Publications by authors named "H Fukushi"
Previous studies showed that deletion of the viral thymidine kinase (TK) gene in several alphaherpesviruses including EHV-1 reduced their virulence. Previously, we found that deletion of ORF37, which is located head-to-head with TK, decreased EHV-1 virulence in mice but did not affect the expression of TK mRNA. Therefore, deletion of ORF38 might also affect virulence by partially deleting the ORF37 promoter.
View Article and Find Full Text PDFEquine herpesvirus type 1 (EHV-1) causes rhinopneumonitis, abortion, and neurological outbreaks (equine herpesvirus myeloencephalopathy, EHM) in horses. EHV-1 also causes lethal encephalitis in small laboratory animals such as mice and hamsters experimentally. EHV-1 ORF76 is a homolog of HSV-1 US9, which is a herpesvirus kinase.
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- * A specific genetic variation (SNP) in the DNA polymerase gene affects the virus's ability to cause neuro-related conditions, with the D752 variant being linked to neuropathogenic effects and the N752 variant being non-neuropathogenic.
- * Experiments on Syrian hamsters showed that while the N752 mutation didn't change viral growth in cells, it significantly reduced the neurovirulence of the virus, indicating that this mutation may have similar implications in both horses and hamsters.
Equine herpesvirus-1 (EHV-1) causes respiratory diseases, abortion, and encephalomyelitis in horses. The EHV-1 immediate-early (IE) protein, essential for viral replication, is transactivated by the binding of a multiprotein complex including the open reading frame 12 (ORF12) and some host factors to the IE promoter region. Promoter-associated non-coding RNAs (pancRNAs), which are transcribed from bidirectional promoters, regulate the transcription of neighboring genes in mammals and pathogens.
View Article and Find Full Text PDFEquine herpesvirus 1 (EHV-1) causes respiratory illness, fetal loss, perinatal mortality, and myeloencephalopathy. This study investigated ORF15's impact on virus infectivity and neurovirulence. The Ab4p neurovirulent strain of EHV1 was used as a backbone to create Ab4p attB, Ab4p∆ORF15, and Ab4p∆ORF15R chimeras via BAC DNA transfection into RK-13 cells.
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