Identification of a variant of gross leukemia virus that induces disease in mice inoculated as adults.

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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“…The virus used in studies was propagated in vivo by i.p. injections of immunocompromised BALB/c mice (11). Mice were infected 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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“…All cell lines reported now to be nonproducers were originally found to be nonproducers within 1 year of explantation. Culture times (years) for cell lines prior to study: >1:12,13,14,18,19,21,22,32,35,36,39,42,43,47,48,52,53,57,58,59,60,61,62, and 63; >2:10 and 17; >4:15; >9:4 and 9.…”

mentioning

confidence: 99%

Evidence for H-2-linked control of retrovirus production in Friend virus-induced tumor cell lines

Wolfe¹,

Blank²

1986

J Virol

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In Friend leukemia virus-induced tumor cell lines derived from mice congenic with respect to the H-2 complex, most cell lines expressing the H-2k haplotype continuously produced infectious exogenous virus in culture, whereas most cell lines expressing the H-2b or H-2d haplotype stopped producing virus during in vitro passage. This apparent H-2-linked control of virus production did not appear to be the result of alteration of the provirus or resistance to superinfection. The implications of this finding with respect to virus-induced leukemogenesis are discussed.

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“…Viruses. Two strains of GMuLV were used in these studies: parental NB tropic GMuLV and the WB91 strain of GMuLV (12) . Virus was expanded by passage in Sc-1 cells, a feral mouse embryo fibroblast line (American Type Culture Collection, Rockville, MD).…”

Section: Methodsmentioning

confidence: 99%

“…To address these questions, the immune response ofmice exposed as neonates to NB-tropic Gross murine leukemia virus (GMuLV) was investigated . Exposure of neonates to GMuLV induces a state ofimmunologic nonresponsiveness that may be linked to intrathymic replication of this retrovirus .1 Abbreviations used in this paper: DTH, delayed-type hypersensitivity; GMuLV, Gross murine leukemia virus ; HAU, hemagglutinating units; LCMV, lymphocytic choriomeningitis virus; PFU, plaque-forming units ; RT, reverse transcriptase.Intraperitoneal injection of neonatal mice with GMuLV leads to the development of lymphatic leukemias typified by the presence of thymic lymphomas, and to a unique form ofpersistent infection within the central nervous system white matter (11)(12)(13) . The data reported here demonstrate that neonatal exposure to these murine retroviruses also induced a state of virus-specific T cell nonresponsiveness, characterized by impaired delayed type hypersensitivity and in vitro proliferative responses.…”

mentioning

confidence: 99%

“…Intraperitoneal injection of neonatal mice with GMuLV leads to the development of lymphatic leukemias typified by the presence of thymic lymphomas, and to a unique form ofpersistent infection within the central nervous system white matter (11)(12)(13) . The data reported here demonstrate that neonatal exposure to these murine retroviruses also induced a state of virus-specific T cell nonresponsiveness, characterized by impaired delayed type hypersensitivity and in vitro proliferative responses.…”

mentioning

confidence: 99%

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Neonatal exposure to thymotropic gross murine leukemia virus induces virus-specific immunologic nonresponsiveness.

Korostoff

Nakada

Faas

et al. 1990

The Journal of Experimental Medicine

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SummaryNeonatal exposure to Gross murine leukemia virus results in a profound inhibition of the virusspecific T and B cell responses of adult animals. Animals exposed to virus as neonates exhibit a marked depression in virus-specific T cell function as measured by the virtual absence of in vivo delayed type hypersensitivity responses and in vitro proliferative responses to virally infected stimulator cells. Further, serum obtained from neonatally treated mice failed to either immunoprecipitate viral proteins or neutralize virus in an in vitro plaque assay, suggesting the concurrent induction of a state of B cell hyporesponsiveness . The specificity of this effect at the levels of both T and B cells was demonstrated by the ability ofneonatally treated mice to respond normally after adult challenge with either irrelevant reovirus or influenza virus. The replication of Gross virus within both stromal and lymphocytic compartments of the neonatal thymus suggests that thymic education plays a key role in the induction ofimmunologic nonresponsiveness to viruses. mmunologic nonresponsiveness to autologous molecules and a variety of exogenous antigens can be linked to their presence during neonatal maturation (1-4). The consequences of neonatal exposure to viruses are considerably more variable (5, 6). Mice infected either neonatally or congenitally with lymphocytic choriomeningitis virus (LCMV)' or endogenous ecotropic retroviruses mount potent Ig responses and produce functional CTL precursors (7-9) . However, several recent studies have shown that exposure of neonatal mice to Moloney murine leukemia virus significantly reduced the frequency ofMoloney virus-specific CTL precursors and Ig levels (6, 10) . These contrasting results raise important questions concerning the ability of different viruses to induce tolerance, and the contributions of T and B cell components to virus-specific tolerance . To address these questions, the immune response ofmice exposed as neonates to NB-tropic Gross murine leukemia virus (GMuLV) was investigated . Exposure of neonates to GMuLV induces a state ofimmunologic nonresponsiveness that may be linked to intrathymic replication of this retrovirus .1 Abbreviations used in this paper: DTH, delayed-type hypersensitivity; GMuLV, Gross murine leukemia virus ; HAU, hemagglutinating units; LCMV, lymphocytic choriomeningitis virus; PFU, plaque-forming units ; RT, reverse transcriptase.Intraperitoneal injection of neonatal mice with GMuLV leads to the development of lymphatic leukemias typified by the presence of thymic lymphomas, and to a unique form ofpersistent infection within the central nervous system white matter (11-13) . The data reported here demonstrate that neonatal exposure to these murine retroviruses also induced a state of virus-specific T cell nonresponsiveness, characterized by impaired delayed type hypersensitivity and in vitro proliferative responses. Concomitant with this T cell defect was the functional inactivation of virus-specific B cells, as evidenced by the absence ofbot...

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Identification of a variant of gross leukemia virus that induces disease in mice inoculated as adults.

Cited by 13 publications

References 11 publications

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

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

Evidence for H-2-linked control of retrovirus production in Friend virus-induced tumor cell lines

Neonatal exposure to thymotropic gross murine leukemia virus induces virus-specific immunologic nonresponsiveness.

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