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- W3048846693 abstract "Expansion of the novel human respiratory coronavirus (SARS-CoV-2) is a global public health emer-gency concern. There is no known successful treatment as of this time and there is a need for medical options to mitigate this current epidemic. SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE2) receptor and is primarily trophic for the lower and upper respiratory tract. A number of current studies on COVID-19 demonstrates the substantial increase in pro-inflammatory factors in the lungs during infection. The virus is also documented in the central nervous system and, in particular, in the brainstem, which plays a key role in respiratory and cardiovascular function. Currently, there are few antiviral approaches, and several alternative drugs are under investigation. Two of these are Idelalisib and Ebastine, already proposed as preventive strategies in airways and al-lergic diseases. The interesting and evolving potentiality of phosphoinositide 3-kinase δ (PI3K in-hibitors, together with Ebastine, lies in their ability to suppress the release of pro-inflammatory cyto-kines, such as IL-1, IL-8, IL-6 and TNF, by T-cells. This may represent an optional therapeutic choice for COVID-19 to reduce inflammatory reactions and mortality, enabling patients to recover faster. This concise communication aims to provide new potential therapeutic targets capable of mitigating and alleviating SARS-CoV-2 pandemic infection." @default.
- W3048846693 created "2020-08-18" @default.
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- W3048846693 date "2020-08-21" @default.
- W3048846693 modified "2023-09-28" @default.
- W3048846693 title "PI3Kδ Inhibition as a Potential Therapeutic Target in COVID-19" @default.
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- W3048846693 doi "https://doi.org/10.3389/fimmu.2020.02094" @default.
- W3048846693 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7472874" @default.
- W3048846693 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32973818" @default.
- W3048846693 hasPublicationYear "2020" @default.
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