COVID-19: combining antiviral and anti-inflammatory treatments

Stebbing, Justin; Phelan, Anne M.; Griffin, Ivan; Tucker, Catherine M.; Oechsle, Olly; Smith, D. Casey; Richardson, Peter J.

doi:10.1016/s1473-3099(20)30132-8

Cited by 1,031 publications

(1,012 citation statements)

References 7 publications

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“…Journal Pre-proof makes the drug a possible candidate for inclusion in combination protocols with antiviral drugs such as lopinavir/ritonavir and remdesivir [109]. Interestingly, tofacitinib shows no detectable inhibition of AAK1 [104], whereas currently no data are available on the possible effect of other JAK inhibitors approved or tested for RA (such as upadacitinib or filgotinib) in relation to coronavirus infection. Unexpectedly, the only clinical trial evaluating the potential role of clathrinmediated endocytosis blockade in the management of COVID-19 is currently ongoing with ruxolitinib (ChiCTR2000029580).…”

Section: J O U R N a L P R E -P R O O Fmentioning

confidence: 99%

COVID-19 infection and rheumatoid arthritis: Faraway, so close!

Favalli

Ingegnoli

Lucia

et al. 2020

Autoimmunity Reviews

429

454

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Section: J O U R N a L P R E -P R O O Fmentioning

confidence: 99%

COVID-19 infection and rheumatoid arthritis: Faraway, so close!

Favalli

Ingegnoli

Lucia

et al. 2020

Autoimmunity Reviews

429

454

View full text Add to dashboard Cite

show abstract

“…The outbreak of the 2019-coronavirus (SARS-CoV-2) has posed the world at a pandemic risk [ [1]]. Coronavirus-19 disease (COVID-19) is an infectious disease caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), an enveloped non-segmented positive-sense RNA β-coronavirus belonging to the same family as severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS) viruses, which causes pneumonia, requires intensive care unit hospitalization in about 10% of cases and can lead to a fatal outcome [2][3][4][5][6]. COVID-19 is characterized in severe cases by an acute respiratory distress syndrome (ARDS) and cytokine release syndrome and there is an immediate need for any agent before the development of a vaccine [2].…”

Section: Introductionmentioning

confidence: 99%

The anti-viral facet of anti-rheumatic drugs: Lessons from COVID-19

Perricone

Triggianese

Bartoloni

et al. 2020

Journal of Autoimmunity

128

131

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“…Fostamatinib, which we prioritized in this study, also inhibits JAK1, JAK2 and AAK1 48 based on curations from DrugBank and was shown to be effective for RA 43 . Of note, two other JAK-STAT signaling inhibitors were recommended by Stebbing et al 45 , while in our analysis JAK-STAT signaling is among the top 10 pathways enriched for top proteins linked to ACE2 expression. Another candidate highlighted by Richardson et al 44 , sunitinib, was also top-listed by our MR-based analysis.…”

Section: On Ace2 Expression and Exploring Drug Candidatesmentioning

confidence: 58%

Exploring diseases/traits and blood proteins causally related to expression of ACE2, the putative receptor of SARS-CoV-2: A Mendelian Randomization analysis highlights tentative relevance of diabetes-related traits

Rao

Lau

2020

Preprint

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The novel coronavirus 2019-nCoV has caused major outbreaks in many parts of the world. A better understanding of the pathophysiology of COVID-19 is urgently needed. Clinically, it is important to identify who may be susceptible to infection and identify treatments for the disease.There is good evidence that ACE2 is a receptor for 2019-nCoV, and studies also suggested that high expression of ACE2 may increase susceptibility to infection. Here we conducted a phenome-wide Mendelian randomization (MR) study to prioritize diseases/traits and blood proteins that may be causally linked to ACE2 expression in the lung. Expression data was based on GTEx. We also explored drug candidates whose targets overlapped with the top-ranked proteins in MR analysis, as these drugs could potentially alter ACE2 expression and may be clinically relevant. Notably, MR is much less vulnerable to confounding and reverse causality compared to observational studies.The most consistent finding was a tentative causal association between diabetes-related traits and increased ACE2 expression. Based on one of the largest GWAS on type II diabetes (T2DM) to date (N=898,130), we found that T2DM is causally linked to raised ACE2 expression (beta=0.1835, 95% CI 0.0853-0.2817; p=2.49E-4; GSMR method). Significant associations (at nominal level; p<0.05) was also observed across multiple datasets, with different analytic methods, and for both type I and II diabetes. Other diseases/traits having nominal significant associations with increased ACE2 included inflammatory bowel disease, (ER+) breast and lung cancers, asthma, smoking and elevated ALT, among others. We also uncovered a number of plasma/serum proteins potentially linked to altered ACE2 expression, and the top enriched pathways included cytokine-cytokine-receptor interaction, VEGF signaling, JAK-STAT signaling etc. We also explored drugs that target some of the top-ranked proteins in the MR analysis.

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COVID-19: combining antiviral and anti-inflammatory treatments

Cited by 1,031 publications

References 7 publications

COVID-19 infection and rheumatoid arthritis: Faraway, so close!

COVID-19 infection and rheumatoid arthritis: Faraway, so close!

The anti-viral facet of anti-rheumatic drugs: Lessons from COVID-19

Exploring diseases/traits and blood proteins causally related to expression of ACE2, the putative receptor of SARS-CoV-2: A Mendelian Randomization analysis highlights tentative relevance of diabetes-related traits

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