Huss Nicholas P, Majeed Sheikh Tahir, Wills Brandon M, Tarakanova Vera L, Brockman Kenneth L, Jondle Christopher N
Department of Investigative Medicine and Center for Immunobiology, Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI, 49007, USA.
Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
Virology. 2024 Sep;597:110153. doi: 10.1016/j.virol.2024.110153. Epub 2024 Jun 22.
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.
γ-疱疹病毒无处不在,是与多种癌症相关的终身病原体,感染了超过95%的成年人口。由于压力和其他影响免疫反应的未知因素导致的病毒再激活增加,通常先于淋巴瘤的发生。我们一生中经历的无数细菌和病毒病原体感染,可能是促进病毒再激活和增加病毒潜伏的一个潜在应激源。利用鼠γ-疱疹病毒68(MHV68)这一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。我们在用不可分型流感嗜血杆菌(NTHi)建立潜伏期间对感染MHV68的小鼠进行攻击,以确定细菌感染对病毒再激活和潜伏的影响。感染MHV68然后用NTHi攻击的小鼠,病毒再激活和病毒潜伏增加。这些数据支持这样的假设,即细菌攻击可促进γ-疱疹病毒再激活和潜伏建立,可能对病毒淋巴瘤的发生产生影响。