PDF(Pubmed)
Abstract：
Gammaherpesviruses are ubiquitous, lifelong pathogens associated with multiple cancers that infect over 95% of the adult population. Increases in viral reactivation, due to stress and other unknown factors impacting the immune response, frequently precedes lymphomagenesis. One potential stressor that could promote viral reactivation and increase viral latency would be the myriad of infections from bacterial and viral pathogens that we experience throughout our lives. Using murine gammaherpesvirus 68 (MHV68), a mouse model of gammaherpesvirus infection, we examined the impact of bacterial challenge on gammaherpesvirus infection. We challenged MHV68 infected mice during the establishment of latency with nontypeable Haemophilus influenzae (NTHi) to determine the impact of bacterial infection on viral reactivation and latency. Mice infected with MHV68 and then challenged with NTHi, saw increases in viral reactivation and viral latency. These data support the hypothesis that bacterial challenge can promote gammaherpesvirus reactivation and latency establishment, with possible consequences for viral lymphomagenesis.
摘要：
γ疱疹病毒无处不在，与多种癌症相关的终生病原体感染超过95％的成年人。病毒再激活的增加，由于压力和其他未知因素影响免疫反应，经常先于淋巴发生。一种可能促进病毒再激活和增加病毒潜伏期的潜在应激源将是我们一生中经历的来自细菌和病毒病原体的无数感染。使用鼠γ疱疹病毒68（MHV68），γ疱疹病毒感染的小鼠模型，我们研究了细菌攻击对γ疱疹病毒感染的影响。我们在用不可分型的流感嗜血杆菌（NTHi）建立潜伏期期间对MHV68感染的小鼠进行了挑战，以确定细菌感染对病毒再激活和潜伏期的影响。小鼠感染了MHV68，然后用NTHi攻击，病毒再激活和病毒潜伏期增加。这些数据支持以下假设：细菌攻击可以促进γ疱疹病毒的再激活和潜伏期的建立，对病毒淋巴发生有可能的后果。
