Abrogation of Fv-1 restriction by genome-deficient virions produced by a retrovirus packaging cell line

Boone, Lawrence R.; Innes, Cynthia L.; Heitman, Catherine K.

doi:10.1128/jvi.64.7.3376-3381.1990

Cited by 29 publications

(6 citation statements)

References 34 publications

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“…The viral determinants for NB-tropism were later mapped to the viral capsid (116). Furthermore, restriction could be abrogated by treatment of cells with inactive viral particles, indicating that Fv1 is a saturable capsid targeting factor (117,118). Unique among the resistance genes described here, Fv1 is also codominant, as Fv1 n/b heterozygous mice are resistant to both N-and B-tropic strains (113).…”

Section: Endogenous Retroelements Repurposed As Restriction Factorsmentioning

confidence: 83%

Mapping Viral Susceptibility Loci in Mice

Kane

Golovkina

2019

Annu. Rev. Virol.

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Genetic alleles that contribute to enhanced susceptibility or resistance to viral infections and virally induced diseases have often been first identified in mice before humans due to the significant advantages of the murine system for genetic studies. Herein we review multiple discoveries that have revealed significant insights into virus-host interactions, all made using genetic mapping tools in mice. Factors that have been identified include innate and adaptive immunity genes that contribute to host defense against pathogenic viruses such as herpes viruses, flaviviruses, retroviruses, and coronaviruses. Understanding the genetic mechanisms that affect infectious disease outcomes will aid the development of personalized treatment and preventive strategies for pathogenic infections.

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Section: Endogenous Retroelements Repurposed As Restriction Factorsmentioning

confidence: 83%

Mapping Viral Susceptibility Loci in Mice

Kane

Golovkina

2019

Annu. Rev. Virol.

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“…This observation puts Lv4 in good company with a growing family of restriction factors that target the retroviral CA. The CA-specific restriction factors Fv1 and TRIM5 can be saturated by virus-like particles (VLPs) bearing restriction-sensitive CA [ 40 , 43 , 81 , 82 ]. Attempts to saturate Lv4 with SIV MAC 239 virus-like particles were unsuccessful, though this result was not unexpected since Lv4 was only observed in blood cells, and saturation of CA-specific restriction activities in non-adherent cells that grow in suspension has not been reported [ 59 ].…”

Section: Discussionmentioning

confidence: 99%

Lv4 Is a Capsid-Specific Antiviral Activity in Human Blood Cells That Restricts Viruses of the SIVMAC/SIVSM/HIV-2 Lineage Prior to Integration

et al. 2015

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HIV-2 and SIVMAC are AIDS-causing, zoonotic lentiviruses that jumped to humans and rhesus macaques, respectively, from SIVSM-bearing sooty mangabey monkeys. Cross-species transmission events such as these sometimes necessitate virus adaptation to species-specific, host restriction factors such as TRIM5. Here, a new human restriction activity is described that blocks viruses of the SIVSM/SIVMAC/HIV-2 lineage. Human T, B, and myeloid cell lines, peripheral blood mononuclear cells and dendritic cells were 4 to >100-fold less transducible by VSV G-pseudotyped SIVMAC, HIV-2, or SIVSM than by HIV-1. In contrast, transduction of six epithelial cell lines was equivalent to that by HIV-1. Substitution of HIV-1 CA with the SIVMAC or HIV-2 CA was sufficient to reduce HIV-1 transduction to the level of the respective vectors. Among such CA chimeras there was a general trend such that CAs from epidemic HIV-2 Group A and B isolates were the most infectious on human T cells, CA from a 1° sooty mangabey isolate was the least infectious, and non-epidemic HIV-2 Group D, E, F, and G CAs were in the middle. The CA-specific decrease in infectivity was observed with either HIV-1, HIV-2, ecotropic MLV, or ALV Env pseudotypes, indicating that it was independent of the virus entry pathway. As2O3, a drug that suppresses TRIM5-mediated restriction, increased human blood cell transduction by SIVMAC but not by HIV-1. Nonetheless, elimination of TRIM5 restriction activity did not rescue SIVMAC transduction. Also, in contrast to TRIM5-mediated restriction, the SIVMAC CA-specific block occurred after completion of reverse transcription and the formation of 2-LTR circles, but before establishment of the provirus. Transduction efficiency in heterokaryons generated by fusing epithelial cells with T cells resembled that in the T cells, indicative of a dominant-acting SIVMAC restriction activity in the latter. These results suggest that the nucleus of human blood cells possesses a restriction factor specific for the CA of HIV-2/SIVMAC/SIVSM and that cross-species transmission of SIVSM to human T cells necessitated adaptation of HIV-2 to this putative restriction factor.

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“…One of the two major alleles of Fv1, Fv1 n , permits infection by N‐tropic but restricts B‐tropic MLV strains, while the other, Fv1 b , permits infection of B‐tropic infection but restricts N‐tropic infection. At low levels of infection, the resistance conferred by Fv1 can be substantial, but is overcome by inoculating cells with high titers of restricted virions (Decleve et al ., 1975; Tennant et al ., 1979; Boone et al ., 1990).…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, the abrogating virus must itself be restricted, and recognized by the restriction factor, in order to saturate it and facilitate infection. For example, treatment of target cells with high levels of N‐MLV abrogates Fv1 b ‐ or Ref1‐mediated restriction of N‐MLV reporter virus infection, whilst treatment with unrestricted B‐MLV does not (Boone et al ., 1990; Towers et al ., 2002).…”

Section: Introductionmentioning

confidence: 99%

Restriction of multiple divergent retroviruses by Lv1 and Ref1

2003

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The mouse gene Fv1 encodes a saturable restriction factor that selectively blocks infection by N‐tropic or B‐tropic murine leukemia virus (MLV) strains. Despite the absence of an Fv1 gene, a similar activity is present in humans that blocks N‐MLV infection (Ref1). Moreover, some non‐human primate cell lines express a potentially related inhibitor of HIV‐1 and/or SIVmac infection (Lv1). Here, we examine the spectrum of retrovirus‐restricting activities expressed by human and African green monkey cell lines. Human cells restrict N‐MLV and equine infectious anemia virus (EIAV), but not HIV‐1, HIV‐2, SIVmac or SIVagm, whilst AGM cells restrict N‐MLV, EIAV, HIV‐1, HIV‐2 and SIVmac. Remarkably, in each example examined, restriction of infection by a given retrovirus can be abrogated at least partially by saturation with another retrovirus, provided that it is also restricted but regardless of whether it is closely related. These data suggest that restriction factors in human and non‐human primate cells are able to recognize and block infection by multiple, widely divergent retroviruses and that the factors themselves may be related.

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Abrogation of Fv-1 restriction by genome-deficient virions produced by a retrovirus packaging cell line

Cited by 29 publications

References 34 publications

Mapping Viral Susceptibility Loci in Mice

Mapping Viral Susceptibility Loci in Mice

Lv4 Is a Capsid-Specific Antiviral Activity in Human Blood Cells That Restricts Viruses of the SIVMAC/SIVSM/HIV-2 Lineage Prior to Integration

Restriction of multiple divergent retroviruses by Lv1 and Ref1

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