ArticleJournal of virology2000
Second-site changes affect viability of amphotropic/ecotropic chimeric enveloped murine leukemia viruses.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Unique Structure and Distinctive Properties of the Ancient and Ubiquitous Gamma-Type Envelope Glycoprotein.Viruses · 2023Review
- Disrupting MLV integrase:BET protein interaction biases integration into quiescent chromatin and delays but does not eliminate tumor activation in a MYC/Runx2 mouse model.PLoS pathogens · 2019Article
- Phosphorylation Requirement of Murine Leukemia Virus p12.Journal of virology · 2016Article
- Repression of the Chromatin-Tethering Domain of Murine Leukemia Virus p12.Journal of virology · 2016Article
- Structural and sequencing analysis of local target DNA recognition by MLV integrase.Nucleic acids research · 2015Article
- Determinants of Moloney murine leukemia virus Gag-Pol and genomic RNA proportions.Journal of virology · 2014Article
- Viral DNA tethering domains complement replication-defective mutations in the p12 protein of MuLV Gag.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Moloney murine leukemia virus genomic RNA packaged in the absence of a full complement of wild type nucleocapsid protein.Virology · 2012Article
- cis-Acting determinants of 7SL RNA packaging by HIV-1.Journal of virology · 2012Article
- MuLV IN mutants responsive to HDAC inhibitors enhance transcription from unintegrated retroviral DNA.Virology · 2012Article
- Identification of residues outside of the receptor binding domain that influence the infectivity and tropism of porcine endogenous retrovirus.Journal of virology · 2008Article
- Effects of identity minimization on Moloney murine leukemia virus template recognition and frequent tertiary template-directed insertions during nonhomologous recombination.Journal of virology · 2007Article
- Adaptive evolution of a tagged chimeric gammaretrovirus: identification of novel cis-acting elements that modulate splicing.Journal of molecular biology · 2007Article
- Revealing domain structure through linker-scanning analysis of the murine leukemia virus (MuLV) RNase H and MuLV and human immunodeficiency virus type 1 integrase proteins.Journal of virology · 2006Article
- G541R within the 4070A TM protein regulates fusion in murine leukemia viruses.Journal of virology · 2003Article
- Role of the mutation Q252R in activating membrane fusion in the murine leukemia virus surface envelope protein.Journal of virology · 2003Article
- Mismatch extension during strong stop strand transfer and minimal homology requirements for replicative template switching during Moloney murine leukemia virus replication.Journal of molecular biology · 2003Article
- Structure and mechanism of a coreceptor for infection by a pathogenic feline retrovirus.Journal of virology · 2003Article
- G100R mutation within 4070A murine leukemia virus Env increases virus receptor binding, kinetics of entry, and viral transduction efficiency.Journal of virology · 2003Article
- Relationship between SU subdomains that regulate the receptor-mediated transition from the native (fusion-inhibited) to the fusion-active conformation of the murine leukemia virus glycoprotein.Journal of virology · 2002Article
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Authors and funding
2 authors.
Funding
Abstract
Chimeras were previously generated between the ecotropic (Moloney-MuLV) and amphotropic (4070A) SU and TM proteins of murine leukemia virus (MuLV). After passage in D17 cells, three chimeras with junctions in the C terminus of SU (AE5, AE6, and AE7), showed improved kinetics of viral spreading, suggesting that they had adapted. Sequencing of the viruses derived from the D17 cell lines revealed second-site changes within the env gene. Changes were detected in the receptor binding domain, the proline-rich region, the C terminus of SU, and the ectodomain of TM. Second-site changes were subcloned into the parental DNA, singly and in combination, and tested for viability. All viruses had maintained their original cloned mutations and junctions. Reconstruction and passage of AE7 or AE6 virus with single point mutations recovered the additional second-site changes identified in the parental population. The AE5 isolate required changes in the VRA, the VRC, the VRB-hinge region, and the C terminus of SU for efficient infection. Passage of virus, including the parental 4070A, in D17 cells resulted in a predominant G100R mutation within the receptor binding domain. Viruses were subjected to titer determination in three cell types, NIH 3T3, canine D17, and 293T. AE6 viruses with changes in the proline-rich region initially adapted for growth on D17 cells could infect all cell types tested. AE6-based chimeras with additional mutations in the C terminus of SU could infect D17 and 293T cells. Infection of NIH 3T3 cells was dependent on the proline-rich mutation. AE7-based chimeras encoding L538Q and G100R were impaired in infecting NIH 3T3 and 293T cells.
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