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Maturation of the HIV reverse transcription complex: putting the jigsaw together
Author(s) -
Warrilow David,
Tachedjian Gilda,
Harrich David
Publication year - 2009
Publication title -
reviews in medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.06
H-Index - 90
eISSN - 1099-1654
pISSN - 1052-9276
DOI - 10.1002/rmv.627
Subject(s) - biology , viral entry , transcription (linguistics) , microbiology and biotechnology , capsid , transcription factor , infectivity , cytoplasm , reverse transcriptase , virology , virus , genetics , viral replication , rna , gene , linguistics , philosophy
Upon HIV attachment, fusion and entry into the host cell cytoplasm, the viral core undergoes rearrangement to become the mature reverse transcription complex (RTC). Reduced infectivity of viral deletion mutants of the core proteins, capsid and negative factor (Nef), can be complemented by vesicular stomatitis virus (VSV) pseudotyping suggesting a role for these viral proteins in a common event immediately post‐entry. This event may be necessary for correct trafficking of the early complex. Enzymatic activation of the complex occurs either before or during RTC maturation, and may be dependent on the presence of deoxynucleotides in the host cell. The RTC initially becomes enlarged immediately after entry, which is followed by a decrease in its sedimentation rate consistent with core uncoating. Several HIV proteins associated with the RTC and recently identified host‐cell proteins are important for reverse transcription while genome‐wide siRNA knockdown studies have identified additional host cell factors that may be required for reverse transcription. Determining precisely how these proteins assist the RTC function needs to be addressed. Copyright © 2009 John Wiley & Sons, Ltd.