Source:http://linkedlifedata.com/resource/pubmed/id/11207313
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2001-3-14
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| pubmed:abstractText |
Whether or not NO plays a critical role in murine CMV (MCMV) infection has yet to be elucidated. In this study, we examined the role of NO in acute infection with MCMV using NO synthase type 2 (NOS2)-deficient mice. NOS2(-/-) mice were more susceptible to lethal infection with MCMV than NOS2(+/+) mice and generated a much higher peak virus titer in the salivary gland after acute infection. A moderate increase in the MCMV titer was also observed in other organs of NOS2(-/-) mice such as the spleen, lung, and liver. The immune responses to MCMV infection including NK cell cytotoxicity and CTL response in NOS2(-/-) mice were comparable with those of NOS2(+/+) mice. Moreover, the ability to produce IFN-gamma is not impaired in NOS2(-/-) mice after MCMV infection. The peritoneal macrophages from NOS2(-/-) mice, however, exhibited a lower antiviral activity than those from NOS2(+/+) mice, resulting in an enhanced viral replication in macrophages themselves. Treatment of these cells from NOS2(+/+) mice with a selective NOS2 inhibitor decreased the antiviral activity to a level below that obtained with NOS2(-/-) mice. In addition, the absence of NOS2 and NOS2-mediated antiviral activity of macrophages resulted in not only an enhanced MCMV replication and a high mortality but also a consequent risk of the latency. It was thus concluded that the NOS2-mediated antiviral activity of macrophages via NO plays a protective role against MCMV infection at an early and late stage of the infection.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
166
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3533-41
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:11207313-Acute Disease,
pubmed-meshheading:11207313-Animals,
pubmed-meshheading:11207313-Cytotoxicity, Immunologic,
pubmed-meshheading:11207313-Herpesviridae Infections,
pubmed-meshheading:11207313-Interferon-gamma,
pubmed-meshheading:11207313-Killer Cells, Natural,
pubmed-meshheading:11207313-Macrophages, Peritoneal,
pubmed-meshheading:11207313-Mice,
pubmed-meshheading:11207313-Mice, Inbred BALB C,
pubmed-meshheading:11207313-Mice, Inbred C57BL,
pubmed-meshheading:11207313-Mice, Knockout,
pubmed-meshheading:11207313-Muromegalovirus,
pubmed-meshheading:11207313-Nitric Oxide Synthase,
pubmed-meshheading:11207313-Nitric Oxide Synthase Type II,
pubmed-meshheading:11207313-Survival Rate,
pubmed-meshheading:11207313-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:11207313-Viral Load,
pubmed-meshheading:11207313-Viral Plaque Assay,
pubmed-meshheading:11207313-Virus Latency,
pubmed-meshheading:11207313-Virus Replication
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| pubmed:year |
2001
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| pubmed:articleTitle |
Role of nitric oxide synthase type 2 in acute infection with murine cytomegalovirus.
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| pubmed:affiliation |
Department of Infectious Diseases, Tokai University School of Medicine, Isehara, Kanagawa, Japan. snoda@is.icc.u-tokai.ac.jp
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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