In Vivo generation of antigenic variants of murine retroviruses

Pozsgay, Judith M.; Klyczek, Karen K.; Blank, Kenneth J.

doi:10.1016/0042-6822(89)90251-1

Cited by 17 publications

(6 citation statements)

References 23 publications

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“…E55+ murine leukemia virus (MuLV) is a replication‐competent retrovirus with high sequence homology to the helper component of Friend virus (33). Unlike Friend virus, which is an acute transforming virus, E55+MuLV is a chronic transforming virus that causes leukemia in susceptible strains of mice (BALB/c) 5–8 months post‐infection (34). E55+MuLV also demonstrates a unique characteristic: resistant strains of mice (C57BL) express high levels of virus early after infection but do not develop leukemia (35).…”

Section: Primary Virus Infections In Aged Micementioning

confidence: 99%

Response of aged mice to primary virus infections

Murasko

Jiang

2005

Immunological Reviews

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Aging is associated with an increased morbidity to virus infections as well as a delay in clearance of symptoms after infection. Studies of sublethal virus infections of aged mice closely mirror the human situation: there is a delay in clearance of virus. The delay in virus clearance is accompanied by a delay and a decrease in T-cell response, particularly of CD8(+) T cells. Intrinsic alterations of T cells of aged mice contribute to this decrease in virus-specific T-cell response; however, evidence suggests that environmental or innate components of the aged host also influence this age-associated decline in clearance of virus. While the changes in the adaptive immune response have been carefully described, the early events in the generation of the T-cell response after virus infection have received limited attention. Importantly, age-associated changes in the innate response to virus infection, particularly production of and response to interferon (IFN)-alpha/beta, cytotoxicity and IFN-gamma production by natural killer cells, interleukin-12 induction, and depletion of non-specific T cells early during virus infection need further evaluation.

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Section: Primary Virus Infections In Aged Micementioning

confidence: 99%

Response of aged mice to primary virus infections

Murasko

Jiang

2005

Immunological Reviews

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“…Mice demonstrating tumors were eliminated from the study. E55ϩMuLV was originally isolated from a spleen of BALB.K mice injected with cell-free culture supernatant from a T cell line derived from a leukemic mouse (10). The virus used in studies was propagated in vivo by i.p.…”

Section: Mice Virus and Infectionmentioning

confidence: 99%

Cutting Edge: T Cells from Aged Mice Are Resistant to Depletion Early During Virus Infection

Jiang

Anaraki

Blank³

et al. 2003

The Journal of Immunology

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Aging is associated with decreased expansion of T cells upon stimulation. In young mice, infection induces a transient T cell depletion followed by the development of an Ag-specific T cell response that controls the infection. We found that T cells were depleted early after infection with E55 + murine leukemia retrovirus in young, but not aged, mice. Adoptive transfer experiments showed donor T cells of young, but not aged, mice were depleted due to apoptosis in various tissues of young recipients. However, T cells of neither young nor aged donors were depleted in aged recipients. These results indicate that both environmental and intrinsic cellular properties limit depletion of T cells of aged mice and suggest a novel explanation for the decreased T cell response associated with aging.

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“…Immune responses to retroviral envelope proteins are regulated by MHC genes (45)(46)(47). Passage of the Gross MuLV in BALB/c-H-2k mice results in the generation of variant viruses that have lost specific gp70en°epitopes (48) . Although the structural differences between Gross virus and these variants have not yet been analyzed in detail, some MHC-controlled immunoselective pressure seems to be involved, in that sera from immunized H-2k mice fail to neutralize the variants, while immune sera from congenic H-2b mice can neutralize both wild-type and variant viruses.…”

Section: Resultsmentioning

confidence: 99%

A host gene regulates the structure of the transmembrane envelope protein of murine leukemia viruses.

Coppola

Thomas

1990

The Journal of Experimental Medicine

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Heterogeneity in the structure of the envelope proteins has been observed in many human and animal retroviruses and may influence pathogenicity. However, the biological significance of this heterogeneity and the mechanisms by which it is generated are poorly understood. We have studied a mouse model in which the envelope gene structure of lymphoma-associated viruses appears to be controlled by a single host gene. The inoculation of HRS and CWD mice with a leukemogenic murine leukemia virus (MuLV) results in recombination between the injected virus and envelope gene sequences of endogenous retroviruses. The genomes of HRS (class I) env recombinants and CWD (class II) env recombinants differ in the sequences encoding the NH2-terminal portion of the transmembrane envelope protein (TM). We have shown that an HRS gene linked to the MHC on chromosome 17 mediates a dominant selection for recombinant retroviruses with the class I envelope gene structure. CBA mice, which share the H-2k haplotype with HRS, also carry the dominant allele at this locus. This system provides a useful model for studies of host factors involved in the selection of specific variants of pathogenic retroviruses.

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In Vivo generation of antigenic variants of murine retroviruses

Cited by 17 publications

References 23 publications

Response of aged mice to primary virus infections

Response of aged mice to primary virus infections

Cutting Edge: T Cells from Aged Mice Are Resistant to Depletion Early During Virus Infection

A host gene regulates the structure of the transmembrane envelope protein of murine leukemia viruses.

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