The p13(II) protein of HTLV type 1: Comparison with mitochondrial proteinscoded by other human viruses

Citation
Dm. D'Agostino et al., The p13(II) protein of HTLV type 1: Comparison with mitochondrial proteinscoded by other human viruses, AIDS RES H, 16(16), 2000, pp. 1765-1770
Citations number
42
Categorie Soggetti
Immunology
Journal title
AIDS RESEARCH AND HUMAN RETROVIRUSES
ISSN journal
08892229 → ACNP
Volume
16
Issue
16
Year of publication
2000
Pages
1765 - 1770
Database
ISI
SICI code
0889-2229(20001101)16:16<1765:TPPOHT>2.0.ZU;2-D
Abstract
In addition to the essential regulatory proteins Rex and Tax, the HTLV-1 ge nome encodes several accessory proteins of yet undefined function, One of t hese "orphan" proteins, named p13(II), was recently shown to be selectively targeted to mitochondria and to induce specific changes in mitochondrial m orphology suggestive of altered inner membrane permeability and swelling. T his represented the first report of a retroviral gene product targeted to m itochondria, and suggested that p13(II)-induced alterations in the function of this organelle may play a role in HTLV-1 replication and/or pathogenesi s, The more recent findings that both Vpr and Tat of HIV-1 are targeted to mitochondria reinforces the proposed relevance of mitochondrial metabolism to the life cycle of retroviruses, Thus, p13(II), Vpr, and Tat can be added to the growing list of mitochondrial proteins produced by clinically impor tant human viruses, including Epstein-Barr virus, human cytomegalovirus, an d hepatitis B virus, Mitochondria are known to play a critical role by prov iding an amplification loop required for the execution of signaling pathway s leading to programmed cell death, The functional consequences of the inte ractions between viral proteins and mitochondria described so far have been attributed to either the positive or negative? control of apoptotic respon ses mediated by this organelle, Further analysis of the effects of p13(II) on mitochondrial function is likely to add to our understanding of the mech anisms underlying the development of HTLV-1-associated diseases.