Link to the University of Pittsburgh Homepage
Link to the University Library System Homepage Link to the Contact Us Form

The base excision repair pathway is required for efficient lentivirus integration

Yoder, KE and Espeseth, A and Wang, XH and Fang, Q and Russo, MT and Lloyd, RS and Hazuda, D and Sobol, RW and Fishel, R (2011) The base excision repair pathway is required for efficient lentivirus integration. PLoS ONE, 6 (3).

[img]
Preview
PDF
Published Version
Available under License : See the attached license file.

Download (1MB) | Preview
[img] Plain Text (licence)
Available under License : See the attached license file.

Download (1kB)

Abstract

An siRNA screen has identified several proteins throughout the base excision repair (BER) pathway of oxidative DNA damage as important for efficient HIV infection. The proteins identified included early repair factors such as the base damage recognition glycosylases OGG1 and MYH and the late repair factor POLß, implicating the entire BER pathway. Murine cells with deletions of the genes Ogg1, Myh, Neil1 and Polß recapitulate the defect of HIV infection in the absence of BER. Defective infection in the absence of BER proteins was also seen with the lentivirus FIV, but not the gammaretrovirus MMLV. BER proteins do not affect HIV infection through its accessory genes nor the central polypurine tract. HIV reverse transcription and nuclear entry appear unaffected by the absence of BER proteins. However, HIV integration to the host chromosome is reduced in the absence of BER proteins. Pre-integration complexes from BER deficient cell lines show reduced integration activity in vitro. Integration activity is restored by addition of recombinant BER protein POLß. Lentiviral infection and integration efficiency appears to depend on the presence of BER proteins. © 2011 Yoder et al.


Share

Citation/Export:
Social Networking:
Share |

Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Yoder, KE
Espeseth, A
Wang, XH
Fang, Q
Russo, MT
Lloyd, RS
Hazuda, D
Sobol, RWrws9@pitt.eduRWS9
Fishel, R
Centers: Other Centers, Institutes, Offices, or Units > Hillman Cancer Center
Other Centers, Institutes, Offices, or Units > Pittsburgh Cancer Institute
Date: 28 March 2011
Date Type: Publication
Journal or Publication Title: PLoS ONE
Volume: 6
Number: 3
DOI or Unique Handle: 10.1371/journal.pone.0017862
Schools and Programs: Graduate School of Public Health > Human Genetics
School of Medicine > Pharmacology and Chemical Biology
Refereed: Yes
MeSH Headings: Active Transport, Cell Nucleus; Animals; Cell Line; Cell Nucleus--metabolism; Cell Survival; DNA Damage; DNA Repair--genetics; DNA, Complementary--genetics; DNA, Viral--genetics; Gene Deletion; HIV Infections--genetics; Humans; Lentivirus--physiology; Lentivirus Infections--genetics; Mice; Reverse Transcription--genetics; Signal Transduction--genetics; Time Factors; Virus Integration--genetics
Other ID: NLM PMC3063173
PubMed Central ID: PMC3063173
PubMed ID: 21448280
Date Deposited: 30 Aug 2012 14:33
Last Modified: 05 Feb 2019 16:55
URI: http://d-scholarship.pitt.edu/id/eprint/13815

Metrics

Monthly Views for the past 3 years

Plum Analytics

Altmetric.com


Actions (login required)

View Item View Item