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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-4-28
pubmed:abstractText
In this work, a role for the genes encoding glycoproteins I (gI) and E (gE) and the US9 protein of bovine herpesvirus type 5 (BHV-5) in neuropathogenicity and reactivation of latent infections was examined. Calves infected intranasally with a gI/gE/US9 deleted recombinant shed up to 10(2.85) TCID50/ml infectious virus in nasal secretions. Calves infected with the wild type BHV-5 parental virus shed up to 10(5) TCID50/ml virus. No signs of disease were observed in calves infected with the recombinant virus, whereas those infected with wild type virus displayed respiratory and neurological signs. The recombinant was only able to reach the basal portions of the central nervous system. In contrast, wild type virus was found widespread within the brain. Reactivation with dexamethasone 60 days post-infection resulted in reactivation of wild type virus, whereas the recombinant virus could not be reactivated. These studies demonstrate that genes gI, gE and US9 of BHV-5 are important for its neuropathogenicity and its ability to reactive from latency.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0147-9571
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
187-96
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Experimental infection of calves with a gI, gE, US9 negative bovine herpesvirus type 5.
pubmed:affiliation
Laboratório de Virologia, Faculdade de Veterinária, Universidade Federal de Pelotas (UFPel), Campus Universitário, Caixa Postal 356, CEP 96010-900 Pelotas, RS, Brazil. sohubner@yahoo.com.br
pubmed:publicationType
Journal Article