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Hypercontractility of the cardiac sarcomere may be essential for the underlying pathological hypertrophy and fibrosis in genetic hypertrophic cardiomyopathies. Aficamten (CK-274) is a novel cardiac myosin inhibitor that was discovered from the optimization of indoline compound 1. The important advancement of the optimization was discovery of an Indane analogue (12) with a less restrictive structure-activity relationship that allowed for the rapid improvement of drug-like properties. Aficamten was designed to provide a predicted human half-life (t1/2) appropriate for once a day (qd) dosing, to reach steady state within two weeks, to have no substantial cytochrome P450 induction or inhibition, and to have a wide therapeutic window in vivo with a clear pharmacokinetic/pharmacodynamic relationship. In a phase I clinical trial, aficamten demonstrated a human t1/2 similar to predictions and was able to reach steady state concentration within the desired two-week window.

Ferroptosis is a regulated form of cell death associated with the iron-dependent accumulation of lipid peroxides. Inducing ferroptosis is a promising approach to treat therapy resistant cancer. Ferroptosis suppressor protein 1 (FSP1) promotes ferroptosis resistance in cancer by generating the antioxidant form of coenzyme Q10 (CoQ). Despite the important role of FSP1, few molecular tools exist that target the CoQ-FSP1 pathway. Exploiting a series of chemical screens, we identify several structurally diverse FSP1 inhibitors. The most potent of these compounds, ferroptosis sensitizer 1 (FSEN1), is an uncompetitive inhibitor that acts selectively through on target inhibition of FSP1 to sensitize cancer cells to ferroptosis. Furthermore, a synthetic lethality screen reveals that FSEN1 synergizes with endoperoxide-containing ferroptosis inducers, including dihydroartemisinin, to trigger ferroptosis. These results provide new tools that catalyze the exploration of FSP1 as a therapeutic target and highlight the value of combinatorial therapeutic regimes targeting FSP1 and additional ferroptosis inducers.

Toxoplasma gondiiis a widespread apicomplexan parasite that can cause severe disease in its human hosts. The ability ofT. gondiiand other apicomplexan parasites to invade into, egress from, and move between cells of the hosts they infect is critical to parasite virulence and disease progression. An unusual and highly conserved parasite myosin motor (TgMyoA) plays a central role inT. gondiimotility. The goal of this work was to test whether pharmacological inhibition of TgMyoA can alter disease progression in an animal model of infection. To this end, we sought to identify small molecule inhibitors of TgMyoA by screening a collection of 50,000 structurally diverse small molecules for inhibitors of the recombinant motors actin-activated ATPase activity. The top hit to emerge from the screen, KNX-002, inhibited TgMyoA with little to no effect on any of the vertebrate myosins tested. KNX-002 was also active against parasites, inhibiting parasite motility and growth in culture in a dose-dependent manner. We used chemical mutagenesis, selection in KNX-002, and targeted sequencing to identify a mutation in TgMyoA (T130A) that renders the recombinant motor less sensitive to compound. Compared to wild-type parasites, parasites expressing the T130A mutation showed reduced sensitivity to KNX-002 in motility and growth assays, confirming TgMyoA as a biologically relevant target of KNX-002. Finally, KNX-002 was shown to slow disease progression in mice infected with wild-type parasites, but not parasites expressing the resistance-conferring TgMyoA T130A mutation. These data demonstrate the specificity of KNX-002 for TgMyoA, bothin vitroandin vivo, and validate TgMyoA as a druggable target for toxoplasmosis. Since TgMyoA is essential for virulence, conserved in apicomplexan parasites, and distinctly different from the myosins found in humans, pharmacological inhibition of MyoA offers a promising new approach to treating the devastating diseases caused byT. gondiiand other apicomplexan parasites.

Malaria is responsible for more than a half million deaths per year. The Plasmodium parasites responsible continue to develop resistance to all known agents, despite treatment with different antimalarial combinations. The atypical Myosin A motor (PfMyoA) is part of a core macromolecular complex called the glideosome, essential for Plasmodium parasite mobility and therefore an attractive drug target. Here, we characterize the interaction of a small molecule (KNX-002) with PfMyoA. KNX-002 inhibits PfMyoA ATPase activity in vitro and blocks asexual blood stage growth of merozoites, one of three motile Plasmodium life-cycle stages. Combining biochemical assays, X-ray crystallography and molecular dynamics, we demonstrate that KNX-002 targets a novel pocket in PfMyoA, sequestering it in a post-rigor state detached from actin. KNX-002 binding affects Mg2+ coordination near ATP, preventing ATP hydrolysis and thus inhibiting motor activity. This first-in-class small-molecule inhibitor of PfMyoA paves the way for developing a new generation of antimalarial treatments.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a range of symptoms in infected individuals, from mild respiratory illness to acute respiratory distress syndrome. A systematic understanding of host factors influencing viral infection is critical to elucidate SARS-CoV-2–host interactions and the progression of Coronavirus disease 2019 (COVID-19). Here, we conducted genome-wide CRISPR knockout and activation screens in human lung epithelial cells with endogenous expression of the SARS-CoV-2 entry factors ACE2 and TMPRSS2. We uncovered proviral and antiviral factors across highly interconnected host pathways, including clathrin transport, inflammatory signaling, cell-cycle regulation, and transcriptional and epigenetic regulation. We further identified mucins, a family of high molecular weight glycoproteins, as a prominent viral restriction network that inhibits SARS-CoV-2 infection in vitro and in murine models. These mucins also inhibit infection of diverse respiratory viruses. This functional landscape of SARS-CoV-2 host factors provides a physiologically relevant starting point for new host-directed therapeutics and highlights airway mucins as a host defense mechanism.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has emerged as a major global health threat. The COVID-19 pandemic has resulted in over 80 million cases and 1.7 million deaths to date while the number of cases continues to rise. With limited therapeutic options, the identification of safe and effective therapeutics is urgently needed. The repurposing of known clinical compounds holds the potential for rapid identification of drugs effective against SARS-CoV-2. Here we utilized a library of FDA-approved and well-studied preclinical and clinical compounds to screen for antivirals against SARS-CoV-2 in human pulmonary epithelial cells. We identified 13 compounds that exhibit potent antiviral activity across multiple orthogonal assays. Hits include known antivirals, compounds with anti-inflammatory activity, and compounds targeting host pathways such as kinases and proteases critical for SARS-CoV-2 replication. We identified seven compounds not previously reported to have activity against SARS-CoV-2, including B02, a human RAD51 inhibitor. We further demonstrated that B02 exhibits synergy with remdesivir, the only antiviral approved by the FDA to treat COVID-19, highlighting the potential for combination therapy. Taken together, our comparative compound screening strategy highlights the potential of drug repurposing screens to identify novel starting points for development of effective antiviral mono- or combination therapies to treat COVID-19.

The SARS coronavirus 2 (SARS-CoV-2) has caused an ongoing global pandemic with currently 29 million confirmed cases and close to a million deaths. At this time, there are no FDA-approved vaccines or therapeutics for COVID-19, but Emergency Use Authorization has been granted for remdesivir, a broad-spectrum antiviral nucleoside analog. However, remdesivir is only moderately efficacious against SARS-CoV-2 in the clinic, and improved treatment strategies are urgently needed. To accomplish this goal, we devised a strategy to identify compounds that act synergistically with remdesivir in preventing SARS-CoV-2 replication. We conducted combinatorial high-throughput screening in the presence of submaximal remdesivir concentrations, using a human lung epithelial cell line infected with a clinical isolate of SARS-CoV-2. We identified 20 approved drugs that act synergistically with remdesivir, many with favorable pharmacokinetic and safety profiles. Strongest effects were observed with established antivirals, Hepatitis C virus nonstructural protein 5 A (HCV NS5A) inhibitors velpatasvir and elbasvir. Combination with their partner drugs sofosbuvir and grazoprevir further increased efficacy, increasing remdesivir’s apparent potency 25-fold. We therefore suggest that the FDA-approved Hepatitis C therapeutics Epclusa (velpatasvir/sofosbuvir) and Zepatier (elbasvir/grazoprevir) should be fast-tracked for clinical evaluation in combination with remdesivir to improve treatment of acute SARS-CoV-2 infections.

The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection causes Coronavirus Disease 2019 (COVID-19), a pandemic that seriously threatens global health. SARS-CoV-2 propagates by packaging its RNA genome into membrane enclosures in host cells. The packaging of the viral genome into the nascent virion is mediated by the nucleocapsid (N) protein, but the underlying mechanism remains unclear. Here, we show that the N protein forms biomolecular condensates with viral genomic RNA both in vitro and in mammalian cells. While the N protein forms spherical assemblies with homopolymeric RNA substrates that do not form base pairing interactions, it forms asymmetric condensates with viral RNA strands. Cross-linking mass spectrometry (CLMS) identified a region that drives interactions between N proteins in condensates, and deletion of this region disrupts phase separation. We also identified small molecules that alter the size and shape of N protein condensates and inhibit the proliferation of SARS-CoV-2 in infected cells. These results suggest that the N protein may utilize biomolecular condensation to package the SARS-CoV-2 RNA genome into a viral particle., The packaging of the SARS-CoV-2 genome is mediated by the nucleocapsid (N) protein; this study shows that the N protein forms liquid condensates with viral genomic RNA and identifies small molecules that alter these condensates.

Hypercontractility of the cardiac sarcomere appears to underlie pathological hypertrophy and fibrosis in select genetic hypertrophic cardiomyopathies. Here, we characterize the small molecule, CK-3773274, as a novel cardiac myosin inhibitor that decreases contractility in vitro and in vivo . In bovine cardiac myofibrils, CK-3773274 decreased myosin ATPase activity in a concentration-dependent fashion (IC 50 :1.26 μM). CK-3773274 specifically inhibited myosin activity, as it reduced myosin ATPase activity in a concentration-dependent manner in the absence of other sarcomere proteins, including actin, troponin, and tropomyosin. CK-3773274 (10 μM) reduced fractional shortening by 84% in electrically paced, isolated adult rat cardiomyocytes relative to control without any effect on the calcium transient. The effect of CK-3773274 on cardiac contractility in vivo was assessed in healthy male Sprague Dawley (SD) rats using single oral doses ranging from 0.5 to 4 mg/kg. Fractional shortening (FS) and left ventricular dimensions were determined by echocardiography at select time points over a 24-hour period. One hour after dose administration, CK-3773274 significantly reduced fractional shortening in a dose-related fashion by 20-70% relative to vehicle treatment (FS %: vehicle: 47.9± 1%; 0.5 mg/kg: 39 ± 2%; 4 mg/kg: 15 ± 4%; mean ±SEM, pin vitro and in vivo . Cardiac myosin inhibition may be a viable approach to treat the underlying hypercontractility of the cardiac sarcomere in hypertrophic cardiomyopathies.

This third study of the author is based on findings of the previous studies. The first study showed how Becker et. al. constructed the SARS CoV-2 Spike Protein in 2008, with approaches of reverse genetics, and inserted into the backbone of the SARS CoV from 2006 (1). The second study showed, how the three US research groups, involved in the synthetic production of the SARS CoV-2 spike protein, developed and matured the SARS CoV-2 virus by decades of laboratory experiments on recombinant human-animal coronavirus RNA through targeted RNA manipulation (2). This overview aims to investigate the publications on whether the constructed SARS CoV-2 virus can be transmitted between individuals. Requirements for infection and transmission of a virus are translation and replication of viral genome in the host. The findings show that the public has been deliberately deceived with false statements in publications to create the narrative of a bat-evolved virus that can be transmitted between humans. But in fact, a spike protein antigen RNA, called SARS CoV-2, was constructed that has neither the efficient function of translation or replication. The only function of the antigen is to enter the human cells to manipulate the human genome. The antigen is then activated by recurrent external injections misleadingly called vaccines, in order to initiate the spike protein antigen synthesis with a sensitive RNA Probe. Consequently, the entry of synthetic foreign genes into the human genome activates an alert system through a cascade of exacerbated immune reactions, which initiates a self destruction mechanism that leads to exodus of the individual. This prevents, at the price of human life, alien genetic material from being incorporated into the human genome and passed to next generations., This is the english version of the following study "Kann das SARS CoV-2 ��bertragen werden?" published December 1, 2021. The author declares no conflict of interests., {"references":["1. M.A. Emergence of synthetic recombinant bat-human spike protein in the Wuhan SARS CoV-2. Zenodo 2020.https://doi.org/10.5281/zenodo.4532195.","2. M.A. The Story about the constructed SARS COV-2 Virus - A Review of three Research Groups.2021;https://doi.org/10.5281/zenodo.4570941.","3. Lan T. Phan, Thuong V. Nguyen, Quang C. Luong, Thinh V. Nguyen, Hieu T. Nguyen, Hung Q. Le, Thuc T. Nguyen, Thang M. Cao, Quang D. Pham,Importation and Human-to-Human Transmission of a Novel Coronavirus in Vietnam. N Engl J med 2020; 382 (9).","4. Chaolin Huang, Yeming Wang, Xingwang Li, Lili Ren, Jianping Zhao, Yi Hu, Li Zhang, Guohui Fan, Jiuyang Xu, Xiaoying Gu,Zhenshun Cheng, Ting Yu, Jiaan Xia, Yuan Wei, Wenjuan Wu, Xuelei Xie, Wen Yin, Hui Li, Min Liu, Yan Xiao, Hong Gao, Li Guo, Jungang Xie,Guangfa Wang, Rongmeng Jiang, Zhancheng Gao, Qi Jin, Jianwei Wang, Bin Cao, Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. The Lancet 2020; 395: 497-506","5. World Health Organization. Classifications https://www.who.int/standards/classifications/classification-of-diseases, 2021 [accessed 28.11.2021]","6. Sufang Tian, Yong Xiong, Huan Liu, Li Niu, Jianchun Guo, Meiyan Liao, Shu-Yuan Xiao, Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies.Modern Pathology 2020; 33:1007–1014.","7. https://www.gatesfoundation.org/How-We-Work/Quick-Links/Grants-Database#q/k=chinese%20academy&page=2, 2021 [accessed 2.3.2021]","8. Puja Mehta, Daniel F McAuley, Michael Brown, Emilie Sanchez, Rachel S Tattersall, Jessica J Manson, HLH Across Speciality Collaboration, UK, COVID-19: consider cytokine storm syndromes and immunosuppression.Lancet 2020;395(10229):1033-1034.","9. Xinjuan Sun, Tianyuan Wang, Dayong Cai , Zhiwei Hu , Jin'an Chen, Hui Liao, Liming Zhid , Hongxia Weie , Zhihong Zhang, Yuying Qiug , Jing Wang, Aiping Wang,Cytokine storm intervention in the early stages of COVID-19 pneumonia. Cytokine and Growth Factor Reviews.2020; 53:38–42.","10. Qiurong Ruan, Kun Yang, Wenxia Wang, Lingyu Jiang and Jianxin Song, Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020;46(5):846-848.","11. Yasmin A. Malik,Properties of Coronavirus and SARS-CoV-2.Malaysian J Pathol2020;42(1):3-11.","12. Wycliffe E. Wei, Zongbin Li, Calvin J. Chiew,; Sarah E. Yong, ; Matthias P. Toh, ; Vernon J. Lee, Presymptomatic Transmission of SARS-CoV-2 — Singapore, January 23–March 16, 2020.US Department of Health and Human Services/Centers for Disease Control and Prevention 2020;69.","13. Inga-Marie Schaefer, Robert F. Padera, Isaac H. Solomon, Sanjat Kanjilal2, Mark M. Hammer, Jason L. Hornick, Lynette M. Sholl,In situ detection of SARS-CoV-2 in lungs and airways of patients with COVID-19.Modern pathology 2020;33,2104–2114.","14. Francesca Caccuri, Antonella Bugatti , Alberto Zani, Antonella De Palma, Dario Di Silvestre Ekta Manocha, Federica Filippini, Serena Messali, Paola Chiodelli, Giovanni Campisi Simona Fiorentini , Fabio Facchetti, Pierluigi Mauri and Arnaldo Caruso,SARS-CoV-2 Infection Remodels the Phenotype and Promotes Angiogenesis of Primary Human Lung Endothelial Cells.Microorganisms 2021; 9, 1438.","15. Joanne M Willey, Linda Sherwood, Christopher J. Woolverton, Lansing M. Prescott, and Joanne M. Willey. Prescott's microbiology. 2011. New York.McGraw-Hill :from p.744.","16. Sarah S. Elsoukkary, Maria Mostyka, Alicia Dillard, Diana R. Berman, Lucy X. Ma, Amy Chadburn, Rhonda K. Yantiss, Jose Jessurun, Surya V. Seshan, Alain C. Borczuk, Steven P. Salvatore, Autopsy Findings in 32 Patients with COVID-19: A Single-Institution Experience. Pathobiology 2021;88:56-68.","17. Silke Stertz, Mike Reichelt, Martin Spiegel, Thomas Kuri, Luis Martínez-Sobrido,Adolfo García-Sastre, Friedemann Weber, Georg Kochs,The intracellular sites of early replication and budding of SARS-coronavirus.Virology 2007; 361: 304–315.","18. Katharina Schubert , Evangelos D. Karousis, Ahmad Jomaa , Alain Scaiola  , Blanca Echeverria1, Lukas-Adrian Gurzeler , Marc Leibundgut, Volker Thiel , Oliver Mühlemann  and Nenad Ban , SARS-CoV-2 Nsp1 binds the ribosomal mRNA channel to inhibit translation. Nature Structural & Molecular Biology 2020;27:959-966.","19. Yuichiro J. Suzuki, Sofia I. Nikolaienko, Vyacheslav A. Dibrova, Yulia V. Dibrova ,Volodymyr M. Vasylyk, Mykhailo Y. Novikov, Nataliia V. Shults, Sergiy G. Gychka,SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells.Vascular Pharmacology 2021;137:1537-1891.","20. Michelle M. Becker, Rachel L. Graham, Eric F. Donaldson, Barry Rockx, Amy C. Sims, Timothy Sheahan, Raymond J. Pickles, Davide Corti, Robert E. Johnston , Ralph S. Baric, and Mark R. Denison, Synthetic recombinant bat SARS-like coronavirus is infectious in cultured cells and in mice. PNAS 2008; 105(50): 19944–19949","21. Swapnil B. Kadam,Geetika S. Sukhramani,Pratibha Bishnoi,Anupama A. Pable,Vitthal T. Barvkar,SARS‐CoV‐2, the pandemic coronavirus: Molecular and structural insights. Journal of Basic Microbiology 2021;61:180-202.","22. Yue Li, Xinai Yang, Na Wang, Haiyan Wang, Bin Yin, Xiaoping Yang, Wenqing Jiang,GC usage of SARS-CoV-2 genes might adapt to the environment of human lung expressed genes.Molecular Genetics and Genomics 2020;295:1537–1546.","23. Jacomine Krijnse-Locker, Maria Ericsson, Peter J. M. Rottier, and Gareth Grittiths, Characterization of the Budding Compartment of Mouse Hepatitis Virus: Evidence That Transport from the RER to the Golgi Complex Requires only One Vesicular Transport Step.The Journal of Cell Biology 1994;124:55-70.","24. Lili Kuo and Paul S. Masters, Genetic Evidence for a Structural Interaction between the Carboxy Termini of the Membrane and Nucleocapsid Proteins of Mouse Hepatitis Virus. JOURNAL OF VIROLOGY 2001;76(10): 4987–4999.","25. Makoto Ujike, Cheng Huang, Kazuya Shirato, Shinji Makino and Fumihiro Taguchi,The contribution of the cytoplasmic retrieval signal of severe acute respiratory syndrome coronavirus to intracellular accumulation of S proteins and incorporation of S protein into virus-like particles. Journal of General Virology 2016;97:1853–1864.","26. Yu Chen, Qianyun Liu, Deyin Guo, Emerging coronaviruses: Genome structure, replication, and pathogenesis. 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Diese dritte Studie baut auf Erkenntnissen der vorherigen Studien auf. In der ersten Studie wurde nachgewiesen, wie Becker et. al. im Jahre 2008 das SARS CoV-2 Spike Protein durch Verfahren des Reverse Genetics hergestellt und in das R��ckgrat des SARS CoV aus dem Jahre 2006 eingef��gt haben(1). Die zweite Studie zeigte, dass die drei US-Forschungsgruppen, die an der k��nstlichen Herstellung des SARS CoV-2 Spike Proteins beteiligt waren, durch Jahrzehnte langen Laborexperimenten an rekombinanten Mensch-Tier Coronavirus RNA, das SARS CoV-2 Virus durch gezielte RNA Manipulation entwickelt und ausgereift haben(2). Diese Arbeit hat sich zur Aufgabe gemacht, die wissenschaftlichen Ver��ffentlichungen auf die Fragestellung zu untersuchen, ob das k��nstlich erstellte SARS CoV-2 Virus ��berhaupt zwischen Menschen ��bertragen werden kann. Die notwendige Voraussetzung zur Infektion und ��bertragung einer Viruserkrankung ist die Virusvermehrung durch Transkription und Replikation des viralen Genoms im Wirtsk��rper. Die Studienlage zeigt, dass die ��ffentlichkeit gezielt durch falsche Behauptungen in wissenschaftlichen Publikationen get��uscht wurde, um das Narrativ eines von Flederm��usen abstammenden Virus zu erschaffen, welches zwischen Menschen ��bertragen werden k��nnte. Tats��chlich wurde eine k��nstliche RNA mit einem Spike Protein Antigen, genannt SARS CoV-2, erstellt, welches weder eine effiziente Transkriptions- noch Replikationsf��higkeit hat. Dabei hat das Antigen zur Aufgabe in die menschlichen Zellen einzudringen, um dort Manipulationen am Genom vorzunehmen. Das Antigen wird dann durch externe Injektionen, hierbei irref��hrend Impfungen genannt, aktiviert, um die Spike Proteinsynthese, die durch rezidivierende Injektionen mit einer Spike Protein sensitiven RNA Probe auszul��sen. Die Folgen eines Eindringens k��nstlich fremden Genmaterials in das menschliche Genom ist die Ausl��sung von Warnmechanismen, die durch eine Kaskade von exazerbierten Immunreaktionen, eine Art Selbstzerst��rungsmechanismus einleitet und zum Exodus f��hren. Somit wird der Einbau fremden Genmaterials ins menschliche Genom, und die Vererbung an n��chste Generationen, auf Kosten menschlichen Lebens, verhindert., The author declares no conflict of interests., {"references":["1. M.A. Emergence of synthetic recombinant bat-human spike protein in the Wuhan SARS CoV-2. Zenodo 2020.https://doi.org/10.5281/zenodo.4532195.","2. M.A. The Story about the constructed SARS COV-2 Virus - A Review of three Research Groups.2021;https://doi.org/10.5281/zenodo.4570941.","3. Lan T. Phan, Thuong V. Nguyen, Quang C. Luong, Thinh V. Nguyen, Hieu T. Nguyen, Hung Q. Le, Thuc T. Nguyen, Thang M. Cao, Quang D. Pham,Importation and Human-to-Human Transmission of a Novel Coronavirus in Vietnam. N Engl J med 2020; 382 (9).","4. Chaolin Huang, Yeming Wang, Xingwang Li, Lili Ren, Jianping Zhao, Yi Hu, Li Zhang, Guohui Fan, Jiuyang Xu, Xiaoying Gu,Zhenshun Cheng, Ting Yu, Jiaan Xia, Yuan Wei, Wenjuan Wu, Xuelei Xie, Wen Yin, Hui Li, Min Liu, Yan Xiao, Hong Gao, Li Guo, Jungang Xie,Guangfa Wang, Rongmeng Jiang, Zhancheng Gao, Qi Jin, Jianwei Wang, Bin Cao, Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. The Lancet 2020; 395: 497-506.","5. World Health Organization. Classifications https://www.who.int/standards/classifications/classification-of-diseases, 2021 [accessed 28.11.2021]","6. Sufang Tian, Yong Xiong, Huan Liu, Li Niu, Jianchun Guo, Meiyan Liao, Shu-Yuan Xiao, Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies.Modern Pathology 2020; 33:1007–1014.","7. https://www.gatesfoundation.org/How-We-Work/Quick-Links/Grants-Database#q/k=chinese%20academy&page=2, 2021 [accessed 2.3.2021]","8. Puja Mehta, Daniel F McAuley, Michael Brown, Emilie Sanchez, Rachel S Tattersall, Jessica J Manson, HLH Across Speciality Collaboration, UK, COVID-19: consider cytokine storm syndromes and immunosuppression.Lancet 2020;395(10229):1033-1034.","9. Xinjuan Sun, Tianyuan Wang, Dayong Cai , Zhiwei Hu , Jin'an Chen, Hui Liao, Liming Zhid , Hongxia Weie , Zhihong Zhang, Yuying Qiug , Jing Wang, Aiping Wang,Cytokine storm intervention in the early stages of COVID-19 pneumonia. Cytokine and Growth Factor Reviews.2020; 53:38–42.","10. Qiurong Ruan, Kun Yang, Wenxia Wang, Lingyu Jiang and Jianxin Song, Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020;46(5):846-848.","11. Yasmin A. Malik,Properties of Coronavirus and SARS-CoV-2.Malaysian J Pathol2020;42(1):3-11.","12. Wycliffe E. Wei, Zongbin Li, Calvin J. Chiew,; Sarah E. Yong, ; Matthias P. Toh, ; Vernon J. Lee, Presymptomatic Transmission of SARS-CoV-2 — Singapore, January 23–March 16, 2020.US Department of Health and Human Services/Centers for Disease Control and Prevention 2020;69.","13. Inga-Marie Schaefer, Robert F. Padera, Isaac H. Solomon, Sanjat Kanjilal2, Mark M. Hammer, Jason L. Hornick, Lynette M. Sholl,In situ detection of SARS-CoV-2 in lungs and airways of patients with COVID-19.Modern pathology 2020;33,2104–2114.","14. Francesca Caccuri, Antonella Bugatti , Alberto Zani, Antonella De Palma, Dario Di Silvestre Ekta Manocha, Federica Filippini, Serena Messali, Paola Chiodelli, Giovanni Campisi Simona Fiorentini , Fabio Facchetti, Pierluigi Mauri and Arnaldo Caruso,SARS-CoV-2 Infection Remodels the Phenotype and Promotes Angiogenesis of Primary Human Lung Endothelial Cells.Microorganisms 2021; 9, 1438.","15. Joanne M Willey, Linda Sherwood, Christopher J. Woolverton, Lansing M. Prescott, and Joanne M. Willey. Prescott's microbiology. 2011. 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