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Functional conservation of HTLV-1 rex balances the immune pressure for sequence variation in the rex gene.

Abstract：

:Naturally occurring mutations in Human T-cell Leukemia Virus Type 1 (HTLV-1) Tax protein lead to loss of recognition by cytotoxic T-lymphocytes. Most of these mutations also abolish or severely impair the transactivation function of Tax. Ninety percent of the rex gene, which encodes the viral regulator of mRNA splicing (Rex), overlaps with the tax gene. In this paper, we report that four previously described point mutations in tax that abolished CTL recognition and activity did not alter either the dimerisation function or the ability to export viral mRNA of the corresponding Rex proteins. Rex proteins containing two other amino acid changes were likewise functional. However, five Rex deletion mutants, predominantly but not exclusively found in HAM/TSP patients, had all lost these functions. We conclude that, although the Tax protein is subject to strong CTL-mediated selection, there are stronger functional constraints on amino acid variation in Rex. This may limit the variation in the tax/rex nucleotide sequence which results in immune evasion.

journal_name

Virology

journal_title

Virology

authors

Smith RE,Niewiesk S,Booth S,Bangham CR,Daenke S

doi

10.1006/viro.1997.8789

subject

Has Abstract

pub_date

1997-10-27 00:00:00

pages

397-403

issue

2

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(97)98789-4

journal_volume

237

pub_type

杂志文章

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