Duplicated sequence motif in the long terminal repeat of maedi-visna virus extends cell tropism and is associated with neurovirulence

Thordur Oskarsson, Hulda S. Hreggvidsdóttir, Gudrún Agnarsdóttir, Sigrídur Matthíasdóttir, Ólafur Sigmar Andrésson, Sigurður Ingvarsson, Valgerður Andrésdóttir

Research output: Contribution to conferenceAbstract

Abstract

Maedi-visna virus (MVV) is a member of the lentivirus subfamily of retroviruses, causing encephalitis (visna), pneumonia (maedi), mastitis and arthritis in sheep. The primary target cells of MVV infection are cells of the monocyte/macrophage lineage, and virus expression is activated upon macrophage maturation. We have previously shown that a duplicated sequence in the long terminal repeat (LTR) of MVV broadens the cell tropism of the virus from being strictly macrophage tropic to being able to grow in a variety of cell types. We have demonstrated that deletion of a CAAAT sequence from either one of the repeated copies resulted in poor growth in sheep choroid plexus cells but had no effect on growth in macrophages. A duplication in the LTR encompassing the CAAAT sequence was found in three neurological field cases sequenced, but no duplication was found in the LTR of six maedi cases, indicating that the duplication in the LTR is associated with neurovirulent strains.
Original languageIcelandic
Pages103-103
Number of pages1
Publication statusPublished - 12 Apr 2004
EventMolecular Mechanism of HIV Pathogenesis (X7). Keystone Symposia - Whistler Conference Centre, Whistler, Canada
Duration: 12 Apr 200418 Apr 2004
https://tks.keystonesymposia.org/index.cfm?e=web.Meeting.Program&meetingid=694

Conference

ConferenceMolecular Mechanism of HIV Pathogenesis (X7). Keystone Symposia
Country/TerritoryCanada
CityWhistler
Period12/04/0418/04/04
Internet address

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