ArticleJournal of virology1995
Involvement of a spliced and defective human foamy virus in the establishment of chronic infection.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- Smoldering oncolysis by foamy virus carrying CD19 as a CAR target escapes CAR T detection by genomic modification.Molecular therapy. Oncology · 2024Article
- Foamy Viruses, Bet, and APOBEC3 Restriction.Viruses · 2021Review
- Genome Analysis and Replication Studies of the African Green Monkey Simian Foamy Virus Serotype 3 Strain FV2014.Viruses · 2020Article
- Review
- Role of the single deaminase domain APOBEC3A in virus restriction, retrotransposition, DNA damage and cancer.The Journal of general virology · 2016Review
- Review
- Lentivirus restriction by diverse primate APOBEC3A proteins.Virology · 2013Article
- HTLV-3/4 and simian foamy retroviruses in humans: discovery, epidemiology, cross-species transmission and molecular virology.Virology · 2013Review
- Restriction of foamy viruses by APOBEC cytidine deaminases.Journal of virology · 2006Article
- Retroviral superinfection resistance.Retrovirology · 2005Review
- The antiretroviral activity of APOBEC3 is inhibited by the foamy virus accessory Bet protein.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Persistent infection with primate foamy virus type 1 increases human immunodeficiency virus type 1 cell binding via a Bet-independent mechanism.Journal of virology · 2004Article
- Early steps of retrovirus replicative cycle.Retrovirology · 2004Review
- A new retroelement constituted by a natural alternatively spliced RNA of murine replication-competent retroviruses.The EMBO journal · 2003Article
- The promyelocytic leukemia protein does not mediate foamy virus latency in vitro.Journal of virology · 2003Article
- Reactivation of a complex retrovirus is controlled by a molecular switch and is inhibited by a viral protein.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Further characterization of equine foamy virus reveals unusual features among the foamy viruses.Journal of virology · 2002Article
- Intra- and intercellular trafficking of the foamy virus auxiliary bet protein.Journal of virology · 2002Article
- Cell-type-specific regulation of the two foamy virus promoters.Journal of virology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human foamy retrovirus (HFV) is found as two proviruses (HFV and delta HFV) which differ by a splice-induced deletion within the bel1 transactivator gene. The defective delta HFV (which lacks a functional Bel1 but harbors an intronless bet gene) is predominantly found in nonlytic infections in vitro as well as in vivo. Here, we show that infection of cell lines stably transduced by delta HFV DNA with the highly lytic HFV leads to chronic infections characterized by an absence of lysis, a balanced ratio of HFV to delta HFV, and a persistent Bet expression accompanied by a shutoff of structural genes. While this system only partially reflects the natural situation, in which target cells are infected by HFV and delta HFV simultaneously, it strongly suggests that delta HFV is a defective interfering retrovirus. Accordingly, previous or concomitant exposure to delta HFV viruses greatly enhances the formation of lysis-resistant clones in culture after HFV infection. The inability of delta HFV proviruses encoding a mutated bet gene to induce chronic infection suggests a role for Bet in this process. Through a specific, splice-induced, genomic deletion, resulting in a switch from Bel1 to Bet expression, the lytic properties of HFV are progressively lost. Such programmed inactivation of a key gene represents a new regulatory mechanism of gene expression in retroviruses.
Indexed as
Identifiers
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.