A mouse gene on chromosome 5 that restricts infectivity of mink cell focus-forming recombinant murine leukemia viruses.

Hartley, Janet W.; Yetter, Robert A.; Morse, H C

doi:10.1084/jem.158.1.16

Cited by 89 publications

(76 citation statements)

References 22 publications

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“…Interference with a cellular receptor has also been observed for mouse gammaretroviruses. Mouse cells harboring certain integrated proviruses, ecotropic Fv4 or polytropic Rmcf or Rmcf2, which express MLV envelope genes, are resistant to exogenous ecotropic or polytropic MLV infection, respectively (5,16,18,50). Although the entry pathway for BVDV is CD46-dependent (30), we found that CD46 expression in MDBK-E1 * E2p7 * cells did not differ from pBabe control cells.…”

Section: Discussionmentioning

confidence: 62%

Transdominant Inhibition of Bovine Viral Diarrhea Virus Entry

Tscherne

Evans

MacDonald

et al. 2008

J Virol

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Bovine viral diarrhea virus (BVDV) is a positive-strand RNA virus and a member of the genus Pestivirus in the family Flaviviridae. To identify and characterize essential factors required for BVDV replication, a library expressing random fragments of the BVDV genome was screened for sequences that act as transdominant inhibitors of viral replication by conferring resistance to cytopathic BVDV-induced cell death. We isolated a BVDV-nonpermissive MDBK cell clone that harbored a 1.2-kb insertion spanning the carboxy terminus of the envelope glycoprotein 1 (E1), the envelope glycoprotein E2, and the amino terminus of p7. Confirming the resistance phenotype conferred by this library clone, naïve MDBK cells expressing this fragment were found to be 100-to 1,000-fold less permissive to both cytopathic and noncytopathic BVDV infection compared to parental MDBK cells, although these cells remained fully permissive to vesicular stomatitis virus. This restriction could be overcome by electroporation of BVDV RNA, indicating a block at one or more steps in viral entry prior to translation of the viral RNA. We determined that the E2 ectodomain was responsible for the inhibition to BVDV entry and that this block occurred downstream from BVDV interaction with the cellular receptor CD46 and virus binding, suggesting interference with a yet-unidentified BVDV entry factor.

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Section: Discussionmentioning

confidence: 62%

Transdominant Inhibition of Bovine Viral Diarrhea Virus Entry

Tscherne

Evans

MacDonald

et al. 2008

J Virol

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“…It has been noticed that DBA mice show immunological protection against FLV infection (36), whereas the immunological functions of C3H mice were severely deteriorated after infection with FLV (16,17). In addition, DBA mice have a gene called Rmcf (11) which causes resistance to the replication of Friend mink cell focus-inducing virus (MCFV) (33), whereas C3H mice are susceptible to it. Therefore, the state of Friend MCFV-induced erythroid cell proliferation may differ between DBA and C3H mice.…”

Section: Discussionmentioning

confidence: 99%

Friend Leukemia Virus Infection Enhances DNA Damage-Induced Apoptosis of Hematopoietic Cells, Causing Lethal Anemia in C3H Hosts

Kitagawa

Yamaguchi

Hasegawa

et al. 2002

J Virol

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Exposure of hematopoietic progenitors to gamma irradiation induces p53-dependent apoptosis. However, host responses to DNA damage are not uniform and can be modified by various factors. Here, we report that a split low-dose total-body irradiation (TBI) (1.5 Gy twice) to the host causes prominent apoptosis in bone marrow cells of Friend leukemia virus (FLV)-infected C3H mice but not in those of FLV-infected DBA mice. In C3H mice, the apoptosis occurs rapidly and progressively in erythroid cells, leading to lethal host anemia, although treatment with FLV alone or TBI alone induced minimal apoptosis in bone marrow cells. A marked accumulation of P53 protein was demonstrated in bone marrow cells from FLV-infected C3H mice 12 h after treatment with TBI. Although a similar accumulation of P53 was also observed in bone marrow cells from FLV-infected DBA mice treated with TBI, the amount appeared to be parallel to that of mice treated with TBI alone and was much lower than that of FLV-plus TBI-treated C3H mice. To determine the association of p53 with the prominent enhancement of apoptosis in FLV-plus TBI-treated C3H mice, p53 knockout mice of the C3H background (C3H p53 ؊/؊ ) were infected with FLV and treated with TBI. As expected, p53 knockout mice exhibited a very low frequency of apoptosis in the bone marrow after treatment with FLV plus TBI. Further, C3H p53 ؊/؊ 3 C3H p53 ؉/؉ bone marrow chimeric mice treated with FLV plus TBI survived even longer than the chimeras treated with FLV alone. These findings indicate that infection with FLV strongly enhances radiation-induced apoptotic cell death of hematopoietic cells in host animals and that the apoptosis occurs through a p53-associated signaling pathway, although the response was not uniform in different host strains.The specific induction of apoptosis to abnormal cells is one of the major treatment strategies for tumors as well as for virus-induced diseases. Therefore, trials to control apoptotic cell processes would be an attractive option for new therapeutic approaches to tumors or virus-induced diseases. To introduce apoptotic signals to the cell, many kinds of cell lines and stimuli have been employed in various experimental systems under physiological and pathological conditions. However, animal models still have priority when establishing the potential efficacy of a treatment in the sense that host reactions can be analyzed totally. In the present study, we investigated how retroviral infection modifies signals for DNA damage-induced apoptosis in hematopoietic cells by using an in vivo model of a Friend leukemia virus (FLV) infection system. The FLV is a murine retrovirus that can cause splenomegaly and induce erythroleukemia in susceptible mouse strains. The virus is a complex of two viruses: a replication-competent helper murine FLV and a replication-defective spleen focus-forming virus. It has been well established that FLV-induced leukemogenesis is genetically controlled by multiple non-H-2-linked virus susceptibility and/or resistance genes as well as H...

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“…Attempts to infect large numbers of cats with biologically cloned and replication-competent FeLV-B isolates was successful in only 15 to 20% of cats . Although FeLV-B resistance might be due to a more efficient immune response, we should also consider the possibility that the outbred cat population is heterogeneous at a genetic locus analogous to the murine Rmcf locus, which confers resistance to MCF virus replication (Hartley et al, 1983).…”

Section: Discussionmentioning

confidence: 99%