@article{d31bde4ee1d548f8b34a5e3a1e340906,
title = "Role of toll-like receptor 7/8 pathways in regulation of interferon response and inflammatory mediators during SARS-CoV2 infection and potential therapeutic options",
abstract = "Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2) is the causative agent of Corona Virus Disease 2019 (COVID-19). Lower production of type I and III interferons and higher levels of inflammatory mediators upon SARS-CoV2 infection contribute to COVID-19 pathogenesis. Optimal interferon production and controlled inflammation are essential to limit COVID-19 pathogenesis. However, the aggravated inflammatory response observed in COVID-19 patients causes severe damage to the host and frequently advances to acute respiratory distress syndrome (ARDS). Toll-like receptor 7 and 8 (TLR7/8) signaling pathways play a central role in regulating induction of interferons (IFNs) and inflammatory mediators in dendritic cells. Controlled inflammation is possible through regulation of TLR mediated response without influencing interferon production to reduce COVID-19 pathogenesis. This review focuses on inflammatory mediators that contribute to pathogenic effects and the role of TLR pathways in the induction of interferon and inflammatory mediators and their contribution to COVID-19 pathogenesis. We conclude that potential TLR7/8 agonists inducing antiviral interferon response and controlling inflammation are important therapeutic options to effectively eliminate SARS-CoV2 induced pathogenesis. Ongoing and future studies may provide additional evidence on their safety and efficacy to treat COVID-19 pathogenesis.",
keywords = "COVID-19, IL-1β, IL-6, SARS-CoV2, TLR7, TLR7/8 agonists, TLR8, Type I interferons",
author = "Dyavar, {Shetty Ravi} and Rahul Singh and Rohini Emani and Pawar, {Ganesh P.} and Chaudhari, {Vinod D.} and Podany, {Anthony T.} and Avedissian, {Sean N.} and Fletcher, {Courtney V.} and Salunke, {Deepak B.}",
note = "Funding Information: This work was supported by P30 MH062261, UNMC Nebraska Neuroscience Alliance COVID-19 Rapid Response grant and Nebraska Research Initiative (NRI) Collaborative Grant (2019-20 RFA) awarded to S.R.D, R01-AI124965 to C.V.F. from the National Institute of Allergy and Infectious Diseases (NIAID) and 1K23AI134307-01A1 to A.T.P. The work was also supported by the Ministry of Human Resource Development , Govt. of India grant ( SPARC/2018-2019/P386/SL ) and Ramalingaswami Fellowship of Govt. of India by DBT, New Delhi (BT/RLF/Re-entry/16/2013) awarded to D.B.S. Funding Information: This work was supported by P30 MH062261, UNMC Nebraska Neuroscience Alliance COVID-19 Rapid Response grant and Nebraska Research Initiative (NRI) Collaborative Grant (2019-20 RFA) awarded to S.R.D, R01-AI124965 to C.V.F. from the National Institute of Allergy and Infectious Diseases (NIAID) and 1K23AI134307-01A1 to A.T.P. The work was also supported by the Ministry of Human Resource Development, Govt. of India grant (SPARC/2018-2019/P386/SL) and Ramalingaswami Fellowship of Govt. of India by DBT, New Delhi (BT/RLF/Re-entry/16/2013) awarded to D.B.S. Publisher Copyright: {\textcopyright} 2021 The Authors",
year = "2021",
month = sep,
doi = "10.1016/j.biopha.2021.111794",
language = "English (US)",
volume = "141",
journal = "Biomedicine and Pharmacotherapy",
issn = "0753-3322",
publisher = "Elsevier Masson",
}