Boname Jessica M, Coleman Heather M, May Janet S, Stevenson Philip G
Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK.
J Gen Virol. 2004 Jan;85(Pt 1):131-135. doi: 10.1099/vir.0.19592-0.
A murine gammaherpesvirus-68 (MHV-68) mutant with deregulated transcription of its ORF50 transactivator was severely impaired in latency establishment. The deregulated virus showed reduced immunogenicity, probably reflecting a lower antigen load. However, it still elicited effective immunity to a subsequent wild-type (WT) virus challenge. Infection was not completely prevented, but was very substantially reduced in extent and the long-term level of WT viral DNA in lungs and spleens remained low. Thus latency-deficient MHV-68 illustrates a possible general approach to creating attenuated gammaherpesvirus vaccines that can protect against pathogenic WT infections.
一种其ORF50反式激活因子转录失调的鼠γ疱疹病毒68（MHV - 68）突变体在潜伏感染建立过程中严重受损。转录失调的病毒免疫原性降低，这可能反映出抗原负载较低。然而，它仍然能引发对随后野生型（WT）病毒攻击的有效免疫。感染并未被完全阻止，但程度上大幅降低，并且肺和脾中WT病毒DNA的长期水平仍然很低。因此，潜伏缺陷型MHV - 68阐明了一种可能的通用方法，用于制备能够预防致病性WT感染的减毒γ疱疹病毒疫苗。
