首页> 外文期刊>Advances in Microbiology >Kinetics of &i&Candida albicans&/i& and &i&Staphylococcus aureus&/i& Biofilm Initiation on Herpes Simplex Virus (HSV-1 and HSV-2) Infected Cells
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Kinetics of &i&Candida albicans&/i& and &i&Staphylococcus aureus&/i& Biofilm Initiation on Herpes Simplex Virus (HSV-1 and HSV-2) Infected Cells

机译:& i&念珠菌的动力学& / i&和& i&金黄色葡萄球菌& / i&生物膜在单纯疱疹病毒(HSV-1和HSV-2)感染细胞上发起

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This study examines the kinetics of S. aureus and C. albicans adherence as it relates to HSV replication and corresponding dynamic display of shared receptors. HeLa cells infected for various times with HSV-1 gL86 or HSV-2 333gJ-(MOI 50) were incubated with S. aureus ATCC 25923 or C. albicans yeast and CFU measured. Over time, S. aureus adherence to HSV-1 infected cells was relatively stable for 45 min then decreased to 0.8 of virus-free control, before cycling at 15-to-30 min intervals. In contrast, staphylococcal adherence to HSV-2 infected cells proceeded at a more gradual rate, increasing to control levels at ~105 min before decreasing to a nadir at 165 min. Yeast adherence to HSV-1 infected cells remained relatively unchanged for the first 75 min then increased 2-fold before returning to its original level. This pattern is repeated over the next 90 min. While a similar pattern with C. albicans and HSV-2 was measured, it occurred more rapidly. Our model shows that while the interaction of both HSV-1 and HSV-2 with S. aureus is both dynamic and inhibitory, C. albicans interaction with HSV-2 is more permissive than HSV-1. However, the interaction of both microbes with HSV-infected cells in this model system appears to be independent of α5B1, CD36 and HSP60 viral-regulated receptor expression. These findings indicate that microbiome interactions across taxonomic kingdoms are more complex than previously thought.
机译:本研究检查了 s的动力学。金黄色葡萄球菌和 c。与HSV复制和共享受体的相应动态显示相似,Albackans遵守。用HSV-1GL86或HSV-2 333GJ-(MOI 50)感染各种时间的Hela细胞与孵育。金黄色葡萄球菌ATCC 25923或 C. albicans酵母和CFU测量。随着时间的推移, s。在循环以15至30分钟的间隔循环之前,AUREUS对HSV-1感染细胞的粘附性相对稳定45分钟,然后在无病毒对照中降低至0.8。相反,对HSV-2感染细胞的葡萄球菌粘附以更逐渐的速率进行,在165分钟下降到Nadir之前,在〜105分钟的控制水平增加。对于首次75分钟,对HSV-1感染细胞的酵母粘附仍保持相对不变,然后在恢复到原始水平之前增加2倍。在接下来的90分钟内重复这种模式。虽然与 c类似的模式。被测量了别代人和HSV-2,它发生得更迅速。我们的模型表明,HSV-1和HSV-2的相互作用与 s。金黄色葡萄球菌是动态和抑制性的, c。与HSV-2的albicans相互作用比HSV-1更允许。然而,微生物与该模型系统中HSV感染细胞的相互作用似乎与α5B1,CD36和HSP60病毒调节的受体表达无关。这些发现表明,分类王国的微生物组相互作用比以前想象的更复杂。

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