Interaction of SARS-COV2 and influenza virus with particulate matter air pollution
- Funded by UK Research and Innovation (UKRI)
- Total publications:0 publications
Grant number: 2721869
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Key facts
Disease
COVID-19, UnspecifiedStart & end year
20222026Known Financial Commitments (USD)
$0Funder
UK Research and Innovation (UKRI)Principal Investigator
N/A
Research Location
United KingdomLead Research Institution
Imperial College LondonResearch Priority Alignment
N/A
Research Category
Pathogen: natural history, transmission and diagnostics
Research Subcategory
Pathogen morphology, shedding & natural history
Special Interest Tags
N/A
Study Type
Non-Clinical
Clinical Trial Details
N/A
Broad Policy Alignment
Pending
Age Group
Not Applicable
Vulnerable Population
Not applicable
Occupations of Interest
Not applicable
Abstract
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