Abstract
Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are complex retroviruses that persist in the host, eventually causing leukemia and neurological disease in a small percentage of infected individuals. In addition to structural and enzymatic proteins, HTLV encodes regulatory (Tax and Rex) and accessory (open reading frame I and II) proteins. The viral Tax and Rex proteins positively regulate virus production. Tax activates viral and cellular transcription to promote T-cell growth and, ultimately, malignant transformation. Rex acts posttranscriptionally to facilitate cytoplasmic expression of viral mRNAs that encode the structural and enzymatic gene products, thus positively controlling virion expression. Here, we report that both HTLV-1 and HTLV-2 have evolved accessory genes to encode proteins that act as negative regulators of both Tax and Rex. HTLV-1 p30II and the related HTLV-2 p28II inhibit virion production by binding to and retaining tax/rex mRNA in the nucleus. Reduction of viral replication in a cell carrying the provirus may allow escape from immune recognition in an infected individual. These data are consistent with the critical role of these proteins in viral persistence and pathogenesis in animal models of HTLV-1 and HTLV-2 infection.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 11077-11083 |
| Number of pages | 7 |
| Journal | Journal of Virology |
| Volume | 78 |
| Issue number | 20 |
| DOIs | |
| State | Published - Oct 2004 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology
Cite this
Repression of human T-cell leukemia virus type 1 and type 2 replication by a viral mRNA-encoded posttranscriptional regulator. / Younis, Ihab; Khair, Lyne; Dundr, Miroslav; Lairmore, Michael Dale; Franchini, Genoveffa; Green, Patrick L.
In: Journal of Virology, Vol. 78, No. 20, 10.2004, p. 11077-11083.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Repression of human T-cell leukemia virus type 1 and type 2 replication by a viral mRNA-encoded posttranscriptional regulator
AU - Younis, Ihab
AU - Khair, Lyne
AU - Dundr, Miroslav
AU - Lairmore, Michael Dale
AU - Franchini, Genoveffa
AU - Green, Patrick L.
PY - 2004/10
Y1 - 2004/10
N2 - Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are complex retroviruses that persist in the host, eventually causing leukemia and neurological disease in a small percentage of infected individuals. In addition to structural and enzymatic proteins, HTLV encodes regulatory (Tax and Rex) and accessory (open reading frame I and II) proteins. The viral Tax and Rex proteins positively regulate virus production. Tax activates viral and cellular transcription to promote T-cell growth and, ultimately, malignant transformation. Rex acts posttranscriptionally to facilitate cytoplasmic expression of viral mRNAs that encode the structural and enzymatic gene products, thus positively controlling virion expression. Here, we report that both HTLV-1 and HTLV-2 have evolved accessory genes to encode proteins that act as negative regulators of both Tax and Rex. HTLV-1 p30II and the related HTLV-2 p28II inhibit virion production by binding to and retaining tax/rex mRNA in the nucleus. Reduction of viral replication in a cell carrying the provirus may allow escape from immune recognition in an infected individual. These data are consistent with the critical role of these proteins in viral persistence and pathogenesis in animal models of HTLV-1 and HTLV-2 infection.
AB - Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are complex retroviruses that persist in the host, eventually causing leukemia and neurological disease in a small percentage of infected individuals. In addition to structural and enzymatic proteins, HTLV encodes regulatory (Tax and Rex) and accessory (open reading frame I and II) proteins. The viral Tax and Rex proteins positively regulate virus production. Tax activates viral and cellular transcription to promote T-cell growth and, ultimately, malignant transformation. Rex acts posttranscriptionally to facilitate cytoplasmic expression of viral mRNAs that encode the structural and enzymatic gene products, thus positively controlling virion expression. Here, we report that both HTLV-1 and HTLV-2 have evolved accessory genes to encode proteins that act as negative regulators of both Tax and Rex. HTLV-1 p30II and the related HTLV-2 p28II inhibit virion production by binding to and retaining tax/rex mRNA in the nucleus. Reduction of viral replication in a cell carrying the provirus may allow escape from immune recognition in an infected individual. These data are consistent with the critical role of these proteins in viral persistence and pathogenesis in animal models of HTLV-1 and HTLV-2 infection.
UR - http://www.scopus.com/inward/record.url?scp=4644248241&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=4644248241&partnerID=8YFLogxK
U2 - 10.1128/JVI.78.20.11077-11083.2004
DO - 10.1128/JVI.78.20.11077-11083.2004
M3 - Article
C2 - 15452228
AN - SCOPUS:4644248241
VL - 78
SP - 11077
EP - 11083
JO - Journal of Virology
JF - Journal of Virology
SN - 0022-538X
IS - 20
ER -