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Equine 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. Viral growth kinetics, plaque size, transcription, and growth were assessed in MDBK cells, mouse neurons, and fetal equine brain cells. Neurovirulence was evaluated post-intranasal inoculation into male CBA/N1 SPF mice, measuring signs, virus titers, and histopathological changes. Deletion of EUL45 (Ab4p-∆EUL45) reduced viral replication efficiency, resulting in decreased release and smaller plaques. EUL45 deletion also upregulated neighbouring genes (EUL46 and EUL44). Ab4p-∆EUL45 exhibited reduced virulence and poor growth in neural cells compared to wild-type viruses. This study sheds light on EUL45's role in EHV-1, viral replication, and regulation of EUL46 and EUL44 expression, suggesting potential as a vaccine candidate. • EHV-1 is associated with respiratory illness, fetal loss, perinatal mortality, and myeloencephalopathy. • Deletion of ORF15 (EUL45) (Ab4p-∆EUL45) reduced viral replication efficiency. • EUL45 deletion also upregulated neighbouring genes (EUL46 and EUL44). • Deletion of EUL45 reduced the virulence and lead to poor growth in neural cells compared to wild-type viruses. [ABSTRACT FROM AUTHOR]

Background: X-linked retinitis pigmentosa (XLRP) is a rare inherited retinal disease predominantly affecting males., Materials and Methods: A comprehensive literature review was conducted to determine the prevalence of retinitis pigmentosa GTPase regulator (RPGR) -mutated XLRP. Identified studies were used to estimate four components among males: the prevalence of retinitis pigmentosa (RP), the proportion of RP that was X-linked, the proportion of misclassified inheritance type among RP cases, and the proportion of XLRP that was RPGR -mutated. Studies providing a direct estimate of XLRP prevalence were also included. The components' sample size-weighted averages were combined to determine an overall prevalence estimate., Results: The prevalence of XLRP was estimated to be between 2.7-3.5 per 100,000 males in the US, Europe, and Australia. After correction for misclassification, the prevalence increased to 4.0-5.2 per 100,000 males. Finally, the proportion of XLRP cases due to RPGR mutations was applied, resulting in an RPGR -mutated XLRP estimate of 3.4-4.4 per 100,000 males. Studies from other countries were consistent with the results for the overall XLRP prevalence but were not included in the final calculation because of regional variations and lack of detailed information., Conclusions: These findings address an important gap in the understanding of RPGR -mutated XLRP by summarizing the global burden of this condition.