Cellular expression of murine leukemia virus gp70-related antigen on thymocytes of uninfected mice correlates with Fv-4 gene-controlled resistance to friend leukemia virus infection

Ikeda, Hidetoshi; Odaka, Takeshi

doi:10.1016/0042-6822(83)90324-0

Cited by 69 publications

(53 citation statements)

References 27 publications

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“…Understanding how these gene transfers influence the immunologic distinction between host "self " and viral "nonself " is of practical importance. Interestingly, several host genes derived from retroviruses limit infection by related viruses (Ikeda and Odaka 1983;Hainaut et al 1990;Mura et al 2004;Aswad and Katzourakis 2012;Fujino et al 2014;Yap et al 2014), demonstrating that lateral gene flow from viruses to their vertebrate hosts can mediate transgenerational immune memory; all known examples are mediated by production of dominant negative proteins. RNA-mediated transgenerational antiviral immunity, while common via the CRISPR/Cas system in prokaryotes (Sorek et al 2008), has thus far been reported in only one metazoan, Caenorhabditis elegans (Rechavi et al 2011).…”

Section: Introductionmentioning

confidence: 99%

piRNAs derived from ancient viral processed pseudogenes as transgenerational sequence-specific immune memory in mammals

Parrish

Fujino

Shiromoto

et al. 2015

RNA

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Endogenous bornavirus-like nucleoprotein elements (EBLNs) are sequences within vertebrate genomes derived from reverse transcription and integration of ancient bornaviral nucleoprotein mRNA via the host retrotransposon machinery. While species with EBLNs appear relatively resistant to bornaviral disease, the nature of this association is unclear. We hypothesized that EBLNs could give rise to antiviral interfering RNA in the form of PIWI-interacting RNAs (piRNAs), a class of small RNA known to silence transposons but not exogenous viruses. We found that in both rodents and primates, which acquired their EBLNs independently some 25-40 million years ago, EBLNs are present within piRNA-generating regions of the genome far more often than expected by chance alone (P = 8 × 10 −3 -6 × 10 −8 ). Three of the seven human EBLNs fall within annotated piRNA clusters and two marmoset EBLNs give rise to bona fide piRNAs. In both rats and mice, at least two of the five EBLNs give rise to abundant piRNAs in the male gonad. While no EBLNs are syntenic between rodent and primate, some of the piRNA clusters containing EBLNs are; thus we deduce that EBLNs were integrated into existing piRNA clusters. All true piRNAs derived from EBLNs are antisense relative to the proposed ancient bornaviral nucleoprotein mRNA. These observations are consistent with a role for EBLN-derived piRNA-like RNAs in interfering with ancient bornaviral infection. They raise the hypothesis that retrotransposon-dependent virus-to-host gene flow could engender RNA-mediated, sequence-specific antiviral immune memory in metazoans analogous to the CRISPR/Cas system in prokaryotes.

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Section: Introductionmentioning

confidence: 99%

piRNAs derived from ancient viral processed pseudogenes as transgenerational sequence-specific immune memory in mammals

Parrish

Fujino

Shiromoto

et al. 2015

RNA

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“…In human immunodeficiency virus (HIV)-infected cells, CD4 receptor molecules are depleted from the cell surface possibly because of the formation of intracellular complexes between viral envelope protein (Env) and receptor (Kawamura eta]., 1989;Crise et aI., 1990;Hart & Cloyd, 1990). The depletion of receptor is thought to be a cause of resistance to superinfection (Rubin, 1960;Vogt & Ishizaki, 1966;Rein, 1982;Granowitz et al, 1991) and natural resistance to retroviral infection in mice and chickens that carry certain endogenous envelope sequences (Gardner et al, 1980;Robinson eta]., 1981; Ikeda & Odaka, 1983;Ikeda eta]., 1985;Ikeda & Sugimura, 1989;lnaguma et al, 1992;Matano et al, 1993). In addition to Env, HIV encodes two proteins that play additional roles in the down-regulation of CD4: Vpu, an 81 amino acid protein encoded by the bicistronic mRNA that also encodes Env, accelerates degradation of CD4 (Willey et al, 1992;Chen et al, 1993) and Nef, Author for correspondence: Jonathan Silver.…”

Section: Introductionmentioning

confidence: 99%

Bimodal down-regulation of CD4 in cells expressing human immunodeficiency virus type 1 Vpu and Env

Fujita

Maldarelli²,

Silver³

1996

Journal of General Virology

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“…Ecotropic murine retroviruses generally have a restricted host range, due not only to the limited availability of their cellular receptor, mCAT-1 (58), but also to the various intrinsic restriction factors present in a specific host (7). Fv1 and Fv4 are the expression products of defective endogenous retroviruses that are present as germ line integrations and can interfere with and even block the infectivities of ecotropic retroviruses (6,25).…”

mentioning

confidence: 99%

The AKV Murine Leukemia Virus Is Restricted and Hypermutated by Mouse APOBEC3

Langlois

Kemmerich

Rada

et al. 2009

J Virol

107

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APOBEC3 proteins are potent restriction factors against retroviral infection in primates. This restriction is accompanied by hypermutations in the retroviral genome that are attributable to the cytidine deaminase activity of the APOBEC3 proteins. Studies of nucleotide sequence diversity among endogenous gammaretroviruses suggest that the evolution of endogenous retroelements could have been shaped by the mutagenic cytidine deaminase activity of APOBEC3. In mice, however, APOBEC3 appears to restrict exogenous murine retroviruses in the absence of detectable levels of deamination. AKV is an endogenous retrovirus that is involved in causing a high incidence of thymic lymphoma in AKR mice. A comparative analysis of several mouse strains revealed a relatively low level of APOBEC3 expression in AKR mice. Here we show that endogenous mouse APOBEC3 restricts AKV infection and that this restriction likely reflects polymorphisms affecting APOBEC3 abundance rather than differences in the APOBEC3 isoforms expressed. We also observe that restriction of AKV by APOBEC3 is accompanied by G3A hypermutations in the viral genome. Our findings demonstrate that APOBEC3 acts as a restriction factor in rodents affecting the strain tropism of AKV, and they provide good support for the proposal that APOBEC3-mediated hypermutation contributed to the evolution of endogenous rodent retroviral genomes.

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Cellular expression of murine leukemia virus gp70-related antigen on thymocytes of uninfected mice correlates with Fv-4 gene-controlled resistance to friend leukemia virus infection

Cited by 69 publications

References 27 publications

piRNAs derived from ancient viral processed pseudogenes as transgenerational sequence-specific immune memory in mammals

piRNAs derived from ancient viral processed pseudogenes as transgenerational sequence-specific immune memory in mammals

Bimodal down-regulation of CD4 in cells expressing human immunodeficiency virus type 1 Vpu and Env

The AKV Murine Leukemia Virus Is Restricted and Hypermutated by Mouse APOBEC3

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