs were collected at sacrifice for histological examination.…”

Section: Methodsmentioning

confidence: 99%

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Inhibitory effect of 9-(2-phosphonylmethoxyethyl)adenine on visna virus infection in lambs: a model for in vivo testing of candidate anti-human immunodeficiency virus drugs.

Thormar

Georgsson

Pálsson

et al. 1995

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

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The acyclic nucleoside phosphonate analog 9-(2-phosphonylmethoxyethyl)adenine (PMEA) was recently found to be effective as an inhibitor of visna virus replication and cytopathic effect in sheep choroid plexus cultures. To study whether PMEA also affects visna virus infection in sheep, two groups of four lambs each were inoculated intracerebrally with 1063 TCID50 of visna virus strain KV1772 and treated subcutaneously three times a week with PMEA at 10 and 25 mg/kg, respectively. The treatment was begun on the day of virus inoculation and continued for 6 weeks. A group of four lambs were infected in the same way but were not treated. The lambs were bled weekly or biweekly and the leukocytes were tested for virus. At 7 weeks after infection, the animals were sacrificed, and cerebrospinal fluid (CSF) and samples of tissue from various areas of the brain and from lungs, spleen, and lymph nodes were collected for isolation of virus and for histopathologic examination. The PMEA treatment had a striking effect on visna virus infection, which was similar for both doses of the drug. Thus, the frequency of virus isolations was much lower in PMEA-treated than in untreated lambs.The difference was particularly pronounced in the blood, CSF, and brain tissue. Furthermore, CSF cell counts were much lower and inflammatory lesions in the brain were much less severe in the treated lambs than in the untreated controls. The results indicate that PMEA inhibits the propagation and spread of visna virus in infected lambs and prevents brain lesions, at least during early infection. The drug caused no noticeable side effects during the 6 weeks of treatment.

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Section: Resultsmentioning

confidence: 79%

Section: Methodsmentioning

confidence: 99%

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Inhibitory effect of 9-(2-phosphonylmethoxyethyl)adenine on visna virus infection in lambs: a model for in vivo testing of candidate anti-human immunodeficiency virus drugs.

Thormar

Georgsson

Pálsson

et al. 1995

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

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“…Data indicates that the antibody response is skewed in SRLV-infected sheep and goats. Only immunoglobulin G1 (IgG1) subtype responses are detected in sheep whilst in goats IgG1 dominates the humoral response [19,102,103,104,105]. …”

Section: Host Genetic Factors Involved In Srlv-induced Pathogenesismentioning

confidence: 99%

“…Evidence backing this is the up regulation of Type 2 cytokines such as anti-inflammatory cytokines IL4 and IL10 [20,80,102,105]. …”

Section: Host Genetic Factors Involved In Srlv-induced Pathogenesismentioning

confidence: 99%

Retroviral Infections in Sheep and Goats: Small Ruminant Lentiviruses and Host Interaction

Larruskain

Jugo

2013

Viruses

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Small ruminant lentiviruses (SRLV) are members of the Retrovirus family comprising the closely related Visna/Maedi Virus (VMV) and the Caprine Arthritis-Encephalitis Virus (CAEV), which infect sheep and goats. Both infect cells of the monocyte/macrophage lineage and cause lifelong infections. Infection by VMV and CAEV can lead to Visna/Maedi (VM) and Caprine Arthritis-Encephalitis (CAE) respectively, slow progressive inflammatory diseases primarily affecting the lungs, nervous system, joints and mammary glands. VM and CAE are distributed worldwide and develop over a period of months or years, always leading to the death of the host, with the consequent economic and welfare implications. Currently, the control of VM and CAE relies on the control of transmission and culling of infected animals. However, there is evidence that host genetics play an important role in determining Susceptibility/Resistance to SRLV infection and disease progression, but little work has been performed in small ruminants. More research is necessary to understand the host-SRLV interaction.

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In Vivoandin VitroInfection with Two Different Molecular Clones of Visna Virus

et al. 1997

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The behavior of two genetically different molecular clones of visna virus KV1772-kv72/67 and LV1-1KS1 was compared in vivo and in vitro. On intracerebral inoculation, clone KV1772-kv72/67 induced a similar response in five sheep as has already been reported with neurovirulent derivates of visna virus. Virus was frequently isolated from blood, cerebrospinal fluid (CSF), and lymphoid organs and induced characteristic central nervous system (CNS) lesions. A strong humoral immune response was detected by ELISA, immunoblotting, and neutralization. Six sheep infected with clone LV1-1KS1 showed a completely different picture. No virus could be isolated from blood or CSF during 6 months of infection. At sacrifice all organs were virus-negative except the CNS of one sheep. None of the six sheep developed significant neutralizing antibodies and only low titer antibodies were detected by ELISA and immunoblotting. Minimal CNS lesions were present in one sheep. The molecular clones were also tested in sheep choroid plexus cells (SCP) and macrophages. In macrophages LV1-1KS1 replicated to a significantly lower titer but induced much more cell fusion than KV1772-kv72/67. The clones replicated equally well in SCP cells. Thus, these molecular clones of visna virus, which differ only by 1% in nucleotide sequence, showed a profound difference in replication and pathogenicity both in vitro and in vivo. These results can be used to map viral genetic determinants important for host-lentivirus interactions.

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Pathogenesis of central nervous system lesions in visna: Cell-mediated immunity and lymphocyte subsets in blood, brain and cerebrospinal fluid

Cited by 40 publications

References 29 publications

Inhibitory effect of 9-(2-phosphonylmethoxyethyl)adenine on visna virus infection in lambs: a model for in vivo testing of candidate anti-human immunodeficiency virus drugs.

Inhibitory effect of 9-(2-phosphonylmethoxyethyl)adenine on visna virus infection in lambs: a model for in vivo testing of candidate anti-human immunodeficiency virus drugs.

Retroviral Infections in Sheep and Goats: Small Ruminant Lentiviruses and Host Interaction

In Vivoandin VitroInfection with Two Different Molecular Clones of Visna Virus

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