| pubmed-article:15371153 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15371153 | lifeskim:mentions | umls-concept:C0971868 | lld:lifeskim |
| pubmed-article:15371153 | lifeskim:mentions | umls-concept:C0017968 | lld:lifeskim |
| pubmed-article:15371153 | lifeskim:mentions | umls-concept:C0332197 | lld:lifeskim |
| pubmed-article:15371153 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:15371153 | pubmed:dateCreated | 2004-9-16 | lld:pubmed |
| pubmed-article:15371153 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15371153 | pubmed:abstractText | Bovine herpesvirus type 5 (BHV-5) is an alphaherpesvirus that causes fatal encephalitis in calves. Envelope glycoproteins E (gE) and gI of alphaherpesviruses are important for the pathogenesis in vivo. Previously the authors determined that BHV-5 gE is important for BHV-5 neurovirulence. To determine the role of gI in BHV-5 neurovirulence, the authors have constructed gI-deleted and gI-revertant BHV-5 and analyzed their neuropathogenic properties in a rabbit seizure model. Following intranasal infection, 40% of the rabbits infected with the gI-deleted virus showed severe neurological signs. gI-deleted BHV-5 invaded all the central nervous system (CNS) structures invaded by the gI-revertant BHV-5; however, the number of neurons infected by the gI-deleted virus was similar or slightly reduced (two to four fold). Thus, the gI-deleted virus retained significant neurovirulence and/or neuroinvasive properties when compared with the gE-deleted BHV-5. Pulse-chase analysis revealed that the gE of gI-deleted virus was processed to a larger and a diffused 94- to 100-kDa protein (instead of 94 kDa). The 94- to 100-kDa protein was processed in the Golgi with delayed kinetics but it was endoglycosidase H (EndoH) resistant. In cells infected with gI-deleted virus, there was a reduction in cell-surface gE expression compared to wild-type, which correlated to reduced amount of gE processed in the Golgi. The authors believe that in the absence of gI, BHV-5 gE is sufficient for BHV-5 neurovirulence. | lld:pubmed |
| pubmed-article:15371153 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15371153 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15371153 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15371153 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15371153 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15371153 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15371153 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15371153 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15371153 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:15371153 | pubmed:issn | 1355-0284 | lld:pubmed |
| pubmed-article:15371153 | pubmed:author | pubmed-author:ChowdhuryS... | lld:pubmed |
| pubmed-article:15371153 | pubmed:author | pubmed-author:Al-MubarakAA | lld:pubmed |
| pubmed-article:15371153 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15371153 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:15371153 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15371153 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15371153 | pubmed:pagination | 233-43 | lld:pubmed |
| pubmed-article:15371153 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:meshHeading | pubmed-meshheading:15371153... | lld:pubmed |
| pubmed-article:15371153 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15371153 | pubmed:articleTitle | In the absence of glycoprotein I (gI), gE determines bovine herpesvirus type 5 neuroinvasiveness and neurovirulence. | lld:pubmed |
| pubmed-article:15371153 | pubmed:affiliation | Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan 66506, USA. | lld:pubmed |
| pubmed-article:15371153 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15371153 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15371153 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15371153 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15371153 | lld:pubmed |
