Coxsackievirus B3-resistant mice become susceptible in Se/vitamin E deficiency
The severity of the heart damage caused by a coxsackievirus infection in mice is determined by several factors, including the genotype of the infecting virus as well as the genetic background of the infected host. Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype...
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| Veröffentlicht in: | Free radical biology & medicine 2003-05, Vol.34 (10), p.1263-1270 |
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| creator | Beck, Melinda A Williams-Toone, Deitra Levander, Orville A |
| description | The severity of the heart damage caused by a coxsackievirus infection in mice is determined by several factors, including the genotype of the infecting virus as well as the genetic background of the infected host. Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. Our results demonstrate the powerful influence of host nutritional status on the course of viral infection compared to other variables traditionally considered to play major roles in determining the extent of virally induced inflammatory heart disease. |
| doi_str_mv | 10.1016/S0891-5849(03)00101-1 |
| format | Article |
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Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. 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Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. Our results demonstrate the powerful influence of host nutritional status on the course of viral infection compared to other variables traditionally considered to play major roles in determining the extent of virally induced inflammatory heart disease.</description><subject>alpha-Tocopherol - metabolism</subject><subject>Animals</subject><subject>Cell Division - drug effects</subject><subject>Coxsackievirus</subject><subject>Diet</subject><subject>Disease resistance</subject><subject>Disease Susceptibility</subject><subject>Drug Resistance, Viral</subject><subject>Enterovirus B, Human - genetics</subject><subject>Enterovirus B, Human - pathogenicity</subject><subject>Enterovirus Infections - genetics</subject><subject>Enterovirus Infections - metabolism</subject><subject>Enterovirus Infections - pathology</subject><subject>Enterovirus Infections - virology</subject><subject>Free radicals</subject><subject>Genotype</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Humans</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocarditis</subject><subject>Myocarditis - genetics</subject><subject>Myocarditis - metabolism</subject><subject>Myocarditis - pathology</subject><subject>Myocarditis - virology</subject><subject>Nutritional Status</subject><subject>Oxidative damage</subject><subject>Oxidative Stress</subject><subject>Selenium</subject><subject>Selenium - deficiency</subject><subject>Spleen - metabolism</subject><subject>Tocopherol</subject><subject>Virus</subject><subject>Vitamin E</subject><subject>Vitamin E Deficiency - complications</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1PwzAMhiMEYmPwE0A9ITiUOU3SpicE0_iQJjgMzlGSulKgXUfSTuzf030IjpxsWc9rWw8h5xRuKNB0PAeZ01hInl8BuwbohzE9IEMqMxZzkaeHZPiLDMhJCB8AwAWTx2RAkyxJc8qH5GXSfAdtPx2unO9CdM9ij8GFVi_aqHYWI4O2qTEKXbC4bJ2pMHKLaI7jlWt13bfTqMDSWYcLuz4lR6WuAp7t64i8P0zfJk_x7PXxeXI3iy3nvI2lAF5qbnIAZqQwhlrGLdMGNcg0F2AomiIVqRHG0tJaliCYns0SLtNSsBG53O1d-uarw9Cq2vX_VZVeYNMFlbEkFTRj_4IJSM6ZhB4UO9D6JgSPpVp6V2u_VhTUxrjaGlcbnQqY2hpXtM9d7A90psbiL7VX3AO3OwB7HyuHXoWtKyycR9uqonH_nPgBI3mP9w</recordid><startdate>20030515</startdate><enddate>20030515</enddate><creator>Beck, Melinda A</creator><creator>Williams-Toone, Deitra</creator><creator>Levander, Orville A</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20030515</creationdate><title>Coxsackievirus B3-resistant mice become susceptible in Se/vitamin E deficiency</title><author>Beck, Melinda A ; Williams-Toone, Deitra ; Levander, Orville A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-8504fa4b9003b85bb1c34c3abea086950b1ebd656b5bc1fcc32e0b03b72486f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>alpha-Tocopherol - metabolism</topic><topic>Animals</topic><topic>Cell Division - drug effects</topic><topic>Coxsackievirus</topic><topic>Diet</topic><topic>Disease resistance</topic><topic>Disease Susceptibility</topic><topic>Drug Resistance, Viral</topic><topic>Enterovirus B, Human - genetics</topic><topic>Enterovirus B, Human - pathogenicity</topic><topic>Enterovirus Infections - genetics</topic><topic>Enterovirus Infections - metabolism</topic><topic>Enterovirus Infections - pathology</topic><topic>Enterovirus Infections - virology</topic><topic>Free radicals</topic><topic>Genotype</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Humans</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Myocarditis</topic><topic>Myocarditis - genetics</topic><topic>Myocarditis - metabolism</topic><topic>Myocarditis - pathology</topic><topic>Myocarditis - virology</topic><topic>Nutritional Status</topic><topic>Oxidative damage</topic><topic>Oxidative Stress</topic><topic>Selenium</topic><topic>Selenium - deficiency</topic><topic>Spleen - metabolism</topic><topic>Tocopherol</topic><topic>Virus</topic><topic>Vitamin E</topic><topic>Vitamin E Deficiency - complications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beck, Melinda A</creatorcontrib><creatorcontrib>Williams-Toone, Deitra</creatorcontrib><creatorcontrib>Levander, Orville A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beck, Melinda A</au><au>Williams-Toone, Deitra</au><au>Levander, Orville A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coxsackievirus B3-resistant mice become susceptible in Se/vitamin E deficiency</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2003-05-15</date><risdate>2003</risdate><volume>34</volume><issue>10</issue><spage>1263</spage><epage>1270</epage><pages>1263-1270</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>The severity of the heart damage caused by a coxsackievirus infection in mice is determined by several factors, including the genotype of the infecting virus as well as the genetic background of the infected host. Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. Our results demonstrate the powerful influence of host nutritional status on the course of viral infection compared to other variables traditionally considered to play major roles in determining the extent of virally induced inflammatory heart disease.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12726914</pmid><doi>10.1016/S0891-5849(03)00101-1</doi><tpages>8</tpages></addata></record> |
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| subjects | alpha-Tocopherol - metabolism Animals Cell Division - drug effects Coxsackievirus Diet Disease resistance Disease Susceptibility Drug Resistance, Viral Enterovirus B, Human - genetics Enterovirus B, Human - pathogenicity Enterovirus Infections - genetics Enterovirus Infections - metabolism Enterovirus Infections - pathology Enterovirus Infections - virology Free radicals Genotype Glutathione Peroxidase - metabolism Humans Killer Cells, Natural - immunology Killer Cells, Natural - metabolism Male Mice Mice, Inbred C57BL Myocarditis Myocarditis - genetics Myocarditis - metabolism Myocarditis - pathology Myocarditis - virology Nutritional Status Oxidative damage Oxidative Stress Selenium Selenium - deficiency Spleen - metabolism Tocopherol Virus Vitamin E Vitamin E Deficiency - complications |
| title | Coxsackievirus B3-resistant mice become susceptible in Se/vitamin E deficiency |
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