Quinolinic acid levels in a murine retrovirus-induced immunodeficiency syndrome

Yoshitatsu Sei, Ian A. Paul, Kuniaki Saito, Richard Layar, Janet W. Hartley, Herbert C. Morse, Phil Skolnick, Melvyn P. Heyes

研究成果: Article

37 引用 (Scopus)

抄録

Mice infected with the retrovirus mixture designated LP-BM5 murine leukemia virus (MuLV) develop an immunosuppressive disease. Quinolinic acid (QUIN) is an endogenous neurotoxic N-methyl-D-aspartate agonist that may contribute to the pathogenesis of HIV-associated neurologic disease. In the present study, the levels of QUIN in brain and blood were measured in mice infected with LP-BM5 MuLV and compared with those in uninfected mice and mice infected with the nonpathogenic strain of ecotropic MuLV (helper component of LP-BM5 MuLV). Infection with LP-BM5 MuLV resulted in progressive increases in blood QUIN levels beginning 2 weeks after inoculation that peaked by 16 weeks postinfection. QUIN levels were also increased in cerebral cortex, hippocampus, and striatum. In systemic tissues, QUIN levels were increased in lung, liver, and spleen. In contrast, infection with the ecotropic vital component of the LP-BM5 MuLV mixture was not associated with any changes in brain, blood, or systemic tissue QUIN levels, even though helper virus burdens were comparable to those in mice infected with LP-BM5 MuLV. Treatment of LP-BM5 MuLV-infected mice with the antiretroviral agent zidovudine (azidothymidine) significantly reduced blood and brain QUIN levels in association with reductions in vital load in brain and spleen. These observations suggest that elevated QUIN production is not attributable to productive infection with retrovirus per se but occurs in response to an agent or agents, such as cytokines, that are produced by the host in response to virus infection.

元の言語English
ページ(範囲)296-302
ページ数7
ジャーナルJournal of Neurochemistry
66
発行部数1
出版物ステータスPublished - 01-01-1996
外部発表Yes

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Quinolinic Acid
Murine Leukemia Viruses
Retroviridae
Viruses
Brain
Blood
Zidovudine
Spleen
Retroviridae Infections
Helper Viruses
Anti-Retroviral Agents
Viral Structures
Tissue
Virus Diseases
N-Methylaspartate
Immunosuppressive Agents
Infection
Nervous System Diseases
Cerebral Cortex
Hippocampus

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

これを引用

Sei, Y., Paul, I. A., Saito, K., Layar, R., Hartley, J. W., Morse, H. C., ... Heyes, M. P. (1996). Quinolinic acid levels in a murine retrovirus-induced immunodeficiency syndrome. Journal of Neurochemistry, 66(1), 296-302.
Sei, Yoshitatsu ; Paul, Ian A. ; Saito, Kuniaki ; Layar, Richard ; Hartley, Janet W. ; Morse, Herbert C. ; Skolnick, Phil ; Heyes, Melvyn P. / Quinolinic acid levels in a murine retrovirus-induced immunodeficiency syndrome. :: Journal of Neurochemistry. 1996 ; 巻 66, 番号 1. pp. 296-302.
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abstract = "Mice infected with the retrovirus mixture designated LP-BM5 murine leukemia virus (MuLV) develop an immunosuppressive disease. Quinolinic acid (QUIN) is an endogenous neurotoxic N-methyl-D-aspartate agonist that may contribute to the pathogenesis of HIV-associated neurologic disease. In the present study, the levels of QUIN in brain and blood were measured in mice infected with LP-BM5 MuLV and compared with those in uninfected mice and mice infected with the nonpathogenic strain of ecotropic MuLV (helper component of LP-BM5 MuLV). Infection with LP-BM5 MuLV resulted in progressive increases in blood QUIN levels beginning 2 weeks after inoculation that peaked by 16 weeks postinfection. QUIN levels were also increased in cerebral cortex, hippocampus, and striatum. In systemic tissues, QUIN levels were increased in lung, liver, and spleen. In contrast, infection with the ecotropic vital component of the LP-BM5 MuLV mixture was not associated with any changes in brain, blood, or systemic tissue QUIN levels, even though helper virus burdens were comparable to those in mice infected with LP-BM5 MuLV. Treatment of LP-BM5 MuLV-infected mice with the antiretroviral agent zidovudine (azidothymidine) significantly reduced blood and brain QUIN levels in association with reductions in vital load in brain and spleen. These observations suggest that elevated QUIN production is not attributable to productive infection with retrovirus per se but occurs in response to an agent or agents, such as cytokines, that are produced by the host in response to virus infection.",
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Sei, Y, Paul, IA, Saito, K, Layar, R, Hartley, JW, Morse, HC, Skolnick, P & Heyes, MP 1996, 'Quinolinic acid levels in a murine retrovirus-induced immunodeficiency syndrome', Journal of Neurochemistry, 巻. 66, 番号 1, pp. 296-302.

Quinolinic acid levels in a murine retrovirus-induced immunodeficiency syndrome. / Sei, Yoshitatsu; Paul, Ian A.; Saito, Kuniaki; Layar, Richard; Hartley, Janet W.; Morse, Herbert C.; Skolnick, Phil; Heyes, Melvyn P.

:: Journal of Neurochemistry, 巻 66, 番号 1, 01.01.1996, p. 296-302.

研究成果: Article

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T1 - Quinolinic acid levels in a murine retrovirus-induced immunodeficiency syndrome

AU - Sei, Yoshitatsu

AU - Paul, Ian A.

AU - Saito, Kuniaki

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AU - Hartley, Janet W.

AU - Morse, Herbert C.

AU - Skolnick, Phil

AU - Heyes, Melvyn P.

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N2 - Mice infected with the retrovirus mixture designated LP-BM5 murine leukemia virus (MuLV) develop an immunosuppressive disease. Quinolinic acid (QUIN) is an endogenous neurotoxic N-methyl-D-aspartate agonist that may contribute to the pathogenesis of HIV-associated neurologic disease. In the present study, the levels of QUIN in brain and blood were measured in mice infected with LP-BM5 MuLV and compared with those in uninfected mice and mice infected with the nonpathogenic strain of ecotropic MuLV (helper component of LP-BM5 MuLV). Infection with LP-BM5 MuLV resulted in progressive increases in blood QUIN levels beginning 2 weeks after inoculation that peaked by 16 weeks postinfection. QUIN levels were also increased in cerebral cortex, hippocampus, and striatum. In systemic tissues, QUIN levels were increased in lung, liver, and spleen. In contrast, infection with the ecotropic vital component of the LP-BM5 MuLV mixture was not associated with any changes in brain, blood, or systemic tissue QUIN levels, even though helper virus burdens were comparable to those in mice infected with LP-BM5 MuLV. Treatment of LP-BM5 MuLV-infected mice with the antiretroviral agent zidovudine (azidothymidine) significantly reduced blood and brain QUIN levels in association with reductions in vital load in brain and spleen. These observations suggest that elevated QUIN production is not attributable to productive infection with retrovirus per se but occurs in response to an agent or agents, such as cytokines, that are produced by the host in response to virus infection.

AB - Mice infected with the retrovirus mixture designated LP-BM5 murine leukemia virus (MuLV) develop an immunosuppressive disease. Quinolinic acid (QUIN) is an endogenous neurotoxic N-methyl-D-aspartate agonist that may contribute to the pathogenesis of HIV-associated neurologic disease. In the present study, the levels of QUIN in brain and blood were measured in mice infected with LP-BM5 MuLV and compared with those in uninfected mice and mice infected with the nonpathogenic strain of ecotropic MuLV (helper component of LP-BM5 MuLV). Infection with LP-BM5 MuLV resulted in progressive increases in blood QUIN levels beginning 2 weeks after inoculation that peaked by 16 weeks postinfection. QUIN levels were also increased in cerebral cortex, hippocampus, and striatum. In systemic tissues, QUIN levels were increased in lung, liver, and spleen. In contrast, infection with the ecotropic vital component of the LP-BM5 MuLV mixture was not associated with any changes in brain, blood, or systemic tissue QUIN levels, even though helper virus burdens were comparable to those in mice infected with LP-BM5 MuLV. Treatment of LP-BM5 MuLV-infected mice with the antiretroviral agent zidovudine (azidothymidine) significantly reduced blood and brain QUIN levels in association with reductions in vital load in brain and spleen. These observations suggest that elevated QUIN production is not attributable to productive infection with retrovirus per se but occurs in response to an agent or agents, such as cytokines, that are produced by the host in response to virus infection.

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Sei Y, Paul IA, Saito K, Layar R, Hartley JW, Morse HC その他. Quinolinic acid levels in a murine retrovirus-induced immunodeficiency syndrome. Journal of Neurochemistry. 1996 1 1;66(1):296-302.