ArticleJournal of virology2002
Characterization of producer cell-dependent restriction of murine leukemia virus replication.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Early detection of a two-long-terminal-repeat junction molecule in the cytoplasm of recombinant murine leukemia virus-infected cells.Journal of virology · 2004Article
- Lv2, a novel postentry restriction, is mediated by both capsid and envelope.Journal of virology · 2004Article
- As(2)O(3) enhances retroviral reverse transcription and counteracts Ref1 antiviral activity.Journal of virology · 2003Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that the human bronchocarcinoma cell line A549 produces poorly infectious gibbon ape leukemia virus-pseudotyped Moloney murine leukemia virus (MLV). In contrast, similar amounts of virions recovered from human fibrosarcoma HT1080 cells result in 10-fold-higher transduction rates (G. Duisit, A. Salvetti, P. Moullier, and F. Cosset, Hum. Gene Ther. 10:189-200, 1999). We have now extended this initial observation to other type-C envelope (Env) pseudotypes and analyzed the mechanism involved. Structural and morphological analysis showed that viral particles recovered from A549 (A549-MLV) and HT1080 (HT1080-MLV) cells were normal and indistinguishable from each other. They expressed equivalent levels of mature Env proteins and bound similarly to the target cells. Furthermore, incoming particles reached the cytosol and directed the synthesis of linear viral DNA equally efficiently. However, almost no detectable circular DNAs could be detected in A549-MLV-infected cells, indicating that the block of infection resulted from defective nuclear translocation of the preintegration complex. Interestingly, pseudotyping of A549-MLV with vesicular stomatitis virus glycoprotein G restored the amount of circular DNA forms as well as the transduction rates to HT1080-MLV levels, suggesting that the postentry blockage could be overcome by endocytic delivery of the core particles downstream of the restriction point. Thus, in contrast to the previously described target cell-dependent Fv-1 (or Fv1-like) restriction in mammalian cells (P. Pryciak and H. E. Varmus, J. Virol. 66:5959-5966, 1992; G. Towers, M. Bock, S. Martin, Y. Takeuchi, J. P. Stoye, and O. Danos, Proc. Natl. Acad. Sci. USA 97:12295-12299, 2000), we report here a new restriction of MLV replication that relies only on the producer cell type.
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.