Interaction of SARS-COV2 and influenza virus with particulate matter air pollution

感染流感和SARS-CoV-2的患者死亡的可能性是单独感染SARS-CoV-2的患者的两倍多（Stowe J, 2020）。有证据表明，当受试者同时暴露于高水平的环境颗粒物（PM）污染时，传播率更高，健康状况恶化（Lu, 2020）。正如COVID-19大流行所记录的那样，来自意大利伦巴第的证据表明，较高的环境水平和每日污染波动会增加COVID-19的感染率（Setti L， 2020年）。通过RNA提取和聚合酶链反应（PCR）间接在污染的PM上检测到SARS-CoV-2 （Setti L et al, 2020）。在直径为250-500 nm的PM超细部分中发现了活的SARS-CoV-2病毒（通过PCR检测和阳性培养）（Lednicky JA, 2021），这提高了这些颗粒可能作为SARS-CoV-2载体的可能性，但没有直接的视觉证据证明这些颗粒是否形成杂交体。如果PM与呼吸道病毒在空气中相互作用，产生的颗粒杂交可能影响空气传播、传播和传染性。另一方面，PM的特定成分具有氧化还原活性，最近有证据表明柴油PM可以使流感病毒失活（Hsiao TC, 2021）。该博士将验证PM作为SARS-CoV-2和流感病毒载体的假设，增加了病毒在空气中传播、传染性和促进细胞炎症反应的可能性。此外，它将确定流感或SARS-COV-2是否与PM的特定成分相互作用，以及特定PM化学物质是否会放大或保护细胞免受损伤。研究结果将为哪些受污染的微环境可能对感染最不安全提供指导，并可能阐明新的治疗干预措施。任务1将优化人上皮细胞的感染和PM剂量。任务2将确定人鼻上皮细胞（HNE）对sars - cov -2感染和PM的反应。任务3将评估在细胞环境中SARS-CoV2是否附着在PM上。EPSRC研究领域：粒子技术和生物物理学

Patients infected with influenza and SARS-CoV-2 are more than twice as likely to die as someone with SARS-CoV-2 alone (Stowe J, 2020) There is evidence of higher transmission rates and worsening of health outcomes when subjects are also exposed to high levels of ambient particulate matter (PM) pollution (Lu, 2020). As documented with the COVID-19 pandemic, evidence from Lombardy, Italy, suggested that higher ambient levels and daily fluctuations of pollution, increase the rate of COVID-19 infection (Setti L, 2020). SARS-CoV-2 has been detected indirectly on PM in pollution via RNA extraction and polymerase chain reaction (PCR) (Setti L et al, 2020). Viable SARS-CoV-2 virus (detected by PCR and positive culture) has been shown in the ultrafine fraction of PM with diameters of 250-500 nm (Lednicky JA, 2021), raising the possibility that these particles could act as a vector for SARS-CoV-2, but there is no direct visual evidence as to whether these particles form hybrids. If PM and the respiratory viruses interact in air, the resulting particle-hybrid could affect airborne spread, transmission and infectivity. On the other hand specific components of PM are redox active and there is very recent evidence that diesel PM can deactivate influenza viruses (Hsiao TC, 2021). This PhD will test the hypothesis that PM acts as a vector for SARS-CoV-2 and influenza viruses, increasing the potential for airborne spread of the virus, infectivity and for boosting cellular inflammatory response. In addition, it will establish whether influenza or SARS-COV-2 interact with specific components of PM and whether specific PM chemistries amplify or protect against cellular damage. The outcomes will provide guidance around which polluted microenvironments are potentially most unsafe for infection and could shed light on new therapeutic interventions.Task 1 will optimise infection and PM dosing of human epithelial cells. Task 2 will determine response of human nasal epithelial cells Human Nasal Airway Epithelial Cells (HNE) to SARS-CoV-2-infected and PM. Task 3 will assess whether SARS-CoV2 adheres to PM in the cellular environment. EPSRC areas: particle technology and biophysics