Homologies between small nuclear RNAs and LAV HTLV-III sequences and their possible role in the cytopathic effect of the virus

J. Mináróvits, J. Segesdi, Z. Kovács, I. Földes

Research output: Article

2 Citations (Scopus)

Abstract

The mechanism of action of LAV HTLV-III resulting in a pronounced cytopathic effect is still unknown. We demonstrate that the long terminal repeat (LTR) sequence and env gene of LAV HTLV-III contain regions of 70-80% homology and/or complementarity with regions of small nuclear (sn) RNAs U1 and U2. On this basis, we hypothesize that the cytotoxic effect of LAV HTLV-III is due - at least partly - to the inhibition of processing of cellular hnRNAs by competing for splice junction sites and/or by complexing with U1 and especially U2 RNAs.

Original languageEnglish
Pages (from-to)27-33
Number of pages7
JournalMedical Hypotheses
Volume22
Issue number1
DOIs
Publication statusPublished - 1987

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Small Nuclear RNA
Terminal Repeat Sequences
HIV
Viruses
env Genes
U2 small nuclear RNA

ASJC Scopus subject areas

  • Developmental Biology
  • Medicine(all)
  • Drug Discovery

Cite this

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abstract = "The mechanism of action of LAV HTLV-III resulting in a pronounced cytopathic effect is still unknown. We demonstrate that the long terminal repeat (LTR) sequence and env gene of LAV HTLV-III contain regions of 70-80{\%} homology and/or complementarity with regions of small nuclear (sn) RNAs U1 and U2. On this basis, we hypothesize that the cytotoxic effect of LAV HTLV-III is due - at least partly - to the inhibition of processing of cellular hnRNAs by competing for splice junction sites and/or by complexing with U1 and especially U2 RNAs.",
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AU - Segesdi, J.

AU - Kovács, Z.

AU - Földes, I.

PY - 1987

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AB - The mechanism of action of LAV HTLV-III resulting in a pronounced cytopathic effect is still unknown. We demonstrate that the long terminal repeat (LTR) sequence and env gene of LAV HTLV-III contain regions of 70-80% homology and/or complementarity with regions of small nuclear (sn) RNAs U1 and U2. On this basis, we hypothesize that the cytotoxic effect of LAV HTLV-III is due - at least partly - to the inhibition of processing of cellular hnRNAs by competing for splice junction sites and/or by complexing with U1 and especially U2 RNAs.

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