ArticleVirology2008
APOBEC3G-independent reduction in virion infectivity during long-term HIV-1 replication in terminally differentiated macrophages.
Article in Virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Microglia: The Real Foe in HIV-1-Associated Neurocognitive Disorders?Biomedicines · 2021Review
- The Role of Macrophages in HIV-1 Persistence and Pathogenesis.Frontiers in microbiology · 2019Review
- HIV-1 latency in monocytes/macrophages.Viruses · 2014Review
- HIV accessory proteins versus host restriction factors.Current opinion in virology · 2013Review
- Antiviral Mechanism and Biochemical Basis of the Human APOBEC3 Family.Frontiers in microbiology · 2012Article
- Viral determinants of HIV-1 macrophage tropism.Viruses · 2011Review
- Stably expressed APOBEC3F has negligible antiviral activity.Journal of virology · 2010Article
- An extended structure of the APOBEC3G catalytic domain suggests a unique holoenzyme model.Journal of molecular biology · 2009Article
- Vpu enhances HIV-1 virus release in the absence of Bst-2 cell surface down-modulation and intracellular depletion.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Differential sensitivity of "old" versus "new" APOBEC3G to human immunodeficiency virus type 1 vif.Journal of virology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
APOBEC3G (APO3G) is a cellular cytidine deaminase with potent antiviral activity. In the case of HIV, the antiviral activity of APO3G is counteracted by the viral Vif protein. Monocyte-derived macrophages (MDM) are terminally differentiated, non-dividing cells susceptible to HIV infection. Human MDM are known to express APO3G and HIV replication in these cells is dependent on Vif. Here we analyzed the correlation between HIV-1 replication and APO3G expression in MDM. Replication of wild type HIV-1 induced a gradual 4-5-fold reduction in APO3G expression. The efficiency of APO3G downregulation correlated with the efficiency of virus replication. Interestingly, despite downregulation of APO3G, the relative infectivity of viruses rapidly declined during the course of infection and was already reduced approximately 90% prior to peak virus production. Cell-free virus preparations showed increased levels of a 41 kDa MA-CA processing intermediate. Sequence analysis around the MA-CA cleavage site and the protease and LTR regions did not reveal deaminase-induced hypermutation of the viral genome, suggesting that APO3G activity is not responsible for the incomplete Gag processing. Thus, the loss of infectivity of HIV-1 viruses produced from long-term infected primary macrophages is due to an APO3G-independent mechanism.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.