1887

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Volume 85, Issue 10

Dissection of measles virus V protein in relation to its ability to block alpha/beta interferon signal transduction Free

Abstract

Interferon (IFN)- and - are the main cytokines for innate immune responses against viral infections. To replicate efficiently in the hosts, viruses have evolved various countermeasures to the IFN response. The V protein of measles virus (MV) has been shown to block IFN-/ signalling. Here, the wild-type IC-B strain of MV was shown to grow comparably in the presence and absence of IFN-, whereas replication of the Edmonston tag strain recovered from cloned DNA was strongly suppressed in its presence. The V protein of the IC-B strain, but not the Edmonston tag strain, blocked IFN- signalling. The V protein of the Edmonston strain from the ATCC also inhibited IFN- signalling. There were three amino acid differences between the V proteins of the Edmonston ATCC and tag strains, and substitutions of both residues at positions 110 and 272 were required for the Edmonston ATCC V protein to lose IFN-antagonist activity. The P protein of the IC-B strain, which shares the N-terminal 231 aa residues with the V protein, also inhibited IFN- signalling. Indeed, fragments comprising only those 231 residues of the IC-B and Edmonston ATCC V proteins, but not the Edmonston tag V protein, were able to block IFN- signalling. However, the N-terminal region of the Edmonston tag V protein, when attached to the C-terminal region of the Edmonston ATCC V protein, inhibited IFN- signalling. Taken together, our results indicate that both the N- and C-terminal regions contribute to the IFN-antagonist activity of the MV V protein.

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2004-10-01
2024-04-23
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Dissection of measles virus V protein in relation to its ability to block alpha/beta interferon signal transduction
J. Gen. Virol. 85, 2991 (2004); https://doi.org/10.1099/vir.0.80308-0
/content/journal/jgv/10.1099/vir.0.80308-0
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