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Effect of ambient temperature on respiratory tract cells exposed to SARS-CoV-2 viral mimicking nanospheres—An experimental study
Biointerphases ( IF 1.6 ) Pub Date : 2021-01-28 , DOI: 10.1116/6.0000743
Sachin Kumar 1 , Alexandra Paul 1 , Sayantan Chatterjee 2 , Sabine Pütz 2 , Natasha Nehra 1 , Daniel S Wang 1 , Arsalan Nisar 1 , Christian M Jennings 1 , Sapun H Parekh 1
Affiliation  

The novel coronavirus caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has reached more than 160 countries and has been declared a pandemic. SARS-CoV-2 infects host cells by binding to the angiotensin-converting enzyme 2 (ACE-2) surface receptor via the spike (S) receptor-binding protein (RBD) on the virus envelope. Global data on a similar infectious disease spread by SARS-CoV-1 in 2002 indicated improved stability of the virus at lower temperatures facilitating its high transmission in the community during colder months (December–February). Seasonal viral transmissions are strongly modulated by temperatures, which can impact viral trafficking into host cells; however, an experimental study of temperature-dependent activity of SARS-CoV-2 is still lacking. We mimicked SARS-CoV-2 with polymer beads coated with the SARS-CoV-2 S protein to study the effect of seasonal temperatures on the binding of virus-mimicking nanospheres to lung epithelia. The presence of the S protein RBD on nanosphere surfaces led to binding by Calu-3 airway epithelial cells via the ACE-2 receptor. Calu-3 and control fibroblast cells with S-RBD-coated nanospheres were incubated at 33 and 37 °C to mimic temperature fluctuations in the host respiratory tract, and we found no temperature dependence in contrast to nonspecific binding of bovine serum ablumin-coated nanospheres. Moreover, the ambient temperature changes from 4 to 40 °C had no effect on S-RBD-ACE-2 ligand-receptor binding and minimal effect on the S-RBD protein structure (up to 40 °C), though protein denaturing occurred at 51 °C. Our results suggest that ambient temperatures from 4 to 40 °C have little effect on the SARS-CoV-2-ACE-2 interaction in agreement with the infection data currently reported.

中文翻译:

环境温度对暴露于 SARS-CoV-2 病毒模拟纳米球的呼吸道细胞的影响——一项实验研究

由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的新型冠状病毒已蔓延至160多个国家,并已被宣布为大流行。SARS-CoV-2 通过病毒包膜上的刺突 (S) 受体结合蛋白 (RBD) 与血管紧张素转换酶 2 (ACE-2) 表面受体结合来感染宿主细胞。2002 年 SARS-CoV-1 传播的类似传染病的全球数据表明,该病毒在较低温度下的稳定性有所提高,有利于其在寒冷月份(12 月至 2 月)在社区中的高传播。季节性病毒传播受到温度的强烈调节,这会影响病毒向宿主细胞的运输;然而,仍然缺乏对 SARS-CoV-2 温度依赖性活性的实验研究。我们用涂有 SARS-CoV-2 S 蛋白的聚合物珠模拟 SARS-CoV-2,以研究季节性温度对模拟病毒纳米球与肺上皮细胞结合的影响。纳米球表面存在 S 蛋白 RBD,导致 Calu-3 气道上皮细胞通过 ACE-2 受体结合。将带有 S-RBD 涂层纳米球的 Calu-3 和对照成纤维细胞在 33 和 37 °C 下孵育,以模拟宿主呼吸道的温度波动,与牛血清 ablumin 涂层纳米球的非特异性结合相比,我们发现不存在温度依赖性。 。此外,环境温度从 4°C 变化到 40°C 对 S-RBD-ACE-2 配体-受体结合没有影响,对 S-RBD 蛋白质结构影响最小(最高 40°C),尽管蛋白质变性发生在51℃。我们的结果表明,4 至 40 °C 的环境温度对 SARS-CoV-2-ACE-2 相互作用影响不大,与目前报告的感染数据一致。
更新日期:2021-03-01
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