人冠状病毒 NL63 感染增强链球菌对上皮细胞的黏附作用。
Infection with human coronavirus NL63 enhances streptococcal adherence to epithelial cells.
机构信息
Microbiology Department, Faculty of Biochemistry Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, 30-387 Krakow, Poland.
Department of Cardiac Surgery and Transplantology, Silesian Center for Heart Diseases, Szpitalna 2, 41-800 Zabrze, Poland.
出版信息
J Gen Virol. 2011 Jun;92(Pt 6):1358-1368. doi: 10.1099/vir.0.028381-0. Epub 2011 Feb 16.
Abstract
Understanding the mechanisms of augmented bacterial pathogenicity in post-viral infections is the first step in the development of an effective therapy. This study assessed the effect of human coronavirus NL63 (HCoV-NL63) on the adherence of bacterial pathogens associated with respiratory tract illnesses. It was shown that HCoV-NL63 infection resulted in an increased adherence of Streptococcus pneumoniae to virus-infected cell lines and fully differentiated primary human airway epithelium cultures. The enhanced binding of bacteria correlated with an increased expression level of the platelet-activating factor receptor (PAF-R), but detailed evaluation of the bacterium-PAF-R interaction revealed a limited relevance of this process.
摘要
了解病毒感染后增强的细菌致病性的机制是开发有效治疗方法的第一步。本研究评估了人类冠状病毒 NL63（HCoV-NL63）对与呼吸道疾病相关的细菌病原体黏附的影响。结果表明，HCoV-NL63 感染导致肺炎链球菌对病毒感染的细胞系和完全分化的原代人呼吸道上皮培养物的黏附增加。细菌结合增强与血小板激活因子受体（PAF-R）的表达水平增加相关，但对细菌-PAF-R 相互作用的详细评估表明该过程相关性有限。
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