This is what the docs are looking at at the moment. I've posted it before but it was updated yesterday. IDGAF what Prez of his outlets preach.
Investigational approaches — A number of investigational approaches are being explored for antiviral treatment of COVID-19, and enrollment in clinical trials should be discussed with patients or their proxies. A registry of international clinical trials can be found on the WHO website and at clinicaltrials.gov.
Certain investigational agents have been described in observational series or are being used anecdotally based on in vitro or extrapolated evidence. It is important to acknowledge that there are no controlled data supporting the use of any of these agents, and their efficacy for COVID-19 is unknown.
●Remdesivir – Several randomized trials are underway to evaluate the efficacy of remdesivir for moderate or severe COVID-19 [110]. Remdesivir is a novel nucleotide analogue that has activity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in vitro and related coronaviruses (including SARS and MERS-CoV) both in vitro and in animal studies [111,112]. Remdesivir is an intravenous agent; reported side effects include nausea, vomiting, and transaminase elevations. It is also prepared in a cyclodextrin vehicle, so there is concern for potentially toxic accumulation of the vehicle in renal impairment. Exclusion criteria vary by trials but include alanine aminotransferase level >5 times the upper limit of normal and chronic kidney disease (creatinine clearance <30 or <50 mL/min, depending on the trial); some trials also exclude use of a different COVID-19-targeted therapy within 24 hours prior to remdesivir initiation. Remdesivir may be available through compassionate use for pregnant women and children. Use of remdesivir has been described in case series [113,114]; systematic evaluation of the clinical impact of remdesivir on COVID-19 has not yet been published.
●Chloroquine/hydroxychloroquine – Both chloroquine and hydroxychloroquine have been reported to inhibit SARS-CoV-2 in vitro, although hydroxychloroquine appears to have more potent antiviral activity [115].
Clinical data evaluating hydroxychloroquine or chloroquine are limited, and their efficacy against SARS-CoV-2 is unknown. Nevertheless, given the lack of clearly effective interventions and the in vitro antiviral activity, some clinicians think it is reasonable to use hydroxychloroquine in hospitalized patients with severe disease or risk for severe disease who are not eligible for clinical trials. In the United States, the FDA issued an emergency use authorization to allow the use of these agents in adolescents or adults hospitalized for COVID-19 when participation in clinical trials is not feasible [116]. However, if these agents are used outside of a clinical trial, the possibility of drug toxicity (including QTc prolongation, in particular, as well as cardiomyopathy and retinal toxicity) and drug interactions should be considered prior to use, especially in individuals who may be more susceptible to these effects, and the patients should be monitored closely for adverse effects during use. The American College of Cardiology has suggested QTc monitoring parameters in this setting [117]. Optimal dosing is uncertain; the FDA suggests hydroxychloroquine 800 mg on day 1 then 400 mg daily and chloroquine 1 g on day 1 then 500 mg daily, each for four to seven days total depending on clinical response [116]. Other hydroxychloroquine regimens used include 400 mg twice daily on day 1 then daily for five days, 400 mg twice daily on day 1 then 200 mg twice daily for four days, and 600 mg twice daily on day 1 then 400 mg daily for four days [118].
Use of chloroquine is included in treatment guidelines from China's National Health Commission and was reportedly associated with reduced progression of disease and decreased duration of symptoms [119,120]. However, primary data supporting these claims have not been published [121]. A randomized trial of patients with mild COVID-19 pneumonia and no hypoxia reported that adding hydroxychloroquine to standard of care resulted in faster time to improvement in fever, cough, and chest imaging findings and possibly a lower likelihood of progression to severe disease, but the trial has not been published in a peer-reviewed journal [122], and there are concerns about concomitant co-therapies, baseline differences between the groups, and the lack of a placebo control.
Published clinical data on either of these agents are limited. In an open-label study of 36 patients with COVID-19, use of hydroxychloroquine (200 mg three times per day for 10 days) was associated with a higher rate of undetectable SARS-CoV-2 RNA on nasopharyngeal specimens at day 6 compared with no specific treatment (70 versus 12.5 percent) [123]. In this study, the use of azithromycin in combination with hydroxychloroquine appeared to be associated with a more rapid decline in viral RNA; however there are methodologic concerns about the control groups for the study, the biologic basis for using azithromycin in this setting is unclear, and another small observational study in patients with more severe illness did not suggest rapid viral RNA clearance with the combination [124]. In a randomized trial of 30 adults with COVID-19 in Shanghai, the proportion of patients with nasopharyngeal viral clearance at day 7 was not different with hydroxychloroquine (400 mg daily for five days) compared with standard of care, and one patient in the hydroxychloroquine group progressed to severe disease; interferon and other antiviral agents were used in both arms, which could be confounding factors [125].
●IL-6 pathway inhibitors – Clinical features consistent with a cytokine release syndrome with elevated interleukin (IL)-6 levels have been described in patients with severe COVID-19. Anecdotal reports have described good outcomes with the IL-6 receptor inhibitor tocilizumab [78], but there are no published clinical data supporting its use. Treatment guidelines from China's National Health Commission include tocilizumab for patients with severe COVID-19 and elevated IL-6 levels. This agent, as well as sarilumab and siltuximab, which also target the IL-6 pathway, are being evaluated in clinical trials [126].
●Convalescent plasma – In the United States, the Food and Drug Administration is accepting emergency investigational new drug applications for use of convalescent plasma for patients with severe or life-threatening COVID-19 [127]. A case series described administration of plasma from donors who had completely recovered from COVID-19 to five patients with severe COVID-19 on mechanical ventilation and persistently high viral titers despite investigational antiviral treatment [34]. The patients had decreased nasopharyngeal viral load, decreased disease severity score, and improved oxygenation by 12 days after transfusion, but these findings do not establish a causal effect. Finding appropriate donors and establishing testing to confirm neutralizing activity of plasma may be logistical challenges. (See "Clinical use of plasma components", section on 'Convalescent plasma'.)
●Favipiravir – Favipiravir is an RNA polymerase inhibitor that is available in some Asian countries for treatment of influenza and is being evaluated in clinical trials for treatment of COVID-19. Published clinical data are pending.
●Lopinavir-ritonavir – Lopinavir-ritonavir appears to have little to no role in the treatment of SARS-CoV-2 infection. This combined protease inhibitor, which has primarily been used for HIV infection, has in vitro activity against the SARS-CoV [128] and appears to have some activity against MERS-CoV in animal studies [129]. However, there was no difference in time to clinical improvement or mortality at 28 days in a randomized trial of 199 patients with severe COVID-19 given lopinavir-ritonavir (400/100 mg) twice daily for 14 days in addition to standard care versus those who received standard of care alone [130].
I actually laughed when the Prez bashed the WHO and accused them of minimizing things (which is what he did) and said he was putting a strong hold on their funding. Then when questoned if it was a good time to freeze funding for the WHO he said he wasn't doing it. Doublespeak and it works.
The WHO has become the villain through certain outlets and it was predictable. It has to be their fault because we certainly wouldn't have minimized it had we known. Folks were screaming this isn't the flu but no one wanted to believe it in the Admin, as well as their followers. Don't be a blind follower.
