Balb/3T3 cells chronically infected with N-tropic murine leukemia virus continue to express Fv-1b restriction

Duran-Troise, Graciela; Bassin, Robert H.; Wallace, Brenda F.; Rein, Alan

doi:10.1016/0042-6822(81)90329-9

Cited by 10 publications

(6 citation statements)

References 20 publications

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“…They show that mutations in the PR cleavage sites flanking CA result in the formation of VLPs that cannot abrogate the restriction factor. A requirement for Gag processing would explain why virus-producing cells still show complete Fv1 restriction (8). Further, the lack of abrogation seen with D54A and following expression of CA in mature form strongly suggests that in addition to processing, assembly of CA into cores is also required.…”

Section: Discussionmentioning

confidence: 99%

“…Despite the fact that the restriction factor can be abrogated by exposure to restricted virus at a high multiplicity of infection, chronically infected cell lines in which high levels of restricted Gag polyprotein are expressed can still restrict incoming virus (8,16). Two explanations, not necessarily mutually exclusive, might be advanced to explain this apparent paradox.…”

mentioning

confidence: 99%

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Capsid Processing Requirements for Abrogation of Fv1 and Ref1 Restriction

Dodding

Bock²,

Yap³

et al. 2005

J Virol

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Murine leukemia virus is restricted in mouse cells lines by a host factor known as Fv1 and in human cell lines by Ref1. Genetic evidence indicates that these restriction factors target the virus capsid (CA) protein. Restriction can be overcome by adding virus at a high multiplicity of infection, indicating that the restriction factors can be saturated. Cells preexposed to restricted virus will allow infection by a second virus which would normally be restricted. This phenomenon is known as abrogation; it provides us with a tool with which to study the interaction of virus with restriction factors. We tested the abilities of several Gag processing mutants to abrogate restriction. Our results show that CA must be cleaved from both p12 and nucleocapsid in order for the incoming virion to interact with the restriction factor. Endogenous expression of properly processed CA, however, failed to abrogate restriction. These results suggest that as well as being processed, CA must also be properly assembled in the form of a condensed viral core in order to interact with Fv1 and Ref1. This polymeric structure may contain restriction factor binding sites not present in monomeric CA.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Capsid Processing Requirements for Abrogation of Fv1 and Ref1 Restriction

Dodding

Bock²,

Yap³

et al. 2005

J Virol

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“…The only requirements are that the abrogating virus can enter the cell, and that it shares the restricted phenotype. Furthermore, restriction is not abrogated by the expression of endogenous Gag in the target cells [97]. This hints at a key role for a viral structural component, which requires virus maturation.…”

Section: Restriction Of Murine Leukemia Virus By Fv-1mentioning

confidence: 98%

“…Below the grey boxes are the sequence motifs of the Zn 2+ -coordinating catalytic centers, which have the consensus sequence for cytidine deaminases [316]. Asterisks denote amino acids inside the catalytic centers that, when mutated, have a severe impact on or cause a complete loss of antiviral function (LOF, positions 67,81,97,100,257,259,288,291). Positions 70, 91, 262, and 282 contain aromatic amino acids presumed to be necessary for binding to nucleic acids.…”

Section: Antiretroviral Activity Of Other Apobec Proteinsmentioning

confidence: 99%

Intracellular Restriction Factors In Mammalian Cells - An Ancient Defense System Finds A Modern Foe

Baumann¹

2006

CHR

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Cross-species transmission of retroviruses poses a threat to mammalian species. Zoonoses have given rise to devastating diseases because the host organism is not prepared to resist a new pathogen. Mammals have developed several layers of defense against viruses, including an intracellular antiretroviral defense, a part of innate immunity. Retroviral restrictions had been studied for decades using murine leukemia virus in mice, however it has become clear that primates too have intrinsic mechanisms to ward off infections by retroviruses. Several of these antiretroviral restriction mechanisms have recently been identified, with two particularly well described factors being members of the tripartite motif (Trim) and APOBEC families. Both systems provide a strong barrier against lentiviral infections. The viruses have developed countermeasures that allow them to replicate despite the host factors. This review discusses our current knowledge of this ancient battle between mammalian hosts and their retroviral opponents.

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“…Lv1 abrogation requires Gag cleavage, suggesting that the interacting domain on CA͞p2 is masked on the precursor protein, and implying that the interaction can only occur with incoming virions but not with virions in the process of exiting the cell. This would provide an explanation for the old observation that MLV producing cells are fully Fv1 protected (20). These observations would also suggest that unprocessed Gag cannot be used as bait for isolating REF1͞Lv1 either directly or by two hybrid approaches.…”

mentioning

confidence: 90%

An intracellular block to primate lentivirus replication

Stoye¹

2002

Proc. Natl. Acad. Sci. U.S.A.

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Balb/3T3 cells chronically infected with N-tropic murine leukemia virus continue to express Fv-1b restriction

Cited by 10 publications

References 20 publications

Capsid Processing Requirements for Abrogation of Fv1 and Ref1 Restriction

Capsid Processing Requirements for Abrogation of Fv1 and Ref1 Restriction

Intracellular Restriction Factors In Mammalian Cells - An Ancient Defense System Finds A Modern Foe

An intracellular block to primate lentivirus replication

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