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1 The main content of this entry is the early findings surrounding the use of anti-inflammatory therapeutics against COVID-19 infection. As this is an evolving pandemic, the data cited was thought to to be true and correct at the time of writing.
Ronan Lordan
 + 1396 word(s) 1396 2020-05-27 10:26:35 |
2 Edited the article.
Ronan Lordan
 + 24 word(s) 1420 2020-05-27 19:45:52 | |
3 Brief conclusion added
Ronan Lordan
 + 64 word(s) 1460 2020-05-27 20:24:09 | |
4 Some additions were made on the 4th paragraph from the end of the document concerning thrombotic complications in COVID patients and relative therapy. Reference [3] in this paragraph is: https://www.tandfonline.com/doi/full/10.1080/21548331.2020.1772639
Alexandros Tsoupras
 + 98 word(s) 1558 2020-05-28 10:00:41 | |
5 Typing errorcorrected
Alexandros Tsoupras
 + 97 word(s) 1557 2020-05-28 10:34:36 | |
6 Additions related to the COVID-infection and Inflammation
Alexandros Tsoupras
 + 446 word(s) 2003 2020-05-29 14:12:44 | |
7 format change
Nicole Yin
 -2 word(s) 2001 2020-06-08 08:07:19 | |
8 format change
Nicole Yin
 -10 word(s) 1991 2020-11-06 05:07:22 |

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Zabetakis, I.; Lordan, R.; Norton, C.; Tsoupras, A. COVID-19 Treatment. Encyclopedia. Available online: https://encyclopedia.pub/entry/938 (accessed on 22 December 2024).
Zabetakis I, Lordan R, Norton C, Tsoupras A. COVID-19 Treatment. Encyclopedia. Available at: https://encyclopedia.pub/entry/938. Accessed December 22, 2024.
Zabetakis, Ioannis, Ronan Lordan, Catherine Norton, Alexandros Tsoupras. "COVID-19 Treatment" Encyclopedia, https://encyclopedia.pub/entry/938 (accessed December 22, 2024).
Zabetakis, I., Lordan, R., Norton, C., & Tsoupras, A. (2020, May 27). COVID-19 Treatment. In Encyclopedia. https://encyclopedia.pub/entry/938
Zabetakis, Ioannis, et al. "COVID-19 Treatment." Encyclopedia. Web. 27 May, 2020.
COVID-19 Treatment
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This entry is adapted from the peer-reviewed paper 10.3390/nu12051466

The novel coronavirus disease (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has engulfed the world, affecting more than 180 countries. As a result, there has been considerable economic distress globally and a significant loss of life. Sadly, the vulnerable and immunocompromised in our societies seem to be more susceptible to severe COVID-19 complications. Notably, there are several significant risk factors for severe COVID-19 infection. These include the presence of poor nutritional status and pre-existing noncommunicable diseases (NCDs) such as diabetes mellitus, chronic lung diseases, cardiovascular diseases (CVD), obesity, and various other diseases that render the patient immunocompromised. These diseases are characterized by systemic inflammation, which may be a common feature of these NCDs, affecting patient outcomes against COVID-19. As a result, various antiviral treatments and anti-inflammatory agents are under investigation for their potential therapeutic value. The section presented below originates from the following article [1].

COVID-19 SARS-CoV-2 Inflammation Hydroxychloroquine ACE Inhibition anti-inflammatory cytokines

1. Introduction

The novel coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by severe acute inflammation in severe cases [1].

SARS-CoV-2 is an enveloped positive-sense RNA virus that typically affects the respiratory system, whereby the main known route of transmission occurs due to the spread of droplets generated when an infected person sneezes or coughs or through other mucus environments, including saliva or discharge from the nose[2]. SARS-CoV-2 gains entry to the cell via the angiotensin-converting enzyme 2 (ACE2) receptor[3][4][5][6][7][8][9][10][11], whereby it predominantly infects the lower respiratory tract, binding to ACE2 on alveolar epithelial cells[12]. Upon binding, there is a subsequent response of the immune system via inflammation-related manifestations and recruitment of antigen-presenting cells[9][10][11]. COVID-19 infection can manifest as an asymptomatic infection, or patients can present with a mild upper respiratory tract illness that may include a cough, chills, fever, fatigue, and shortness of breath[13]. In severe cases, the most common complications are sepsis, acute respiratory distress syndrome (ARDS), heart failure, and septic shock. However, severe viral pneumonia with respiratory failure can potentially lead to death[14]. Multiple organ dysfunction is likely attributable to uncontrolled acute inflammation and cytokine storm release[9][10][11][15][16][17]. As our knowledge of the disease is evolving, it is clear that other symptoms are being identified, including chilblains[18], sudden anosmia or ageusia[19], and even stroke[20].

2. Current Knowledge of COVID-19 Treatment and Anti-Inflammatory Approaches

The inflammatory response plays a crucial role in the clinical manifestations of COVID-19. Post SARS-CoV-2 entry, host factors trigger an immune response against the virus, which, if uncontrolled, may result in pulmonary tissue damage, functional impairment, and reduced lung capacity, despite the pathogenic effect of the virus[9][10]. Apart from nonspecific inflammatory responses such as edema and inflammatory cell infiltration, severe exfoliation of alveolar epithelial cells, alveolar septal widening, damage to alveolar septa, and alveolar space infiltration has been detected in a distinctly organized manner[9][10]. Thus, SARS-CoV-2 infection can cause pathological changes, degeneration, infiltration, and hyperplasia[9]. Apart from respiratory failure, other common features amongst critical COVID-19 patients include a sudden decline of the patient’s health status approximately two weeks after onset[10], infiltration of monocytes and macrophages into lung lesions, a decrease of lymphocytes such as natural killer (NK) cells in peripheral blood, extremely high levels of inflammatory response due to the proinflammatory cytokine storm, atrophy of the spleen and lymph nodes, along with reduced lymphocytes in lymphoid organs, hypercoagulability, thrombosis, and multiple organ damage[10][21]. These are just a selection of the clinical manifestations that occur as the medical community begins to learn more as the pandemic continues to grow.

It is therefore apparent that a viral infection-related inflammation and the subsequent cytokine storm in severe cases plays a crucial role in patient outcomes[9][10][11][15]. Furthermore, the coexistence of noncommunicable chronic diseases (NCDs) in COVID-19 patients may aggravate and intensify the inflammatory pathology and increase the risk for adverse outcomes and mortality[22]. As a result, anti-inflammatory agents are under investigation for their therapeutic value [1]. 

Classic first-line antiviral treatments are a potential therapeutic against COVID-19, which, when concomitant with organ function support, are very important to reduce mortality for mild and critical patients[10][23]. Antiviral therapy against SARS-CoV-2 consists of using different polymerase inhibitor drugs that are currently on the market and approved for use against other viruses; these include Ribavirin, Remdesivir, Sofosbuvir, Galidesivir, and Tenofovir[23]. These antiviral drugs have previously exhibited anti-inflammatory properties, either individually or combined as highly active antiviral therapies. However, the long-term use of some of these antiviral therapeutics against other persistent viral infections has been associated with inflammation-related cardiovascular side effects[24][25].

Researchers are also targeting inflammation through the investigation of immunomodulatory and anti-inflammatory therapies to reduce systemic inflammation before the onset of multi-organ dysfunction[10][26]. Therefore, biological agents targeting cytokines expression and specific cytokine antagonists, such as IL-6R monoclonal antibodies, TNF inhibitors, IL-1 antagonists, Janus kinase inhibitor (JAK) inhibitors, etc., have been considered[10]. Adopting an approach against specific cytokines entails the danger of only inhibiting one aspect of the inflammatory pathways involved. As a consequence, it may not be very effective in curbing the cytokine storm in COVID-19, as various cytokine pathways are of significant importance, and immunosuppression may actually compromise host defenses[27][28]. Furthermore, some of these specified anti-inflammatory medications, such as JAK inhibitors, may also block the production of the antiviral interferons such as the INF-a, which may have negative consequences for the immune response[10][29].

Researchers are also investigating the possible effects of antimalarial drugs such as chloroquine and hydroxychloroquine against SARS-CoV-2. These molecules are generally prescribed for autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis in patients whose disease status has not improved with other treatments. However, chloroquine and hydroxychloroquine possess a broad spectrum of antiviral effects against several viral infections, including coronaviruses such as SARS-CoV-1[10][30][23][24][31][32]. In vitro experiments in China identified chloroquine as a promising therapeutic against SARS-CoV-2[32][33], while the immunomodulatory effects of its derivative hydroxychloroquine may be more effective at targeting the cytokine storm that occurs in the late phase of critically ill COVID-19 infected patients, with less side effects[31][34].

Hydroxychloroquine interferes with lysosomal activity and autophagy and alters transcription and signaling pathways, which can result in the modulation of cytokine production[35], all of which are postulated to dampen the effects of the proinflammatory cytokine storm of severe COVID-19 patients. Furthermore, hydroxychloroquine has been reported to have better outcomes when combined with other drugs, such as antibiotics like azithromycin, or drugs used for rheumatoid arthritis, such as tocilizumab/atlizumab, in addition to the standard medical management for septic shock and ARDS[36]. Notably, some antibiotics, including azithromycin, have exhibited anti-inflammatory potency[26][37][38], while tocilizumab/atlizumab contains a humanized monoclonal antibody against the IL-6 receptor; thus, it is mainly used for reducing inflammation during autoimmune disorders[39].

Hydroxychloroquine, in combination with azithromycin, has been particularly focused upon due to the results of a French study where 26 COVID-19 patients received the combination treatment versus control groups. However, there were several issues with the study design, including its small sample size, the fact that the control groups were from different hospitals, the study was not blinded, and a myriad of other issues[40]. While the study provided an indication that hydroxychloroquine was worth further investigation, its results have been blown out of proportion in the media. Hydroxychloroquine has even been prematurely touted as a “game-changer” by President Donald Trump of the United States, who has admonished that he may even consider taking this untested drug against COVID-19[41], which is eventually did do. Some countries have allowed compassionate use of these drugs[42][43]. The promotion of hydroxychloroquine or chloroquine without substantial evidence of randomized, controlled trials is a significant safety and efficacy concern and requires further intensive investigation[44][45][46]. Currently, a study from the United States Veterans Health Administration indicated that patients administered hydroxychloroquine alone or in combination with azithromycin were no less likely to require mechanical ventilation and had higher mortality when on hydroxychloroquine alone versus the standard treatment[47]. This example demonstrates the necessity for world leaders to consult with their experts prior to promoting unproven medications against SAR-CoV-2 as a matter of public safety until further research is conducted. Since writing this review, several countries have chosen to stop using hydroxychloroquine and France has barred its use against COVID-19 [48].

Several researchers mention the relationship of anti-CVD-related drugs with COVID-19. Indeed, there is a focus on the anti-inflammatory drug colchicine, which has been previously used effectively against cardiovascular disorders[49]. Since ACE2 is implicated in COVID-19 infection, the role of angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs) of the ACE2 receptor and its rennin-angiotensin system, which are typically used for hypertension, has recently been evaluated[50][51][52][30] . ACEIs/ARBs perform a protective role in the cardiovascular system by also increasing the expression ACE2 in the heart[30]. However, the impact of ACEIs/ARBs on ACE2 in other organs, especially whether they could influence the expression level and activity of ACE2 in the lungs, with a subsequently higher susceptibility to SARS-CoV-2 infection, remains unknown. Thus, if ACEIs/ARBs have the capacity to upregulate the expression and activity of ACE2 in the lungs, they may play a dual role in COVID-19. On one hand, the higher level of ACE2 might increase the susceptibility of cells to SARS-CoV-2 viral host entry and propagation, whereas, on the other hand, the activation of ACE2 might ameliorate the acute lung injury induced by SARS-CoV-2[30][53][54]. Despite these concerns, the European Society of Cardiology recommends that patients continue their usual antihypertensive medications due to lack of evidence[55]. This also may have dietary implications due to the modulatory effects dietary patterns can have on hypertension but also due to the fact that some foods are associated with high levels of ACE inhibitory peptides[56]. Thus, further research is required to investigate the role of ACE2 activation, expression, and its related pathways in COVID-19.

As aforementioned, implementing an anti-inflammatory strategy is challenging, as it is not yet clear if any specific features of the immune response can be inhibited directly without compromising a patient’s overall immune defense[27]. It is important to determine the optimum method to reduce inflammation. Further research is also required to gain an understanding of the temporal features of the COVID-19 inflammatory response and to determine at what stage of the infection should pharmaceutical treatments be administered. Similarly, an understanding of the dosing and sexual dimorphism in drug metabolism and disease presentation is required. Likewise, ethnicity may be a determining factor in severe COVID-19 infections that requires further investigation[57][58].

Furthermore, COVID-19 patients have higher risk for thrombotic disease states including acute coronary syndrome, venous thromboembolism such as deep vein thrombosis or pulmonary embolism, or stroke. Subjects with underlying CVD are also at higher risk for morbidity and mortality if infected [59]. Considering an increased risk of clot development can turn mild cases into more severe and life-threatening emergencies, a preventative approach targeting thrombosis should also be considered[60], particularly those that may also target inflammation[61]. However, management of anticoagulation and/or antiplatelet medications can be difficult in potentially critically ill patients. Therefore, guidance for the utilization of antithrombotic and antiplatelet therapies in patients with known or suspected COVID-19 is needed, and especially in the cardiovascular patient with COVID-19, in the face of a rapidly evolving understanding of this virus and its complications [59].

Reactive oxygen species (ROS) also play a crucial role in the inflammatory response. As such, utilizing compounds with antioxidant properties may also be considered to reduce the cytokine storm induced by the viral infection[62]. Indeed, antioxidative therapies are being considered for ameliorating cardiac injuries in critically ill COVID-19 patients[63].

Among other measures, the nutritional status of an infected patient should also be considered, as nutritional deficiencies may increase a patient’s risk to developing a severe infection of COVID-19[64]. Introducing nutritional interventions should not be overlooked due to their potential for beneficial clinical outcomes[65]; in particular, consideration must be given to intensive care unit (ICU) patients[66]. 

Further research is ongoing to develop and investigate more treatments and antivirals that control or limit the damage caused by various symptoms of the viral infection and reduce the viral load until a vaccine is developed. 

References

  1. Zabetakis, Ioannis; Lordan, Ronan; Norton, Catherine; Tsoupras, Alexandros; COVID-19: The Inflammation Link and the Role of Nutrition in Potential Mitigation. Nutrients 2020, 12, 1466, https://doi.org/10.3390/nu12051466.
  2. Chih-Cheng Lai; Tzu-Ping Shih; Wen-Chien Ko; Hung-Jen Tang; Po-Ren Hsueh; Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease-2019 (COVID-19): The epidemic and the challenges. International Journal of Antimicrobial Agents 2020, 55, 105924, 10.1016/j.ijantimicag.2020.105924.
  3. Zhou, P.; Yang, X.-L.; Wang, X.-G.; Hu, B.; Zhang, L.; Zhang, W.; Si, H.-R.; Zhu, Y.; Li, B.; Huang, C.-L.; et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 2020, 579, 270–273.
  4. Wan, Y.; Shang, J.; Graham, R.; Baric, R.S.; Li, F. Receptor recognition by the novel coronavirus from wuhan: An analysis based on decade-long structural studies of SARS coronavirus. J. Virol. 2020, 94, e00120–e00127.
  5. Yan, R.; Zhang, Y.; Li, Y.; Xia, L.; Guo, Y.; Zhou, Q. Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2. Science 2020, 367, 1444–1448.
  6. Gheblawi, M.; Wang, K.; Viveiros, A.; Nguyen, Q.; Zhong, J.-C.; Turner, A.J.; Raizada, M.K.; Grant, M.B.; Oudit, G.Y. Angiotensin converting enzyme 2: SARS-CoV-2 receptor and regulator of the renin-angiotensin system. Circ. Res. 2020, 126, 1456–1474.
  7. Chen, L.; Hao, G. The role of angiotensin-converting enzyme 2 in coronaviruses/influenza viruses and cardiovascular disease. Cardiovasc. Res. 2020, cvaa093.
  8. Touyz, R.M.; Li, H.; Delles, C. Ace2 the janus-faced protein—From cardiovascular protection to severe acute respiratory syndrome-coronavirus and covid-19. Clin. Sci. (Lond. Engl. 1979) 2020, 134, 747–750.
  9. Li, G.; Fan, Y.; Lai, Y.; Han, T.; Li, Z.; Zhou, P.; Pan, P.; Wang, W.; Hu, D.; Liu, X.; et al. Coronavirus infections and immune responses. J. Med. Virol. 2020, 92, 424–432.
  10. Zhang, W.; Zhao, Y.; Zhang, F.; Wang, Q.; Li, T.; Liu, Z.; Wang, J.; Qin, Y.; Zhang, X.; Yan, X.; et al. The use of anti-inflammatory drugs in the treatment of people with severe coronavirus disease 2019 (COVID-19): The perspectives of clinical immunologists from China. Clin. Immunol. 2020, 214, 108393.
  11. Conti, P.; Ronconi, G.; Caraffa, A.; Gallenga, C.E.; Ross, R.; Frydas, I.; Kritas, S.K. Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by coronavirus-19 (COVID-19 or SARS-CoV-2): Anti-inflammatory strategies. J. Biol. Regul. Homeost. Agents 2020, 34, 1.
  12. Fang Jiang; Liehua Deng; Liangqing Zhang; Yin Cai; Chi‐Wai Cheung; Zhengyuan Xia; Review of the Clinical Characteristics of Coronavirus Disease 2019 (COVID-19). Journal of General Internal Medicine 2020, 35, 1545-1549, 10.1007/s11606-020-05762-w.
  13. Zhe Xu; Lei Shi; Yijin Wang; Jiyuan Zhang; Lei Huang; Chao Zhang; Shuhong Liu; Peng Zhao; Hongxia Liu; Li Zhu; et al.Yanhong TaiChangqing BaiTingting GaoJinwen SongPeng XiaJinghui DongJing‐Min ZhaoFu-Sheng Wang Pathological findings of COVID-19 associated with acute respiratory distress syndrome. The Lancet Respiratory Medicine 2020, 8, 420-422, 10.1016/s2213-2600(20)30076-x.
  14. Fei Zhou; Ting Yu; Ronghui Du; Guohui Fan; Ying Liu; Zhibo Liu; Jie Xiang; Yeming Wang; Bin Song; Xiaoying Gu; et al.Lulu GuanYuan WeiHui LiXudong WuJiuyang XuShengJin TuYi ZhangHua ChenBin Cao Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. The Lancet 2020, 395, 1054-1062, 10.1016/s0140-6736(20)30566-3.
  15. Kritas, S.K.; Ronconi, G.; Caraffa, A.; Gallenga, C.E.; Ross, R.; Conti, P. Mast cells contribute to coronavirus-induced inflammation: New anti-inflammatory strategy. J. Biol. Regul. Homeost. Agents 2020, 34, 34.
  16. Mehta, P.; McAuley, D.F.; Brown, M.; Sanchez, E.; Tattersall, R.S.; Manson, J.J. COVID-19: Consider cytokine storm syndromes and immunosuppression. Lancet 2020, 395, 1033–1034.
  17. Qin, C.; Zhou, L.; Hu, Z.; Zhang, S.; Yang, S.; Tao, Y.; Xie, C.; Ma, K.; Shang, K.; Wang, W.; et al. Dysregulation of immune response in patients with COVID-19 in Wuhan, China. Clin. Infect. Dis. 2020, ciaa248.
  18. Adèle De Masson; Jean-David Bouaziz; Luc Sulimovic; Charles Cassius; Marie Jachiet; Marius-Anton Ionescu; Michel Rybojad; M. Bagot; Tu-Anh Duong; Sndv (French Union Of Dermatologists-Venereologists); et al. Chilblains are a common cutaneous finding during the COVID-19 pandemic: a retrospective nationwide study from France. Journal of the American Academy of Dermatology 2020, null, null, 10.1016/j.jaad.2020.04.161.
  19. Lechien, J.R.; Chiesa-Estomba, C.M.; De Siati, D.R.; Horoi, M.; Le Bon, S.D.; Rodriguez, A.; Dequanter, D.; Blecic, S.; El Afia, F.; Distinguin, L.; et al. Olfactory and gustatory dysfunctions as a clinical presentation of mild-to-moderate forms of the coronavirus disease (COVID-19): A multicenter european study. Eur. Arch. Otorhinolaryngol. 2020. Available online: https://link.springer.com/article/10.1007%2Fs00405-020-05965-1 (accessed on 1 April 2020). [CrossRef]
  20. Akshay Avula; Krishna Nalleballe; Naureen Narula; Steven Sapozhnikov; Vasuki Dandu; Sudhamshi Toom; Allison Glaser; Dany Elsayegh; COVID-19 presenting as stroke.. Brain, Behavior, and Immunity 2020, null, null, 10.1016/j.bbi.2020.04.077.
  21. Taisheng Li; Hongzhou Lu; Wenhong Zhang; Clinical observation and management of COVID-19 patients. Emerging Microbes & Infections 2020, 9, 687-690, 10.1080/22221751.2020.1741327.
  22. World Health Organization. COVID-19 and NCDs. Available online: https://www.who.int/internal-publications-detail/covid-19-and-ncds (accessed on 23 March 2020)
  23. Meredith Wadman; Jennifer Couzin-Frankel; Jocelyn Kaiser; Catherine Matacic; A rampage through the body.. Science 2020, 368, 356-360.
  24. Elfiky, A.A.; Ribavirin, Remdesivir, Sofosbuvir, Galidesivir, and Tenofovir against SARS-CoV-2 RNA dependent rna polymerase (RDRP): A molecular docking study. Life Sci. 2020, 253, 117592, 10.1016/j.lfs.2020.117592.
  25. Alexandros B. Tsoupras; Maria Chini; Nickolaos Tsogas; Elizabeth Fragopoulou; Tzortzis Nomikos; Athina Lioni; Nikolaos Mangafas; Constantinos A. Demopoulos; Smaragdi Antonopoulou; Marios C. Lazanas; et al. Anti-Platelet-Activating Factor Effects of Highly Active Antiretroviral Therapy (HAART): A New Insight in the Drug Therapy of HIV Infection?. AIDS Research and Human Retroviruses 2008, 24, 1079-1086, 10.1089/aid.2007.0263.
  26. David S Fedson; Confronting the next influenza pandemic with anti‐inflammatory and immunomodulatory agents: why they are needed and how they might work. Influenza and Other Respiratory Viruses 2009, 3, 129-142, 10.1111/j.1750-2659.2009.00090.x.
  27. Andrew I Ritchie; Aran Singanayagam; Immunosuppression for hyperinflammation in COVID-19: a double-edged sword?. The Lancet 2020, 395, 1111-1111, 10.1016/s0140-6736(20)30691-7.
  28. Belinda J. Thomas; Rebecca A. Porritt; P J Hertzog; Philip G. Bardin; Michelle D. Tate; Glucocorticosteroids enhance replication of respiratory viruses: effect of adjuvant interferon. Scientific Reports 2014, 4, 7176, 10.1038/srep07176.
  29. Charles E. Samuel; Antiviral Actions of Interferons. Clinical Microbiology Reviews 2001, 14, 778-809, 10.1128/cmr.14.4.778-809.2001.
  30. Rami Sommerstein; Michael M. Kochen; Franz H. Messerli; Christoph Gräni; Coronavirus Disease 2019 (COVID‐19): Do Angiotensin‐Converting Enzyme Inhibitors/Angiotensin Receptor Blockers Have a Biphasic Effect?. Journal of the American Heart Association 2020, 9, e016509, 10.1161/jaha.120.016509.
  31. Cantong Zhang; Shaoying Huang; Fengping Zheng; Yong Dai; Controversial treatments: An updated understanding of the coronavirus disease 2019. Journal of Medical Virology 2020, null, null, 10.1002/jmv.25788.
  32. Philippe Colson; Jean-Marc Rolain; Jean-Christophe Lagier; Philippe Brouqui; Didier Raoult; Chloroquine and hydroxychloroquine as available weapons to fight COVID-19. International Journal of Antimicrobial Agents 2020, 55, 105932, 10.1016/j.ijantimicag.2020.105932.
  33. Manli Wang; Ruiyuan Cao; Leike Zhang; Xinglou Yang; Jia Liu; Mingyue Xu; Zhengli Shi; Zhihong Hu; Wu Zhong; Gengfu Xiao; et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro. Cell Research 2020, 30, 269-271, 10.1038/s41422-020-0282-0.
  34. Xueting Yao; Fei Ye; Miao Zhang; Cheng Cui; Baoying Huang; Peihua Niu; Xu Liu; Li Zhao; Erdan Dong; Chunli Song; et al.Siyan ZhanRoujian LuHaiyan LiWenjie TanDongyang Liu In Vitro Antiviral Activity and Projection of Optimized Dosing Design of Hydroxychloroquine for the Treatment of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Clinical Infectious Diseases 2020, null, ciaa237, 10.1093/cid/ciaa237.
  35. Eva Schrezenmeier; Thomas Dorner; Mechanisms of action of hydroxychloroquine and chloroquine: implications for rheumatology. Nature Reviews Rheumatology 2020, 16, 155-166, 10.1038/s41584-020-0372-x.
  36. Dan Zhou; Sheng-Ming Dai; Qiang Tong; COVID-19: a recommendation to examine the effect of hydroxychloroquine in preventing infection and progression. Journal of Antimicrobial Chemotherapy 2020, null, dkaa114, 10.1093/jac/dkaa114.
  37. Ognjen Culić; Vesna Eraković; Ivana Cepelak; Karmela Barišić; Karmen Brajsa; Zeljko Ferencić; Ruzica Galović; Ines Glojnarić; Zoran Manojlović; Vesna Munić; et al.Renata Novak-MircetićVerica Pavicić-BeljakMirna SucićMarija VeljacaTihana Zanić-GrubisićMichael J. Parnham Azithromycin modulates neutrophil function and circulating inflammatory mediators in healthy human subjects. European Journal of Pharmacology 2002, 450, 277-289, 10.1016/s0014-2999(02)02042-3.
  38. Avraham Beigelman; Cassandra L Mikols; Sean P Gunsten; Carolyn L. Cannon; Steven L. Brody; Michael J Walter; Azithromycin attenuates airway inflammation in a mouse model of viral bronchiolitis. Respiratory Research 2010, 11, 90-90, 10.1186/1465-9921-11-90.
  39. Hiroaki Takatori; Yuka Kanno; Zhi Chen; John J. O’Shea; New complexities in helper T cell fate determination and the implications for autoimmune diseases. Modern Rheumatology 2008, 18, 533-541, 10.3109/s10165-008-0099-z.
  40. Philippe Gautret; Jean-Christophe Lagier; Philippe Parola; Van Thuan Hoang; Line Meddeb; Morgane Mailhe; Barbara Doudier; Johan Courjon; Valérie Giordanengo; Vera Esteves Vieira; et al.Hervé Tissot DupontStéphane HonoréPhilippe ColsonEric ChabrièreBernard La ScolaJean-Marc RolainPhilippe BrouquiDidier Raoult Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial. International Journal of Antimicrobial Agents 2020, null, 105949, 10.1016/j.ijantimicag.2020.105949.
  41. Trump, D.J. White House Coronavirus Task Force Press Conference. Available online: https://www.politico.com/video/2020/04/04/trump-says-he-may-take-hydroxychloroquine-070784 (accessed on 4 April 2020).
  42. Kalil, A.C. Treating COVID-19-off-label drug use, compassionate use, and randomized clinical trials during pandemics. JAMA 2020, 2763802. Available online: https://jamanetwork.com/journals/jama/fullarticle/2763802 (accessed on 4 April 2020).
  43. Brian Owens; Excitement around hydroxychloroquine for treating COVID-19 causes challenges for rheumatology. The Lancet Rheumatology 2020, 2, e257-e257, 10.1016/s2665-9913(20)30089-8.
  44. Singh, R. Need for abundant caution in prophylactic application of chloroquine and hydroxychloroquine for viral infections including COVID-19: Possibility of increased susceptibility. Soc. Sci. Res. Netw. 2020, 3570607. Available online: http://dx.doi.org/10.2139/ssrn.3570607 (accessed on 4 April 2020).
  45. Zhaowei Chen; Jijia Hu; Zongwei Zhang; Shan Shan Jiang; Shoumeng Han; Dandan Yan; Ruhong Zhuang; Ben Hu; Zhan Zhang; Efficacy of hydroxychloroquine in patients with COVID-19: results of a randomized clinical trial. medRxiv 2020, 2020, 20040758, 10.1101/2020.03.22.20040758.
  46. Andrea Cortegiani; Giulia Ingoglia; Mariachiara Ippolito; Antonino Giarratano; Sharon Einav; A systematic review on the efficacy and safety of chloroquine for the treatment of COVID-19. Journal of Critical Care 2020, 57, 279-283, 10.1016/j.jcrc.2020.03.005.
  47. Joseph Magagnoli; Siddharth Narendran; Felipe Pereira; Tammy Cummings; James W Hardin; S Scott Sutton; Jayakrishna Ambati; Outcomes of hydroxychloroquine usage in United States veterans hospitalized with Covid-19. medRxiv 2020, 2020, 20065920, 10.1101/2020.04.16.20065920.
  48. France Bars Use Of Hydroxychloroquine In COVID-19 Cases . npr. Retrieved 2020-5-27
  49. Christian A. Devaux; Jean-Marc Rolain; Philippe Colson; Didier Raoult; New insights on the antiviral effects of chloroquine against coronavirus: what to expect for COVID-19?. International Journal of Antimicrobial Agents 2020, 55, 105938, 10.1016/j.ijantimicag.2020.105938.
  50. Mahmoud Gheblawi; Kaiming Wang; Anissa Viveiros; Quynh Nguyen; Jiu-Chang Zhong; Anthony J. Turner; Mohan K. Raizada; Maria B. Grant; Gavin Y. Oudit; Angiotensin-Converting Enzyme 2: SARS-CoV-2 Receptor and Regulator of the Renin-Angiotensin System. Circulation Research 2020, 126, 1456-1474, 10.1161/circresaha.120.317015.
  51. Li Chen; Guang Hao; The role of angiotensin-converting enzyme 2 in coronaviruses/influenza viruses and cardiovascular disease. Cardiovascular Research 2020, null, cvaa093, 10.1093/cvr/cvaa093.
  52. Rhian Touyz; Hongliang Li; Christian Delles; ACE2 the Janus-faced protein - from cardiovascular protection to severe acute respiratory syndrome-coronavirus and COVID-19.. Clinical Science 2020, 134, 747-750, 10.1042/CS20200363.
  53. Murray Esler; Danielle Esler; Can angiotensin receptor-blocking drugs perhaps be harmful in the COVID-19 pandemic?. Journal of Hypertension 2020, 38, 781-782, 10.1097/hjh.0000000000002450.
  54. Ankit B Patel; Ashish Verma; COVID-19 and Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: What Is the Evidence?. JAMA 2020, 323, 1769–1770, 10.1001/jama.2020.4812.
  55. European Society of Cardiology. Position Statement of the ESC Council on Hypertension on ACE-Inhibitors and Angiotensin Receptor Blockers. Available online: https://www.escardio.org/Councils/Council-on-Hypertension-(CHT)/News/position-statement-of-the-esc-council-on-hypertension-on-ace-inhibitors-and-ang (accessed on 11 April 2020).
  56. B. Murray; Richard J. Fitzgerald; Angiotensin Converting Enzyme Inhibitory Peptides Derived from Food Proteins: Biochemistry, Bioactivity and Production. Current Pharmaceutical Design 2007, 13, 773-791, 10.2174/138161207780363068.
  57. Manish Pareek; Mansoor N Bangash; Nilesh Pareek; Daniel Pan; Shirley Sze; Jatinder S Minhas; Wasim Hanif; Kamlesh Khunti; Ethnicity and COVID-19: an urgent public health research priority. The Lancet 2020, 395, 1421-1422, 10.1016/s0140-6736(20)30922-3.
  58. Akangsha Sur Roy; Montgomery Matson; Rahul Herlekar; Response to ‘Vitamin D concentrations and COVID-19 infection in UK Biobank’. Diabetes & Metabolic Syndrome: Clinical Research & Reviews 2020, 14, 561–565, 10.1016/j.dsx.2020.05.049.
  59. Ryan A. Watson; Drew M. Johnson; Robin N. Dharia; Geno J. Merli; John U. Doherty; Anti-Coagulant and Anti-Platelet Therapy in the COVID-19 Patient: A Best Practices Quality Initiative Across a Large Health System. Hospital Practice 2020, ;, 10.1080/21548331.2020.1772639, https://doi.org/10.1080/21548331.2020.1772639.
  60. Klok, F.A.; Kruip, M.J.H.A.; van der Meer, N.J.M.; Arbous, M.S.; Gommers, D.A.M.P.J.; Kant, K.M.; Kaptein, F.H.J.; van Paassen, J.; Stals, M.A.M.; Huisman, M.V.; et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb. Res. 2020. Available online: https://www.ncbi.nlm.nih.gov/pubmed/32291094 (accessed on 1 April 2020).
  61. Ronan Lordan; Alexandros Tsoupras; Ioannis Zabetakis; Platelet activation and prothrombotic mediators at the nexus of inflammation and atherosclerosis: Potential role of antiplatelet agents.. Blood Reviews 2020, null, 100694, 10.1016/j.blre.2020.100694.
  62. Pandong LuoLiu; Dong Liu; Juan Li; Pharmacological perspective: glycyrrhizin may be an efficacious therapeutic agent for COVID-19. International Journal of Antimicrobial Agents 2020, null, 105995, 10.1016/j.ijantimicag.2020.105995.
  63. Wang, J.-Z.; Zhang, R.-Y.; Bai, J. An anti-oxidative therapy for ameliorating cardiac injuries of critically ill COVID-19-infected patients. Int. J. Cardiol. 2020. Available online: https://www.ncbi.nlm.nih.gov/pubmed/32321655 (accessed on 1 April 2020).
  64. Lei Zhang; Yunhui Liu; Potential interventions for novel coronavirus in China: A systematic review. Journal of Medical Virology 2020, 92, 479-490, 10.1002/jmv.25707.
  65. Riccardo Caccialanza; Alessandro Laviano; Federica Lobascio; Elisabetta Montagna; Raffaele Bruno; Serena Ludovisi; Angelo Guido Corsico; Antonio Di Sabatino; Mirko Belliato; Monica Calvi; et al.Isabella IaconaGiuseppina GrugnettiElisa BonadeoAlba MuzziEmanuele Cereda Early nutritional supplementation in non-critically ill patients hospitalized for the 2019 novel coronavirus disease (COVID-19): Rationale and feasibility of a shared pragmatic protocol. Nutrition 2020, 74, 110835, 10.1016/j.nut.2020.110835.
  66. Rocco Barazzoni; Stephan C. Bischoff; Joao Breda; Kremlin Wickramasinghe; Zeljko Krznaric; Dorit Nitzan; Matthias Pirlich; Pierre Singer; Endorsed By The Espen Council; ESPEN expert statements and practical guidance for nutritional management of individuals with SARS-CoV-2 infection. Clinical Nutrition 2020, 39, 1631-1638, 10.1016/j.clnu.2020.03.022.
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Subjects: Pathology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Ioannis Zabetakis
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Ronan Lordan
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Catherine Norton
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Alexandros Tsoupras
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Entry Collection: COVID-19
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Update Date: 06 Nov 2020
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