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Effects of cell cycle status on early events in retroviral replication
Author(s) -
Katz Richard A.,
Greger James G.,
Skalka Anna Marie
Publication year - 2005
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20358
Subject(s) - retrovirus , biology , cell cycle , viral replication , stem cell , virology , vector (molecular biology) , gene , mitosis , cell type , cell , genetics , computational biology , virus , recombinant dna
The study of retroviruses over the last century has revealed a wide variety of disease‐producing mechanisms, as well as apparently harmless interactions with animal hosts. Despite their potential pathogenic properties, the intrinsic features of retroviruses have been harnessed to create gene transfer vectors that may be useful for the treatment of disease. Retroviruses, as all viruses, have evolved to infect specific cells within the host, and such specificities are relevant to both pathogenesis and retrovirus‐based vector design. The majority of cells of an animal host are not progressing rapidly through the cell cycle, and such a cellular environment appears to be suboptimal for replication of all retroviruses. Retrovirus‐based vectors can therefore be restricted in many important target cells, such as post‐mitotic differentiated cells or stem cells that may divide only infrequently. Despite intense interest, our understanding of how cell cycle status influences retroviral infection is still quite limited. In this review, we focus on the importance of the cell cycle as it relates to the early steps in retroviral replication. Retroviruses have been categorized based on their abilities to complete these early steps in non‐cycling cells. However, all retroviruses are subject to a variety of cell cycle restrictions. Here, we discuss such restrictions, and how they may block retroviral replication, be tolerated, or overcome. J. Cell. Biochem. 94: 880–889, 2005. © 2005 Wiley‐Liss, Inc.