Response to Dr. Spaeder by Massimo Citro Della Riva, M.D.
Dear Colleague,
I have read your response to the letter of Abp. Carlo M. Viganò. I am also a doctor who has spent more than a year and a half treating those who are infected with SARS-CoV-2, and I do not agree with your affirmations; therefore, in order to continue on the path of mutual constructive criticism, I feel I should respond.
When Abp. Viganò writes about gene serums, he does not necessarily intend to allude to a product that integrates itself into our genome, but rather to a messenger RNA that is itself a gene molecule, since it is a ribonucleic acid. These serums cannot be called vaccines, since a vaccine is a pathogen or a part of a pathogen, either attenuated or inactivated, which is capable of inducing immunity. In contrast, the serums are experimental molecules (already used to treat various oncological pulmonary pathologies, such as cystic fibrosis and other diseases, but never until now experimented with to treat a viral infection) that do not induce immunity but rather produce spikes, which in turn must induce antibodies. The spikes are the toxic and poisonous part of this virus and also the most subject to mutation.
In any case, the reverse transcription of viral RNA is also possible,[1] as occurs with other RNA viruses, which is then capable of triggering long-term chronic diseases.[2] The reverse transcription of the vaccine mRNA is for now only hypothetical, just as it is for the DNA of the adenovirus vector: It is, however, plausible due to the presence of retrotransposons. It is known for certain that protein N of SARS-CoV-2 is transcribed into our DNA.[3] The vaccine mRNAs remain potentially oncogenic by integration or by genetic (epigenetic) interference. It has recently been discovered that the spike is located in the nucleus and inhibits the repair of DNA damage, preventing adaptive immunity.[4] Therefore, I would not be so sure that the vaccine mRNA cannot reverse transcribe itself into our DNA.
I am happy that you mentioned that vaccines always carry a component of risk, and so they should only be used when the benefit outweighs the risk. But this is not the case with COVID-19, where the benefit is almost zero and the risks are high. We are talking about an infection that is perfectly treatable, with a lethality of less than 1%; thus there is no need for vaccination. Furthermore, the lack of efficacy is there for all to see: these serums do not interrupt transmission; they do not prevent infection; indeed, most of the time infection follows vaccination. Furthermore, those who are vaccinated are contagious and continue to infect people, thereby increasing the epidemic. These serums induce variants which, as you know, are mutations by which the virus escapes the vaccine. The low efficacy of these vaccines is evident from observing the situation in Israel, where there is a worrisome increase in hospitalizations, above all among people between 40 and 50 years old who are fully vaccinated.[5]
An investigation in hospitals in Israel has documented that almost 100% of those hospitalized had previously been vaccinated,[6] and they are already considering giving a fourth dose of the vaccine in the nation that was the first to inoculate its inhabitants with the third dose.[7] In Norway, where the majority of the population is vaccinated, the number and percentage of hospitalizations related to COVID-19 is increasing among vaccinated patients, and vaccination has not reduced the probability of death in the hospital.[8] Waterford is the county in Ireland with the highest rate of SARS-CoV-2 infection, even though 99.7% of its residents are vaccinated.[9] Gibraltar is the place in the world with the highest percent of vaccinated people (119% [This includes the 19% who travel from abroad to the island]) and the absence of those who are not vaccinated, and yet is recording a continual exponential increase in COVID-19 infections.[10] The number of neutralizing antibodies present after vaccination is lower than in uninfected controls.[11]
There is no difference in viral loads between the vaccinated and the non-vaccinated, and if the vaccinated are infected by the delta variant, they can be a course of transmission of SARS-CoV-2 to others.[12] In the case of the delta variant, the neutralizing antibodies have a reduced affinity for the spike protein.[13] There is no difference in the viral load between the vaccinated and the non-vaccinated who are infected by the delta variant.[14] There is a very poor response to the vaccines among those who have the delta variant.[15] In almost 70 nations the number of COVID-19 is increasing despite all the vaccinations.[16] Here in Italy, the population continues to be infected and the hospitals are full, despite the fact that 85% of the population is vaccinated. These serums are proving to be completely ineffective as well as useless.
It is said the serums help people contract a milder form of infection, but I want to remind you that this infection always begins in a mild form and that before it evolves (in a small number of cases) into a more severe form, several days pass during which it is perfectly treatable. If properly treated right away, people get well. None of my patients who have been treated as soon as they become infected have ever been hospitalized, and the thousands of Italian doctors who treat patients immediately report a rate of hospitalization that is less than 1%.[17] The same holds true for colleagues from other European nations with whom I am in contact.
The treatments you call “alternative” are not at all alternative, and they have existed since the very first case of SARS (I wish to remind you that the current virus is actually the second SARS, that the virus is almost identical to SARS-CoV-1 and so are its clinical manifestations), as can be found in literature beginning in 2003. The fact that hydroxychloroquine (HCQ) can inhibit coronaviruses is found in literature beginning right after SARS; one cannot say this was not known. In SARS-CoVs generally, HCQ increases the endosomal pH and interferes with the terminal glycosylation of the cell receptor (ACE2).[18] Chloroquine inhibits SARS-CoV replication.[19] HCQ is an effective inhibitor of the replication of SARS-CoV both in vitro and also in vivo: SARS-CoV-1 (viral replication reduced by 99% after three days), MERS-CoV, HCoV-229E, HCoV-OC43.[20] In mice, chloroquine transmitted to newborns protects it from the lethal challenge of human HCoV-OC43.[21]
COVID-19 is perfectly treatable, but it must be treated immediately, without wasting time, preferably within the first two days. HCQ also has an anti-viral action: Hydroxychloroquine (400 mg per day) and azythromicin (500 mg per day) for at least five days, up to 10 days.[23] In China, HCQ has even been found to be useful in treating COVID-19 pneumonia, and it is recommended “to include it in the next guidelines for the treatment of COVID-19 pneumonia.[24]
Hydroxychloroquine has all the characteristics to be confirmed as the drug of choice in the prophylaxis of early-stage coronavirus complications, and derivatives from China are being studied by the U.S. FDA as a treatment for COVID-19.[25] As much as 37% of the 6,227 doctors from 30 different nations who have cast an international vote consider HCQ to be the most effective treatment for COVID-19.[26] Colyer and Hinthorn call it “a first-line treatment,” especially when combined with azythromicin.[27] A German research group has invented hydroxychloroquine in an aerosol form and experimented with excellent results: Instead of receiving 400 mg in a systemic way, the patient receives 2-4 mg through inhalation, without toxicity.[28]
Ivermectin, alone or in association, is an anthelmintic with anti-bacterial, anti-viral and anti-tumoral activity, which acts on flaviviruses, HIV, Ebola and Zika,[29] blocks the RNA virus of respiratory diseases in pigs[30] and neutralizes SARS-CoV-2 in 48 hours in vitro.[31] Quercetin is also effective in the first phase of the disease,[32] acting as a powerful viral inhibitor against SARS-CoV-2, of which it blocks the 3CL (3-chymotrypsin-like) proteases, also called Mpro, which are essential in the replication cycle,[33] and this was divulged by a printed communication of the CNR Institute of Nanotechnology,[34] completely ignored by health institutions.
Quercetin has a synergic action with vitamin C in the prevention and treatment of SARS-CoV-2.[35] Cortisone (dexamethasone and betamethasone) also acts on the same proteases.[36] Another SARS-CoV-2 3CL protease inhibitor is ebselen,[37] “an organic selenium compound with anti-inflammatory, anti-oxidant and cyto-protective properties, studied for the treatment of bipolar disorders and hearing loss, with very low toxicity and with a strong clinical potential for the treatment of coronaviruses.”[38] Confirmation of ebselen’s action against SARS-CoV-2 comes from the Milan Politecnico [Clinic],[39] with a confirmatory study describing its mechanism of action.[40] Ebselen is a powerful inhibitor of SARS-CoV-2.[41]
Another inhibitor of these proteases is cinanserin: Already in 2005 the European Commission certified that the treatment for SARS-CoV had been found, since cinanserin inhibits the SARS coronavirus in a significant way and is a ready-to-use drug for treating SARS.[42] This is in an official document of the European Commission. We recall that 3CL, or Mpro, is the main protease present in coronaviruses.[43] The strong inhibition of cinanserin on the replication of SARS-CoV is in [medical] literature: “The binding of cinanserin and its hydrochloride to bacterially expressed 3CLpro of SARS-CoV and of the relative human coronavirus 229E (HCoV-229E) has been demonstrated by resonance technology of the surface plasmon. It is specific for the 3CL coronaviruses,”[44] and these proteases are present in SARS-CoV-2. “The design and development of specific antiviral drugs with direct anti-SARS-CoV-2 action can be made possible by targeting conserved enzymes such as the 3C protease.”[45] Cinanserin inhibits SARS-CoV-2.[46] A virtual screening confirmed the inhibitory activity of cinanserin and ebselen on the SARS-CoV-2 substrate Mpro.[47]
Since thromboembolisms are among the worst complications, the anti-coagulant action of low-molecular-weight heparin (enoxaparin) is needed.[48] Furthermore, the spike-binding domain of SARS-CoV-2 interacts with heparin.[49] When it opens to meet the ACE-2s (which are electronegative), the spike takes on a strong positive charge that allows it to connect.[50] Heparin is a mixture of mucopolysaccharides whose N-sulfate groups give it the highest electronegative charge of any known biomolecules, including ACE-2 receptors.[51] Thus heparin and spike attract one another like a magnet, taking the virus away from our receptors. Early use of heparin reduces the risk of serious development [of the coronavirus]. Hydroxyxchloroquine exercises a safe anti-thrombotic action,[52] and works in synergy with low-molecular-weight heparin.[53] Most importantly: The coagulative complications of coronavirus were in literature ever since SARS and MERS,[54] and have been covered up. Why was the grave danger of thromboembolisms not immediately divulged to all medical personnel? And why instead was it stubbornly concealed? We could have avoided thousands of deaths. As for cortisone, it is known to be the drug of choice for treating the cytokine storm and has been confirmed by clinical practice and a vast literature.
In support of treatment there are cholecalciferol (always associated with menaquinone), ascorbic acid and zinc. In 2020, 300 different works were published about the benefits of cholecalciferol in COVID-19.[55] The D3 is important in the prevention and treatment of COVID-19,[56] it can reduce the risk of this infection,[57] it inhibits the IL-17 mediated response,[58] it has a role in the cytokine storm and in COVID-19 mortality.[59] Its deficiency increases the risk of infection and aggravates ARDS[60] and COVID-19 patients need higher doses of vitamin D3.[61] It protects and prevents ARDS.[62] It is recommended in at-risk patients.[63] It helps to prevent infection from SARS-CoV-2 to inhibit the cytokine storm by suppressing NFkB, IL-6 and TNF, and to prevent the loss of neurosensation by stimulating neurotrophins such as NGF.[64] Compared to the untreated, high doses of D3 reduce fibrinogen and negativize viral RNA.[65]
By improving mucociliar cleareance, zinc removes pathogens from the respiratory pathways,[73] inhibits the “RNA polymerase RNA dependent” enzyme[74] that replicates viruses to RNA, and reduces the activity of ACE-2 receptors.[75] Low levels of zinc are associated with the worsening of COVID-19 patients.[76] Zinc supplements are recommended in COVID-19 patients and the increase of mucociliar clearance is confirmed, epithelial integrity is strengthened, viral replication is inhibited, anti-viral activity is increased, the risks of hyper-inflammation are attenuated and pulmonary damage is reduced as well as the risk of secondary infections.[77] In COVID-19 zinc is just as effective as treatment, above all if it is combined with hydroxychloroquine and azithromyhcin.[78] The hydroxychloroquine-azithromycin-zinc combination is valid.[79] Chloroquine acts as a zinc ionophore, facilitating entry into the cell.[80]
Ascorbic acid is among the most powerful anti-infectives and anti-virals,[81] as confirmed in the previous SARS outbreak[82]; it promotes phagocytosis and protects epithelial barriers.[83] A double-blind, randomized study of those hospitalized with acute respiratory infections found that vitamin C improves the course of the infection.[84, 85] In COVID-19, doses of 2–8 g per day orally prevent respiratory infections and 6–24 g per day intravenously reduces mortality in its severe pulmonary forms.[86] The sick hospitalized through COVID-19 in China have been treated with high doses (even tens of grams) intravenously.[87] In Shanghai, dozens of moderate and serious patients have been treated with high doses of vitamin C intravenously.[88] Intravenous vitamin C has been given in severe cases of COVID-19 with sepsis.[89] Timely high doses of vitamin C improve COVID-19 pneumonia.[90] Two research groups, in Shanghai and Guangszhou, recommend high doses of intravenous ascorbate for the treatment of ARDS, with other supportive treatments, including vitamin D3 and zinc.[91] Intravenous ascorbate along with steroids and vitamin D3 resolve sepsis in critical patients.[92] Vitamin C prevents complications and reduces alveolar fluid by inhibiting the activation of neutrophils and reducing alveolar damage.[93]
Prevention is helpful with the anti-inflammatory and immunomodulating glycoprotein lactoferrin, which has an anti-viral action of ample spectrum, including against coronaviruses and SARS-CoV-2, and is helpful also in treatment.[94] It inhibits the entrys of SARS-CoV-2 in cells by blocking the heparin sulfate, a co-receptor of ACE-2. This glucoprotein restores iron homeostasis and reduces oxidative stress and inflammation.[95]
Archbishop Viganò is perfectly correct when he writes that these drugs have been systematically boycotted by the WHO and regulatory agencies. And I would add: These drugs have been unjustly maligned. It is enough to think of hydroxycholoroquine. Two completely made-up studies in The Lancet and The New England Journal of Medicine claimed to potray this drug as toxic[96]: They were discovered and withdrawn, but they served to make HCQ to be withdrawn almost worldwide. An obvious boycott! All studies adverse to HCQ are financed by the pharmaceutical industry or by agencies tied to Mr. William Henry Gates III or have conflicts of interest, therefore they have zero credibility. Beginning with the three who argued that the cardiotoxicity of HCQ (usually estimated to be less than 1%) was 10%[97], or 19%[98] or even 33%.[99] All of these studies are worthless, and the list goes on and on.
The effectivness of hyperimmune plasma has been well known ever since the first SARS,[100] and it is also well known during this second outbreak.[101] But perhaps plasma was uncomfortable for someone who has more interest in making space for monoclonals. Therefore, Dr. Spaeder, don’t say that there are not treatments, because this makes us co-responsible for millions of deaths of people who have not been treated precisely because, although there were treatments, these treatments were denied them. This pandemic is a true massacre, a second holocaust.
Let us ask ourselves why traditional vaccines with attenuated SARS-CoV-2 have not been prepared. And why did they target the spike and not the M and N proteases, which are not toxic and do not mutate (and thus we would not have had the variants of the vaccine)? Other authors are asking the same thing.[102] Instead, with these serums that produce trillions of spikes, we have obtained dangerous and deadly effects and continuous variations that extend the pandemic. I remind you of them. In addition to the well-known high risk of ADE[103] and of auto-immunity,[104] the spike can behave like a prion,[105] therefore it is neurotoxic,[106] it is cardiotoxic [107] and above all it is harmful to the endothelium, provoking endothelitis with hypercoagulation and thromboembolism.[108]
I remind you it has been demonstrated that the spike is sufficient, apart from the virus, precisely as a product of these serums, to harm the organism and to produce damage to the lungs, the arteries and the endothelium in general.[109] Even the S1 subunit of the spike is sufficient.[110] These two studies demonstrate that, once the replicating capacity of the virus is removed, cells are damaged by the spike, only and exclusively by the spike. And it is precisely this that is produced inside the bodies of those who are vaccinated. Another study confirms that the S1 subunit of the spike significantly increases the pro-inflamatory cytokines (αTNF, IL6, IL1β, IL8) through the activation of the inflammasomes NFkB, p38 MAPK and NLRP3, and confirms that the pre-treatment with cortisone reducese the release of cytokines.[111]
Therefore, Abp. Viganò is perfectly correct in recalling the danger and mortality of these serums. The medical-scientific literature says so, and not only the sites which you cited and called “anti-vaccine propaganda.” Look at the European data reported by EudraVigilance, which certainly cannot be called no-vax.[112] Instead, many now see it is pro-vaccine propaganda, supported and directed by supra-national sovereign groups that have other purposes than the health of the population, propaganda based only on private studies that are worthless because they collude with the industry. Among many other examples, the example of the first study on the Pfizer vaccine applies, which claims the vaccine has a 95% rate of effectiveness and the absence of any toxicity, which is financed by Pfizer and BioNTech.[113, 114] The same applies to the recent study on the vaccination for children from 5 to 11 years, which is called safe and effective, also financed by Pfizer and BioNTech. It has zero scientific value. Or the study done by Moderna, which was financed by Moderna, NIAID and the pharmaceutical industries.[115] All this is not science. It is a criminal scam.
In closing, I would like to remind you, my esteemed Colleague, that we are doctors, and we have the duty to protect our patients, to work for their good and not for the good of those who pursue their own interests, contrary to medicine and the life of the population. We ought to think for ourselves and not robotically repeat the anti-scientific slogans of the mainstream and the oligarchic system illegitimately governing the planet. We have sworn by Asclepius, not by multinationals. I thank Abp. Viganò for his precious contribution to the search for truth, the thing we scientists ought to always do. Apparently, the Archbishop is more of a scientist than us.
Massimo Citro Della Riva, M.D.
[1] Zhang L et al, SARS-CoV-2 RNA reverse-transcribed and integrated into the human genome. https://doi.org/10.1101/2020.12.12.422516.
Zhang L et al, Reverse-transcribed SARS-CoV-2 RNA can integrate into the genome of cultured human cells and can be expressed in patient-derived tissues. PNAS. 2021, 118 (21):e2105968118.
[2] Balada E et al, Implication of human endogenous retroviruses in the development of autoimmune disease. Int Rev Immunol. 2010; 29(4):351-70.
Voisset C et al, Human RNA “rumor” viruses: the search for novel human retroviruses in chronic disease. Microbiol Mol Biol Rev. 2008; 72(1):157-96.
[3] Zhang L et al, cit. PNAS. 2021.
[4] Jiang H et al, SARS–CoV–2 Spike Impairs DNA Damage Repair and Inhibits V(D)J Recombination In Vitro. Viruses. 2021; 13(10):2056.
[5] https://www.adhocnews.it/israele-preoccupante-aumento-dei-ricoveri-tra-i-pienamente-vaccinati/
[6] https://visionetv.it/dea-in-israele-quasi-tutti-i-ricoverati-erano-stati-vaccinati/
[7] https://www.iltempo.it/attualita/2021/09/06/news/quarta-dose-vaccino-israele-calo-anticorpi-pandemia-calo-efficacia-vaccini-dati-numeri-28567896/
[8] Whittaker R et al, Patient trajectories among hospitalised COVID-19 patients vaccinated with an mRNA vaccine in Norway: a register-based cohort study. https://doi.org/10.1101/2021.11.05.21265958
[9] https://www.irishtimes.com/news/health/waterford-city-district-has-state-s-highest-rate-of-covid-19-infections-1.4707344
[10] https://www.secondopianonews.it/attualita/2021/11/22/gibilterra-centro-piu-vaccinato-al-mondo-annulla-il-natale-troppi-contagi.html
[11] Chau N et al, Transmission of SARS-CoV-2 Delta Variant Among Vaccinated Healthcare Workers, Vietnam. Preprint on The Lancet, 2021, oct. 11.
[12] Riemersma KK et al, Vaccinated and unvaccinated individuals have similar viral loads in communities with a high prevalence of the SARS-CoV-2 delta variant. medRxiv 2021.07.31.21261387.
[13] Yahi N et al, Infection-enhancing anti-SARS-CoV-2 antibodies recognize both the original Wuhan/D614G strain and delta variants. A potential risk for mass vaccination? J of Infection. 2021; 83(5):607-35.
[14] Acharya C et al, No significant difference in viral load between vaccinated and unvaccinated, asymptomatic and symptomatic groups when infected with SARS-CoV-2 delta variant. medRxiv 2021.09.28.21264262.
[15] Eyre D et al, The impact of SARS-CoV-2 vaccination on Alpha & Delta variant transmission. MedRxiv. 2021. Doi: 10.1101/2021.09.28.21264260.
[16] Subramanian SV, Kumar A, Increases in COVID-19 are unrelated to levels of vaccination across 68 countries and 2947 counties in the United States. Eur J Epidemiol. 2021 Sep 30: 1–4.
[17] https://www.bing.com/videos/search?q=testimonanzie+medici+cure+domiciliari+precoci+grimaldi+covid&&view=detail&mid=1157CE3EEF5FED45E9691157CE3EEF5FE
[18] Anirudhan V et al, Targeting SARS-CoV-2 viral proteases as a therapeutic strategy to treat COVID-19. J med Virol. 2021; 93(5):2722-34.
[19] Savarino A et al, New insights into the antiviral effects of chloroquine, Lancet Infect Dis. 2006;6(2):67-69.
[20] Keyaerts E et al, In vitro inhibition of severe acute respiratory syndrome coronavirus by chloroquine, cit. 2004.
[21] Keyaerts E et al, Antiviral activity of chloroquine against human coronavirus OC43 infection in newborn mice. Antimicrob Agents Chemother. 2009; 53:3416-21.
[22] Yao X et al, 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), Clin Infect Dis, 2020 Mar 9; ciaa237.
Chandler LC et al, Immunomodulatory Effects of Hydroxychloroquine and Chloroquine in Viral Infections and their potential Application in Retinal Gene Therapy. Int J Mol Sci. 2020; 21(14):4972.
Meo SA et al, Efficacy of Chloroquine and Hydroxychloroquine in the Treatment of COVID-19, Eur Rev Med Pharmacol Sci Actions, 2020;24(8):4539-47.
[23] Raoult D et al, Outcomes of 3,737 COVID-19 patients treated with hydroxychloroquine/azithromycin and other regimens in Marseille, France: A retrospective analysis, Travel Med Infect Dis. 2020 July-August; 36: 101791.
Gautret P et al, Clinical and microbiological effect of a combination of hydroxychloroquine and azithromycin in 80 COVID-19 patients with at least a six-day follow up: A pilot observational study, Travel Med Infect Dis, 2020; 34:101663.
Gautret P et al, Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial, Int J Antimicrob Agents, 2020; 20:105949.
Chen Z et al, Efficacy of hydroxychloroquine in patients with COVID-19: results of a randomized clinical trial. doi.org/10.1101/2020.03.22.20040758.
[24] Gao J et al, Breakthrough: chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies. Biosci Trend. 2020; 14(1):72-73.
[25] Tarek M Abd El-Aziz, JD Stockand, Recent Progress and Challenges in Drug Development against COVID-19 Coronavirus (SARS-CoV-2) – An Update on the Status, Infect Genet Evol, 2020; 83:104327.
[26] Sermo.Com (2020) Breaking Results: Sermo’s COVID-19 Real Time Barometer Study, available at Sermo’s COVID-19-Barometer Web
[27] Sass E, Dr. Jeff Colyer: Combo of existing drugs shows promise against COVID-18. 24/3/20. https://theeconomicstandard.com/combo-of-existing-drugs-shows-promise-against-covid-19
[28] Klimke A et al, Hydroxychloroquine as an aerosol might markedly reduce and even prevent severe clinical symptoms after SARS-CoV-2 infection, Med Hypotheses. 2020; 142: 109783.
[29] Dong S et al, Identification of anti-flaviviral drugs with mosquitocidal and anti-Zika virus activity in Aedes aegypti. PLoS Negl Trop Dis. 2019;13(8):e0007681.
Wagstaff KM et al, Ivermectin is a specific inhibitor of importin α/β-mediated nuclear import able to inhibit replication of HIV-1 and dengue virus. Biochem J. 2012; 443(3):851–6.
[30] Lee YJ, Lee C. Ivermectin inhibits porcine reproductive and respiratory syndrome virus in cultured porcine alveolar macrophages. Arch Virol. 2016 Feb;161(2):257-68.
[31] Caly L et al, The FDA-approved drug ivermectin inhibits the replication of SARS-CoV-2 in vitro. Antiviral Res. 2020; 178: 104787.
[32] Di Pierro F et al, Possible therapeutic effects of adjuvant quercitin supplementation against early-stage COVID-19 infection: A prospective, randomized, controlled and open-label study. Int J Gen Med. 2021; 14:2359-66.
[33] Abian O et al, Structural stability of SARS-CoV-2 3CLpro and identification of quercetin as an inhibitor by experimental screening. Int J Biol Macromolecules. 2000; 164:1693-1703.
[34] https://www.cnr.it/en/press-release/9620/la-molecola-di-origine-naturale-che-inibisce-sars-cov-2
[35] Colunga Biancatelli RM et al, Quercetin and Vitamin C: An Experimental, Synergistic Therapy for the Prevention and Treatment of SARS-CoV-2 Related Disease (COVID-19). Front Immunol. 2020; 11:1451.
[36] Ghosh R et al, Potential therapeutic use of corticosteroids as SARS CoV-2 main protease inhibitors: a computational study. J Biomol Struct Dyn. 2020 :1–14.
[37] Haritha CV, Ebselen, a new candidate therapeutic against SARS-CoV-2. Int J Surg. 2020; 84: 53–56.
[38] Jin Z et al, Structure of Mpro from SARS-CoV-2 and discovery of its inhibitors. Nature. 2020; 582:289–93.
[39] https://scitechdaily.com/ebselen-a-mechanism-to-stop-covid-19-replication.
[40] Daolio A et al, Binding motif of ebselen in solution: chalcogen and hydrogen bonds team up. New J Chemistry. 2020; 47.
[41] Anirudhan V et al, Targeting SARS-CoV-2 viral proteases as a therapeutic strategy to treat COVID-19. J med Virol. 2021; 93(5):2722-34.
[42] https://cordis.europa.eu/article/id/24006-fp6-project-finds-cure-for-sars/it
[43] https://it.abcdef.wiki/wiki/3C-like_protease
[44] Lili Chen et al, Cinanserin is an inhibitor of the 3C-like proteinase of severe acute respiratory syndrome coronavirus and strongly reduces virus replication in vitro. J Virol. 2005;79(11):7095-103.
[45] Ahmad Abu Turab Naqvi et al, Insights into SARS-CoV-2 genome, structure, evolution, pathogenesis and therapies: Structural genomics approach. Biochim Biophys Acta Mol Basis Dis. 2020; 1866(10):165878.
[46] Jin Z et al, Structure of Mpro from SARS-CoV-2 and discovery of its inhibitors. Nature. 2020; 582:289–93.
[47] https://informa.airicerca.org/it/2020/06/24/minireview-mpro-la-principale-proteasi-di-sars-cov-2-e-i-suoi-inibitori
[48] Tang N et al, Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy. J Thromb Haemost. 2020;18(5):1094-9.
[49] Thachil J, The versatile heparin in COVID-19. J Thromb Haemost. 2020; 18(5):1020-2.
[50] Kucherova A et al, Modeling the opening SARS-CoV-2 spike: investigation of its dynamic electro-geometric properties. https://doi.org/10.1101/2020.10.29.361261.
[51] Cox M, Nelson D, Lehninger, Principles of Biochemistry. N.4, Freeman. 2004, p. 1100. ISBN 0-7167-4339-6.
[52] Espinola RG et al, Hydroxychloroquine reverses platelet activation induced by human IgG antiphospholipid antibodies. Thromb Haemost. 2002; 87:518-22.
Szymezak J et al, Hydroxychloroquine: a new therapeutic approach to the thrombotic manifestations of antiphospholipid syndrome. Rev Med Interne. 2010; 31(12):854-7.
Petri M, Use of hydroxychloroquine to prevent thrombosis in systemic lupus erythematosus and in antiphospholipid antibody-positive patients. Curr Rheumatol Rep. 2011; 13(1):77-80.
Schmidt-Tanguy A et al, Antithrombotic effects of hydroxychloroquine in primary antiphospholipid syndrome patients. Thromb Haemost JTH. 2013; 11:1927-9.
Million M et al, Thrombosis and antiphospholipid antibody syndrome during acute Q fever. Medicine (Baltimore) 2017; 96(29):e7578.
Miranda S et al, Hydroxychloroquine reverses the prothrombotic state in a mouse model of antiphospholipid syndrome: Role of reduced inflammation and endothelial dysfunction. PLoS One. 2019; 14(3):e0212614.
[53] Oscanoa TJ et al, A pharmacological perspective of chloroquine in SARS-CoV-2 infection: An old drug for the fight against a new coronavirus? Int J Antimicrob Agents. 2020;56(3):106078.
[54] Dimitrios Gianni et al, Coagulation disorders in coronavirus infected patients: COVID-19, SARS-CoV-1, MERS-CoV and lessons from the past. J Clin Virol. 2020; 127:104362.
Wu YP et al, Analysis of thrombotic factors in severe acute respiratory syndrome (SARS) patients. Thromb Haemost 2006; 96(01): 100-101.
[55] Isaia G, D’Avolio A et al, Vitamina D nella prevenzione e nel trattamento del COVID-19: nuove evidenze. Accademia di Medicina di Torino. 2020. https://www.comune.torino.it/pass/salute.
[56] Laird E et al, Vitamin D and Inflammation: potential implications for severity of Covid-19. Ir Med J. 2020; 113(5):81.
[57] D’Avolio A et al. 25-Hydroxyvitamin D concentration are lower in patients with positive PCR for SARS-CoV-2. Nutrients. 2020; 12(5): 1359.
[58] Fiorino S et al. Cytokine storm in aged people with CoV-2: possible role of vitamins as therapy or preventive strategy. Aging Clin Exp Res. 2020; 32(10): 2115-31.
[59] Daneshkhah A et al, Evidence for possible association of vitamin D status with cytokine storm and unregulated inflammation in Covid-19 patients. Aging Clin Exp Res. 2020; 32(1): 2141-58.
[60] Quesada-Gomez JM et al, Vitamin D receptor stimulation to reduce acute respiratory distress syndrome (ARDS) in patients with coronavirus SARS-CoV-2 infections: Revised Ms SBMB 2020_166. J Steroid Biochem Mol Biol. 2020; 202:105719.
Merzon E et al, Low plasma 25(OH) vitamin D level is associated with increased risk of Covid-19 infection: an Israeli population-based study. FEBS J. 2020; 287(17): 3693-3702.
Boucher B, Vitamin D status as a predictor of Covid-19 risk in Black, Asian and other ethnic minority groups in the UK. Diabetes Metab Res Rev. 2020; 36(8): e3375.
[61] Grant WB et al, Evidence that Vitamin D Supplementation could reduce Risk of Influenza and Covid-19 Infections and Death. Nutrients. 2020; 12(4): 988.
[62] Malaguarnera L, Vitamin D3 and potential treatment adjuncts for Covid-19. Nutrients. 2020; 12(11): 3512.
[63] Nurshad A, Role of vitamin D in preventing of Covid-19 infection, progression and severity. J Infect Public Health. 2020; 13(10): 1373-80.
[64] Yi Xu et al, The importance of vitamin D metabolism as a potential prophylactic, immunoregulatory and neuroprotective treatment for Covid-19. J Transl Med. 2020; 18(1): 322.
[65] Rastogi A et al, Short term, high-dose vitamin D supplementation for COVID-19 disease: a randomized, placebo-controlled, study (SHADE study). Postgraduate Med J. 2020. Doi: 10.1138/postgradmedj-2020-139065.
[66] Jain A et al, Analysis of vitamin D level among asymptomatic and critically ill COVID-19 patients and its correlation with inflammatory markers. Sci Rep. 2020; 10:20191. doi: 10.1038/s41598-020-77093-z
[67] Entrenas Castillo M et al, Effect of calcifediol treatment and best available therapy versus best available therapy on intensive care unit admission and mortality among patients hospitalized for COVID-19: A pilot randomized clinical study. The Journal of Steroid Biochemistry and Molecular Biology. 2020; 203:105751.
[68] Kaufman HW et al, SARS-CoV-2 positivity rates associated with circulating 25-hydroxyvitamin D levels. PLoS ONE. 2020; doi: 10.1371/journal.pone.0239252.
[69] Annweile G et al, Vitamin D supplementation associated to better survival in hospitalized frail elderly COVID-19 patients. The GERIA-COVID quasi-experimental study. Nutrients. 2020; 12(11):3377.
[70] Siuka D et al, Vitamin D supplementation during the Covid.19 pandemic. Mayo Clin Proc. 2020; 95(8): 1804-5.
[71] Ysak H et al, Effects of Vitamin D on Covid-19 Infection and prognosis: A Systematic Review. Risk Manag Health Policy. 2021; 14:31-38.
[72] Giannini S et al, Effectiveness of In-Hospital Cholecalciferol Use on Clinical Outcomes in Comorbid COVID-19 Patients: A Hypothesis-Generating Study. Nutrients. 2021; 13(1): 219.
[73] http://www.medimagazine.it/sars-cov-2-supplementi-di-zinco-rafforzano-gli-antivirali/
[74] Aartjan JW et al, Zn (2+) inhibits Coronavirus and Arterivirus RNA Polymerase Activity in vitro and Zinc Ionophores block the Replication of these Viruses in Cell Culture, PLoS Pathol, 2010; 6(11): e1001176.
[75] Lee MC et al, Zinc supplement augments the suppressive effects of repurposed drugs of NF-kappa B inhibitor on ACE2 expression in human lung cell lines in vitro. doi: https://doi.org/10.1101/2021.01.27.428372
[76] Vogel-Gonzales M et al, Low Zinc Levels at Admission Associates with Poor Clinical Outcomes in SARS-CoV-2 Infection. Nutrients 2021; 13(2):562.
[77] Wessels I et al, The Potential Impact of Zinc Supplementation on COVID-19 Pathogenesis. Front. Immunol., 2020 https://doi.org/10.3389/fimmu.2020.01712.
[78] Shittu MO, Afolami OI, Improving the Efficacy of Chloroquine and Hydroxychloroquine against SARS-CoV-2 may require Zinc Additives – A better Synergy for future COVID-19 clinical trials, Infez Med, 2020; 28(2):192-7.
Derwand R, Scholz M, Does Zinc Supplementation enhance the clinical Efficacy of Chloroquine/Hydroxychloroquine to win Today’s Battle against COVID-19? Med Hypotheses, 2020; 142:109815.
[79] Carlucci PM et al, Hydroxychloroquine and azithromycin plus zinc vs hydroxychloroquine and azithromycin alone: outcomes in hospitalized COVID-19 patients, The Preprint Server for Health Sciences, 2020. doi.org/10.1101/2020.05.02.20080036.
[80] Jing Xue et al, Chloroquine is a zinc ionophore, PLoS One, 2014; 9(10): e109180.
Aartjan JW et al, Zn (2+) inhibits Coronavirus and Arterivirus RNA Polymerase Activity in vitro and Zinc Ionophores block the Replication of these Viruses in Cell Culture, PLoS Pathol, 2010; 6(11): e1001176.
[81] Gorton HC, Jarvis K, The effectiveness of vitamin C in preventing and relieving the symptoms of virus-induced respiratory infections. J Manipulative Physiol Ther. 1999; 22(8): 530-3
[82] Hemilä H, Vitamin C and SARS coronavirus, J of Antimicrobial Chemotherapy. 2003; 52(6): 1049–50.
[83] Carr AC, Maggini S, Vitamin C and immune function. Nutrients. 2017; 9(11):1211.
[84] Hunt C et al, The clinical effects of vitamin C supplementation in elderly hospitalized patients with acute respiratory infections. Int J Vitam Nutr Res.1994;64(3):212-9.
[85] Carr AC, Rowe S, The emerging role of vitamin C in the prevention and treatment of COVID-19. Nutrients. 2020; 12(11):3286.
[86] Holford P et al, Vitamin C—An Adjunctive Therapy for Respiratory Infection, Sepsis and COVID-19. Nutrients. 2020; 12(12): 3760.
[87] https://www.globalresearch.ca/three-intravenous-vitamin-c-research-studies-approved-treating-covid-19/5705405?fbclid=IwAR0S2E
[88] Cheng RZ. Can early and high intravenous dose of vitamin C prevent and treat coronavirus disease 2019 (COVID-19)? Med Drug Discov Published online 2020.
[89] Li J. Evidence is stronger than you think: a meta-analysis of vitamin C use in patients with sepsis. Crit Care. 2018; 22(1):258
[90] Doctor of Growth M.D et al, Orthomolecular Medicine News Service. Chinese special Edition, Feb 16, 2020
[91] Cheng RZ, Kogan M, Davis D, Ascorbate as Prophylaxis and Therapy for COVID-19—Update From Shanghai and U.S. Medical Institutions, Glob Adv Health Med. 2020; 9: 2164956120934768.
[92] Marik PE, Khangoora V, Rivera R, Hooper MH, Catravas J. Hydrocortisone, vitamin C, and thiamine for the treatment of severe sepsis and septic shock: a retrospective before-after study. Chest. 2017; 151(6):1229–38.
[93] Hemilä H, Chalker E. Vitamin C can shorten the length of stay in the ICU: A meta-analysis. Nutrients. 2019; 11(4).
Nabzdyk CS, Bittner EA. Vitamin C in the critically ill – indications and controversies. World J Crit Care Med. 2018; 7(5):52–61.
[94] Chang R et al, Lactoferrin as potential preventative and adjunct treatment for COVID-19. Int J Antimicrob Agents. 2020; 56(3):106118.
[95] Campione E et al, cit. 2020.
[96] Mandeep R Mehra et al, Hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19: a multinational registry analysis, Lancet, 2020, 6736(20)31180-6.
Mandeep R Mehra , Sapan S Desai, SreyRam Kuy , Timothy D Henry , Amit N Patel, Cardiovascular Disease, Drug Therapy, and Mortality in Covid-19. N Engl J Med. DOI: 10.1056/NEJMoa2007621.
[97] Mahévas M et al, Clinical efficacy of hydroxychloroquine in patients with COVID-19 pneumonia who require oxygen: observational comparative study using routine cara data. BMJ. 2020; 369:m1844.
[98] Mercuro NJ et al, Risk of QT interval prolongation associated with use of hydroxychloroquine with or without concomitant azithromycin among hospitalized patients testing positive for coronavirus disease 2019 (COVID-19). JAMA Cardiol. Doi: 10.1001/jamacardio.2020.1834.
[99] Bessière F et al, Assessment of QT intervals in a case series of patients with coronavirus disease 2019 (COVID-19) infection treated with hydroxychloroquine alone or in combination with azithromycin in an intensive care unit. JAMA Cardiol. 2020;e201787.
[100] Cheng Y et al, Use of convalescent plasma therapy in SARS patients in Hong Kong. Eur J Clin Microbiol Infect Dis. 2005;24(1):44-6.
[101] Nguyen AA et al, Immunoglobulins in the treatment of COVID-19 infection: Proceed with caution! Clin Immunol. 2020; 216:108459.
Pravindra Kumar et al, Role of ACE2 receptor and the landscape of treatment options from convalescent plasma therapy to the drug repurposing in COVID-19. Mol Cell Biochem, 2020; doi: 10.1007/s11010-020-03924-2.
Tonn T et al, Stability and neutralizing capacity of SARS-CoV-2-specific antibodies in convalescent plasma, Lancet Microbe, 2020, 1(2): e63.
Perotti C, Baldanti F, De Donno G et al, Mortality reduction in 46 patients with severe COVID-19 treated with hyperimmune plasma. A proof-of-concept, single-arm, multicenter trial. Haematologica. 2020; 105(12): 261784
Chenguang Shen et al, Treatment of 5 Critically III Patients with COVID-19 with Convalescent Plasma. JAMA 2020; 323 (16): 1582-9.
Qing-Lei Zeng et al, Effect of Convalescent Plasma Therapy on Viral Shedding in COVID-19 Patients. J Infect Dis. 2020; jiaa228.
Rojas M et al, Convalescent plasma in Covid-19: Possible mechanisms of action. Autoimmun Rev. 2020;102554.
Gniadek TJ et al, SARS-CoV-2 neutralization and serology testing of COVID-19 convalescent plasma from donors with nonsevere disease. Published online 2020 Oct 2. doi: 10.1111/trf.16101
Duan K et al. Effectiveness of convalescent plasma therapy in severe COVID-19 patients. PNAS, USA. 2020;202004168.
Wang L et al, Antibodies with potent and broad neutralizing activity against antigenically diverse and highly transmissible SARS-CoV-2 variants. bioRxiv. Preprint. 2021 doi: 10.1101/2021.02.25.432969
[102] Mangge H et al, Immune Responses against SARS-CoV-2—Questions and Experiences. Biomedicines 2021; 9(10):1342
Peng Y et al, Broad and strong memory CD4+ and CD8+ T cells induced by SARS-CoV-2 in UK convalescent individuals following COVID-19. Nat Immunol. 2020; 21:1336-45
[103] Iwasaki A et al, The potential danger of suboptimal antibody responses in COVID-19. Nat Rev Immunol. 2020; 20:339-341.
Kumaragurubaran Karthik et al, Role of antibody-dependent enhancement (ADE) in the virulence of SARS-CoV-2 and its mitigation strategies for the development of vaccines and immunotherapies to counter COVID-19. Hum Vaccin Immunother. 2020: 1–6.
Wen Shi Lee et al, Antibody-dependent enhancement and SARS-CoV-2 vaccines and therapies. Nature Microbiology, 2020; 5:1185-91.
Cardozo T, Veazey R, Informed consent disclosure to vaccine trial subjects of risk of COVID-19 vaccines worsening clinical disease. Int J Clin Pract. 2020; e13795. doi: 10.1111/ijcp.13795
[104] Kanduc D, Shoenfeld Y. Molecular mimicry between SARS-CoV-2 spike glycoprotein and mammalian proteomes: implications for the vaccine. Immunol Res. 2020; 68(5):310-313.
Badier L et al, IgA vasculitis in adult patient following vaccination by ChadOx1 nCoV-19. Autoimmunity Rev. 2021; 20(11):102951
Hočevar A, Tomšic M, Immune mediated events timely associated with COVID-19 vaccine. A comment on article by Badier, et al.: “IgA vasculitis in adult patients following vaccination by ChadOx1 nCoV-19”. Autoimmunity Rev, available online 2 November 2021, 102989
Pujol A et al, Thyroid as a target of adjuvant autoimmunity/inflammatory syndrome due to mRNA-based SARS-CoV2 vaccination: from Graves’ disease to silent thyroiditis. J Endocrinol Invest. 2021 Nov 18 : 1–8.
Hotez P et al, The potential role of Th17 immune responses in coronavirus immunopathology and vaccine-induced immune enhancement. Microbes Infect. 2020; 22(4-5):165-7.
[105] J Bart Classen, COVID-19 RNA based vaccines and the risk of prion disease. Microbiology & InfectiousDisease. 2021; 5 (1):1-3.
[106] Rhea EM et al, The S1 protein of SARS-CoV-2 crosses the blood–brain barrier in mice. Nat Neurosci 2021; 24:368–378.
Buždygan T et al, The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier. Neurobiol Dis. 2020; 146:105131.
Filosto M et al, Guillain-Barré syndrome and COVID-19: an observational multicentre study from two Italian hotspot regions. BMJ. 2020; 92(7):751.
Finsterer J et al, Post SARS-CoV-2 vaccination Guillain-Barre syndrome in 19 patients. Clinics (Sao Paulo). 2021 Oct 11;76:e3286.
Finsterer J. Guillain-Barre syndrome 15 days after COVID-19 despite SARS-CoV-2 vaccination. IDCases. 2021 Jul 12; 25:e01226.
Finsterer J. Neurological side effects of SARS-CoV-2 vaccinations. Acta Neurol Scand. 2021. doi: 10.1111/ane.13550.
Kaulen LD et al, Neurological autoimmune diseases following vaccinations against SARS-CoV-2: a case series. Eur J Neurol. 2021. doi: 10.1111/ene.15147.
[107] Sharma A et al, Human iPSC-derived cardiomyocytes are susceptible to SARS-CoV-2 infection. Cell Reports Medicine. 2020; 1(4): 100052.
Shi S et al, Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol. 2020; 5(7):802-10.
Chen L et al, The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc. Res. 2020; 116:1097–1100.
Tucker NR et al, Myocyte Specific Upregulation of ACE2 in Cardiovascular Disease: Implications for SARS-CoV-2 mediated myocarditis. medRxiv. 2020 doi: 2020.04.09.20059204.
Oudit GY et al, SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS. Eur. J. Clin. Invest. 2009; 39:618–625.
Tricarico G, Travagli V, COVID-19 fatal outcomes: Role of the endothelial glycocalyx in both cell adhesion and migration. Biomed J. 2021; 44(4):512–513.
Giardini V et al, Increased sFLT-1/PlGF ratio in COVID-19: A novel link to angiotensin II-mediated endothelial dysfunction. AJH. 2020; 95(8):25882.
Østergaard L, SARS CoV-2 related microvascular damage and symptoms during and after COVID-19: Consequences of capillary transit-time changes, tissue hypoxia and inflammation. https://doi.org/10.14814/phy2.14726
Choi S et al, Myocarditis-induced sudden death after BNT162b2 mRNA COVID-19 vaccination in Korea: case report focusing on histopathological findings. J Korean Med Sci. 2021;36(40):e286.
Dionne A et al, Association of Myocarditis with BNT162b2 Messenger RNA COVID-19 Vaccine in a Case Series of Children. JAMA Cardiol. 2021:e213471
Kim HW et a, Patients with Acute Myocarditis Following mRNA COVID-19 Vaccination. JAMA Cardiol. 2021; 6(10):1196-1201.
Montgomery J et al, Myocarditis Following Immunization With mRNA COVID-19 Vaccines in Members of the US Military. JAMA Cardiol. 2021; 6(10):1202-6
Das BB et al, Myopericarditis after messenger RNA Coronavirus Disease 2019 Vaccination in Adolescents 12 to 18 Years of Age. J Pediatr. 2021; 238:26-32.e1.
Kafil T, Crean A et al, mRNA COVID-19 vaccination and development of CMR-confirmed myopericarditis. Doi.org/10.1101/2021.09.13.21262182.
[108] Tricarico G et al, Clinical Evidence and Therapeutic Treatments at the Time of the Coronaviruses Responsible for SARS: A Perspective and Points of view with a Focus on Vascular Endothelium. Coronaviruses, 2021, 2, e130921191743.
Gundry S, Mrna COVID Vaccines Dramatically Increase Endothelial Inflammatory Markers and ACS Risk as Measured by the PULS: a Warning. Circulation, 2021; 144:A10712.
Sangli S et al, Thrombosis with Thrombocytopenia After the Messenger RNA–1273 Vaccine. Ann Intern Med. 2021: L21-0244.
Carli G et al, Deep vein thrombosis (DVT) occurring shortly after the second dose of mRNA SARS-CoV-2 vaccine. Intern Emerg Med. 2021; doi: 10.1007/s11739-021-02685-0
Andraska EA et al, Three cases of acute venous thromboembolism in females after vaccination for coronavirus disease 2019. J Vasc Surg Venous Lymphat Disord. 2021 doi: 10.1016/j.jvsv.2021.07.009
Shazley O et al, A COVID-Positive 52-Year-Old Man Presented With Venous Thromboembolism and Disseminated Intravascular Coagulation Following Johnson & Johnson Vaccination: A Case-Study. Cureus. 2021 Jul 14;13(7):e16383
Hippisley-Cox J et al, Risk of thrombocytopenia and thromboembolism after covid-19 vaccination and SARS-CoV-2 positive testing: self-controlled case series study. BMJ. 2021; 374:n1931.
[109] Lei Y, Zhang J et al, SARS-CoV-2 spike protein impairs endothelial function via downregulation of ACE2. Circulation Research. 2021; 128(9):1323-6.
[110] Colunga Biancatelli RML et al, The SARS-CoV-2 spike protein subunit S1 induces COVID-19-like acute lung injury in Κ18-hACE2 transgenic mice and barrier dysfunction in human endothelial cells. Am J Physiol Lung Cell Mol Physiol. 2021; 321(2):477-84.
[111] Olajide OA et al, Induction of Exaggerated Cytokine Production in Human Peripheral Blood Mononuclear Cells by a Recombinant SARS-CoV-2 Spike Glycoprotein S1 and Its Inhibition by Dexamethasone. Inflammation. 2021; 44:1865-77.
[112] https://www.vocidallastrada.org/2021/10/eudravigilance-27247-morti-2563768.html
[113] Polack FP et al, Safety and efficacy of the BNT162b2 mRNA COVID-19 vaccine, N Engl J Med. 2020; 383:2603-15.
[114] Walter EB et al, Evaluation of the BNT162b2 Covid-19 Vaccine in Children 5 to 11 Years of Age. DOI: 10.1056/NEJMoa2116298.
[115] Baden LR et al, Efficacy and safety of the mRNA-1273 SARS-CoV-2 vaccine, N Engl J Med. 2021; 384:403-16.
SEARCH LEARN RESIST 
You must be logged in to post a comment.