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Virus Res. 2014 Nov 4;192:92-102. doi: 10.1016/j.virusres.2014.08.015. Epub 2014 Aug 30.

Target silencing of components of the conserved oligomeric Golgi complex impairs HIV-1 replication.

Author information

1
John T. Macdonald Foundation Department of Human Genetics, John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, 1501 NW 10th Ave, Miami, FL 33136, United States. Electronic address: s.liu8@med.miami.edu.
2
John T. Macdonald Foundation Department of Human Genetics, John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, 1501 NW 10th Ave, Miami, FL 33136, United States. Electronic address: mdominska@gmail.com.
3
John T. Macdonald Foundation Department of Human Genetics, John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, 1501 NW 10th Ave, Miami, FL 33136, United States. Electronic address: DDykxhoorn@med.miami.edu.

Abstract

All viruses require host cell factors to replicate. A large number of host factors have been identified that participate at numerous points of the human immunodeficiency virus 1 (HIV-1) life cycle. Recent evidence supports a role for components of the trans-Golgi network (TGN) in mediating early steps in the HIV-1 life cycle. The conserved oligomeric Golgi (COG) complex is a heteroctamer complex that functions in coat protein complex I (COPI)-mediated intra-Golgi retrograde trafficking and plays an important role in the maintenance of Golgi structure and integrity as well as glycosylation enzyme homeostasis. The targeted silencing of components of lobe B of the COG complex, namely COG5, COG6, COG7 and COG8, inhibited HIV-1 replication. This inhibition of HIV-1 replication preceded late reverse transcription (RT) but did not affect viral fusion. Silencing of the COG interacting protein the t-SNARE syntaxin 5, showed a similar defect in late RT product formation, strengthening the role of the TGN in HIV replication.

KEYWORDS:

Conserved oligomeric Golgi complex; HIV-dependency factors; Human immunodeficiency virus; Trans-Golgi network

PMID:
25179963
PMCID:
PMC4447101
DOI:
10.1016/j.virusres.2014.08.015
[Indexed for MEDLINE]
Free PMC Article

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