γ-Herpesviruses establish latent infections of lymphocytes and drive their proliferation, causing cancers and motivating a search for vaccines. Effective vaccination against murid herpesvirus-4 (MuHV-4)-driven lymphoproliferation by latency-impaired mutant viruses suggests that lytic access to the latency reservoir is a viable target for control. However, the vaccines retained the immunogenic MuHV-4 M2 latency gene. Here, a strong reduction in challenge virus load was maintained when the challenge virus lacked the main latency-associated CD8+ T-cell epitope of M2, or when the vaccine virus lacked M2 entirely. This protection was maintained also when the vaccine virus lacked both episome maintenance and the genomic region encompassing M1, M2, M3, M4 and ORF4. Therefore, protection did not require immunity to known MuHV-4 latency genes. As the remaining vaccine virus genes have clear homologs in human γ-herpesviruses, this approach of deleting viral latency genes could also be applied to them, to generate safe and effective vaccines against human disease.

中文翻译：

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当初免病毒缺乏已知的潜伏基因时，可以维持针对多重疱疹病毒4的疫苗保护。

γ-疱疹病毒可建立淋巴细胞的潜伏感染并驱动其增殖，从而引发癌症并促进人们寻找疫苗。对潜伏期受损的突变病毒进行的针对鼠疱疹病毒4（MuHV-4）驱动的淋巴增殖的有效疫苗接种表明，对潜伏期水库的裂解访问是控制的可行目标。但是，疫苗保留了具有免疫原性的MuHV-4 M2潜伏期基因。在这里，当挑战病毒缺少M2的主要潜伏期相关CD8 + T细胞抗原决定簇时，或者当疫苗病毒完全缺乏M2时，挑战病毒的负载会大大降低。当疫苗病毒既缺乏附加体维护，又缺乏涵盖M1，M2，M3，M4和ORF4的基因组区域时，这种保护也得以维持。因此，保护​​不需要免疫已知的MuHV-4潜伏期基因。