Slow Infections of the Central Nervous System: The Legacy of Dr. Bjorn Sigurdsson (Annals of the New York Academy of Sciences)

Ingvarsson, S. (Participant)

Faculty of Medicine

Activity: Participating in or organising an event › Organising a conference, workshop, ...

Period	2 Jun 1993 → 5 Jun 1993
Event type	Conference
Location	Reykjavík, IcelandShow on map
Degree of Recognition	International

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Ingvarsson1993NYAS
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Björn Sigurðsson introduced the concept of slow viral infections in a series of special lectures given at the University of London in 1954. Since then, concern with and knowledge of slow viral infections - both in animals and in humans - has grown greatly. Lentivirus infections affecting the central nervous system are of particular interest: HIV encephalopathy occurs in a high percentage of AIDS patients, with devastating symptoms.
Avian erythroblastosis virus (AEV) which carries two oncogenes, v-erbA and v-erbB causes erythroleukemia and sarcomas in young chickens and transforms embryo fibroblasts and bone marrow cells in culture. The v-erbA oncogene encodes an aberrant version of a gene for a nuclear thyroid hormone receptor (c-erbA, TR) and functions in neoplasia by blocking erythroid differentiation and by altering the growth properties of fibroblasts. Owing to the multiple point mutations and a small C-terminal deletion, v-erbA has lost the ability to bind T3, but still binds to DNA in a sequence-specific fashion. The phenotypic effects of v-erbA are correlated with and probably caused by v-erbA-mediated repression of a set of erythrocyte-specific genes, but their expression seems to be required during normal erythrocyte maturation. In differentiating erythroblasts the v-erbA oncoprotein specifically arrests expression of the avian erythrocyte anion transporter (band 3), CAII and ALA-S genes at the transcriptional level. Overexpression of the TK is required to modulate erythrocyte-specific gene expression in the presence of T3. The v-erbA oncogene might act as a constitutively active repressor of erythrocyte gene transcription, having lost its ability to depress (or activate) these genes in response to T3 or even retinoic acid.