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

Sicen Liu, Monika Dominska-Ngowe, Derek M Dykxhoorn

Research output: Contribution to journalArticle

5 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)92-102
Number of pages11
JournalVirus Research
Volume192
DOIs
StatePublished - Jan 1 2014

Fingerprint

Golgi Apparatus
Virus Replication
HIV-1
trans-Golgi Network
Life Cycle Stages
Reverse Transcription
Coat Protein Complex I
Qa-SNARE Proteins
SNARE Proteins
Glycosylation
Homeostasis
Maintenance
HIV
Viruses
Enzymes
Proteins

Keywords

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

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases
  • Cancer Research

Cite this

Target silencing of components of the conserved oligomeric Golgi complex impairs HIV-1 replication. / Liu, Sicen; Dominska-Ngowe, Monika; Dykxhoorn, Derek M.

In: Virus Research, Vol. 192, 01.01.2014, p. 92-102.

Research output: Contribution to journalArticle

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