This post is a timeline of our notes on the virus SARS-CoV-2, the disease it causes (COVID-19). The notes cover the period from March 18 to April 9, 2020. Our later notes were published in separate articles marked with the tag COVID-19.
On April 8, 2020, France hit a gruesome record as its COVID-19 mortality rate reached 13.35%. Causes: sabotage of bureaucracy and medical incompetence (April 9, 2020).
A COVID-19 mortality rate for patients treated by a COMPETENT medical team can be as low as 0.099%.
Novartis stated they have 50,000,000 doses on hand with another 80,000,000 doses to be ready by May. (April 9, 2020).
Corticosteroid administration depletes lymphocytes and increases neutrophils in peripheral circulation (April 7, 2020).
Reduced lymphocytes counts and increased neutrophils to lymphocytes ratio (NLR) is a prominent feature of COVID-19. Higher NLRs are associated with poor outcomes.
Glucocorticosteroids are elevated during stress and critical illness (read more in another article on this website). Elevated blood levels of endogenous corticosteroids and corticosteroids administered exogenously both change absolute numbers of different fractions of circulating leukocytes. Neutrophils go up. Lymphocytes go down. Administration of exogenous corticosteroids to COVID-19 patients should, therefore, further increase neutrophils to leukocytes ratio (NLR). If higher NLR is associated with poor outcomes in COVID-19, administration of corticosteroids would seem counterproductive. Are steroids used appropriately in the treatment of COVID-19?
High doses of corticosteroid methylprednisolone for 1–2 days early in the course of acute respiratory distress syndrome (ARDS) may be harmful (April 7, 2020).
As of April 6, 2020, the average COVID-19 mortality rate in a selection of European and other developed countries is staggering 10%. An explanation is needed for such abysmally poor results of the medical treatment of COVID-19. One possible explanation is an inappropriate use of steroids. In Italy, corticosteroids were used to treat 30% of the COVID-19 patient as of March 17, 2020.
All pneumonia cases are now “COVID-19” since everybody gets infected with SARS-CoV-2 in the hospital (March 31, 2020).
COVID-19 mortality rates around the world are exaggerated because ALL patients with other causes of pneumonia are being coinfected with SARS-CoV-2 in hospitals and become “COVID-19”.
Ian Lipkin, a New York professor of medicine, director of infection and immunity, used a wrong dosage of hydroxychloroquine to treat his COVID-19 (March 31, 2020).
This is an excerpt from our article with more details (see the link below):
Ian Lipkin started Hydroxychloroquine but used a wrong dosage and protocol. As Ian Lipkin explained it: “I did not feel well after that initial dose of 800mg… I had an episode of diarrhea soon after I took it.”
Apparently, Ian Lipkin, “Professor, Director, Center for Infection and Immunity”, and the physicians who treated him, did not bother to look up the dosages and protocols used in existing trials of hydroxychloroquine in COVID-19 patients. Lipkin most likely used the dosage for treating malaria. Indeed, the drug label information for hydroxychloroquine approved by the FDA for the US mentions 800mg as an initial dose in treating uncomplicated malaria.
Neutrophils role as a part of the inflammatory and immune response and COVID-19 associated pathology (March 31, 2020).
It is emerging that an inflammatory and immune dysfunction is the main cause of the damage to lungs and other organs in complicated cases of COVID-19. COVID-19 in this sense is not different from, for instance, influenza virus pneumonia. In both of these conditions, inflammation may contribute as much to the pathology as viral and microbial toxicity.
It is, therefore, necessary to take another look at the complex mechanisms of the inflammatory and immune response.
Read more in a separate article on this website.
Gautret (the group of Didier Raoult), 2020 (29):
A recent Chinese survey revealed that the median duration of viral shedding was 20.0 days (IQR 17.0–24.0) in survivors, but SARS-CoV-2 was detectable until death in non-survivors. The shortest observed duration of viral shedding among survivors was eight days, whereas the longest was 37 days (18). Therefore, a treatment enabling the viral carriage to be cleared and COVID-patients to be clinically cured at an early stage would help limit the transmission of the virus.
Orwellian “Doublethink”: A New York doctor would not use hydroxychloroquine to treat COVID-19 because it is against “The Party Line” (March 29, 2020).
Daniel Griffin, MD, gives an impression of a sharp infection disease specialist. His involvement in HIV research and propaganda activities apparently cloud his mind. This may be dangerous to his patients.
Griffin is at the frontline of fighting against COVID-19 in one of New York’s hospitals. In a podcast that came out on March 29, 2020, Griffin gave several interesting updates on COVID-19. However, Griffin was again critical of the use of hydroxychloroquine to treat COVID-19 “because one of the patients in the most recent study died”. Then, Griffin said that some data showed that it was ok to use steroids again in treating COVID-19.
The most recent study that Griffin refers to is the study by the group of Didier Raoult ( Gautret, 2020 (29)). The authors showed that a combination of hydroxychloroquine and an antibiotic was effective in clearing viral load in a group of 80 patients with the exception of one.
Gautret (the group of Didier Raoult), 2020 (29):
Virus cultures from patient respiratory samples were negative in 97.5% patients at Day5. This allowed patients to rapidly de discharge from highly contagious wards with a mean length of stay of five days.
It is noteworthy that the only patient who did not survive in the study by Gautret, 2020 (29), was an 86 years old male who was on corticosteroids from the day of the onset of the symptoms.
The study by Gautrer (the group of Didier Raoult), 2020 (29), showed positive results. Hydroxychloroquine is toxic, but COVID-19 turned out to be a deadly disease. Staggering mortality rates of 5 to 10% in many European countries show that doctors do not know how to treat viral pneumonia effectively. Why is Daniel Griffin opposed to the use of hydroxychloroquine to treat COVID-19?
Daniel Griffin is involved in very dubious HIV research and in diverse “educational activities”. These educational activities very often involve outright propaganda. Separating information and propaganda of the Party Line is a challenge when you listen to Griffin.
Respiratory specimens, including nasal and pharyngeal swabs, bronchoalveolar lavage fluid, sputum, or bronchial aspirates were tested for common viruses, including influenza, avian influenza, respiratory syncytial virus, adenovirus, parainfluenza virus, SARS-CoV and MERS-CoV using real-time RT-PCR assays approved by the China Food and Drug Administration. Routine bacterial and fungal examinations were also performed. Given the emergence of the 2019-nCoV pneumonia cases during the influenza season, antibiotics (orally and intravenously) and oseltamivir (orally 75 mg twice daily) were empirically administered. Corticosteroid therapy (methylprednisolone 40–120 mg per day) was given as a combined regimen if severe community-acquired pneumonia was diagnosed by physicians at the designated hospital. Oxygen support (eg, nasal cannula and invasive mechanical ventilation) was administered to patients according to the severity of hypoxaemia. Repeated tests for 2019-nCoV were done in patients confirmed to have 2019-nCoV infection to show viral clearance before hospital discharge or discontinuation of isolation.
Symptomatic COVID-19: If you don’t have dyspnea (difficulty breathing) 8 days after illness onset, you are likely to be OK (March 27, 2020).
COVID-19: Days from illness onset to dyspnoea (difficulties breathing): 8·0 (6·0–17·0) and 6·5 (2·0–10·0) for those who needed ICU care (n=13) and for those who did not(n=28), respectively. There was no statistical difference between the two groups (P=0.22).
Table 1:Demographics and baseline characteristics of patients infected with 2019-nCoV.
Source: Huang, 2020 (28).
Misuse of steroids may explain the 25 times higher COVID-19 mortality rates in Italy and Spain in comparison to Germany (March 27, 2020).
Yuen et al., 2020 (26):
The window in which steroids might be beneficial to patients with COVID- 19 is very narrow. In other words, steroids can only be used when SARS-CoV-2 has already been eliminated by human immune response. Otherwise, SARS-CoV-2 replication will be boosted leading to exacerbation of symptoms, substantial virus shedding, as well as increased risk for nosocomial transmission and secondary infection. In this regard, it will be of interest to determine whether the report of fungal infection in the lungs of some patients in Wuhan might be linked to misuse of steroids.
COVID-19 fatality rates (death rates) as of March 26, 2020. Italy – 10.09%, Spain – 7.21%, Germany – 0.54%, the US – 1.39%, South Korea – 1.33%, Iran – 7.69%.
When total cases cross 5 thousand in a country, daily new cases grow by approximately 10% of the total despite lockdowns.
Wu J.T. et al., 2020 (27):
Considering the totality of the findings they nevertheless indicate that COVID-19 transmission is difficult to control. With a basic reproductive number of around two, we might expect at least half of the population to be infected, even with aggressive use of community mitigation measures.
If you had a cold with symptoms similar to COVID-19 before November 15, 2019, it is very unlikely that it was caused by SARS-CoV-2 virus.
According to Wu J.T. et al. 2020 (27), SARS-CoV-2 would have appeared after a single zoonotic (from animal to human) transmission around November 15, 2019:
Recent phylogenetic analyses suggest that the most recent common ancestor of the sequenced COVID-19 genomes emerged between 23 October and 16 December 2019 (http://virological.org/t/clock-and-tmrca-based-on-27-genomes/347;accessed 12 Feb 2020). As such, we assume that the epidemic in Wuhan was seeded by a single zoonotic event that generated z0 infections on 15 November 2019.
Researchers from Hong Kong calculated that the SYMPTOMATIC case fatality rate (sCFR) was 1.4%, criticized the Chinese bureaucrats for incompetence.
A key public health priority during the emergence of a novel pathogen is estimating clinical severity, which requires properly adjusting for the case ascertainment rate and the delay between symptoms onset and death.
Wu J.T. et al., 2020 (27).
Researchers from Hong Kong have been very critical of the Chinese bureaucracy and its management of the Corona Virus crisis. Wu J.T. et al., 2020 (27), criticize the Chinese bureaucrats for exaggerating the mortality rate and calculated a very useful statistic, the “SYMPTOMATIC case fatality rate” of COVID-19. Wu J.T. et al., 2020 (27):
Using public and published information, we estimate that the overall symptomatic case fatality risk (the probability of dying after developing symptoms) of COVID-19 in Wuhan was 1.4% (0.9–2.1%), which is substantially lower than both the corresponding crude or naïve confirmed case fatality risk (2,169/48,557 = 4.5%) and the approximator1 of deaths/deaths + recoveries (2,169/2,169 + 17,572 = 11%) as of 29 February 2020.
Physiological Literacy on Infection Fatality Rate (IFR), Symptomatic Case Fatality Rate (sCFR), and hospitalization fatality risk (HFR).
Wu J.T. et al., 2020 (27):
The clinical severity of infectious diseases is typically measured in terms of infection fatality risk (IFR), symptomatic case fatality risk (sCFR) and hospitalization fatality risk (HFR). The case definitions underlying these severity measures are as follows:
1. IFR defines a case as a person who would, if tested, be counted as infected and rendered (at least temporarily) immune, as usually demonstrated by seroconversion or other immune response13. Such cases may or may not be symptomatic.
2. sCFR defines a case as someone who is infected and shows certain symptoms.
3. HFR defines a case as someone who is infected and hospitalized. It is typically assumed in such estimates that the hospitalization is for treatment rather than isolation purposes.
Figure 2 summarizes our estimates of age-specific sCFRs and susceptibility to symptomatic infection. Both parameters increase substantially with age. If the probability of developing symptoms after infection, Psym, is 0.5, the sCFR values are 0.3% (0.1–0.7%), 0.5% (0.3–0.8%) and 2.6% (1.7–3.9%) for those aged <30 years, 30–59 years and >59 years, respectively.
Wu J.T. et al., 2020 (27): “We estimate that only 1.8% (0.9–3.3%) of symptomatic cases that occurred between 10 December 2019 and 3 January 2020 were ascertained.”
Italy: “Corona virus” or “Macaroni Virus”? 9 out of 10 COVID-19 deaths in Italy are most likely caused by the incompetence of Italian doctors (March 26, 2020).
It looks like there is an epidemic of incompetence in the Italian health care. Doctors there generate crazy death rates, 22 times more people die in Italy than in Germany. A criminal investigation is needed at this point.
One of the most bizarre facts during the unfolding “Corona Virus Crisis” is the wild difference in the mortality rates. As of March 24, 2020, Germany had almost 30 thousand confirmed cases of COVID-19, the 3rd largest number of cases in Europe. And the mortality rate of COVID-19 in Germany has been below 0.42% throughout the epidemic. At the same time in Italy, the mortality rate is 22 times higher than in Germany and it recently went up to almost 10%. What is going on?
At this point, the most likely explanation is that among those who die from COVID-19 in Italy, 9 out of 10 are killed by the incompetence of Italian doctors.
There are also alarming mortality rates that are reported from Spain, France, the UK, and the Netherlands. The mortality rates of COVID-19 in these countries are around 5%. Another striking figure is the seasonal flu mortality in the US. Indeed, according to the CDC, seasonal flu kills 10% of confirmed cases.
Our medical consultancy is specialized in testing qualifications of medical doctors. We also survey medical doctors active on social networks and in grassroots health conferences. The average level is low. Outright incompetency and even idiotic statements are common.
We know that mainstream medicine can not really treat chronic diseases: “Type 2 diabetes and heart disease kill slowly and there is nothing to do about it. Take some pills”.
There has been an assumption that while modern mainstream medicine can not effectively treat chronic diseases, it can treat infections.
At this point, with an element of satire, we should rename the mysterious deadly Italian virus into the “Macaroni Virus”, a virus that causes utter incompetence of the medical profession.
Until we have another explanation, we should assume that 9 out of 10 COVID-19 deaths in Italy are caused by the incompetence of Italian doctors.
Flu peaked in Wuhan in the beginning of 2020. Are people with flu being reinfected with SARS-CoV-2 in hospitals? (March 25, 2020).
There is an interesting study from Hong Kong. The authors are critical of the Chinese government and make many interesting comments. Yuen et al., 2020 (26):
The activity of seasonal flu in Wuhan also reached a peak at the beginning of 2020. It will be of interest to see whether the flu season had ended and how many people having a fever now are actually infected with influenza virus. Precision control measures for SARS-CoV-2 should be tailor-designed for high-risk groups based on the results of this analysis. Differentiating people having a flu and preventing them from infecting with SARS-CoV-2 in a hospital setting might also be critical.
Yuen et al., 2020 (26):
Is the virus less transmissible after several passages in humans? Retrospective analysis of all confirmed cases in Wuhan should be very informative. The answers to the above questions hold the key to the outcome of the outbreak. If the transmission is weakened, the outbreak may ultimately come to an end at which SARS-CoV-2 is eradicated from humans. On the contrary, if effective transmission can be sustained, the chance is increased that SARS-CoV-2 will become another community-acquired human coronavirus just like the other four human coronaviruses (229E, OC43, HKU1 and NL63) causing common cold only.
A study with a correct title: “Clinical characteristics of SARS-CoV-2 infected pneumonia with diarrhea.”
There is a study in pre-print by a group of authors from China that described clinical characteristics of patients infected by SARS-CoV-2 (Wei et al., 2020 (26)). The clinical characteristics are of interest. What is also positive in this study is its title. Indeed, the title underlines pneumonia and diarrhea while SARS-CoV-2 presence is indicated as “infected”.
At this point, we should be open to the possibility that SARS-CoV-2 indeed causes a higher proportion of severe cases than other common coronaviruses and common cold viruses and influenzas. There are, indeed, alarming data on mortality rates that are coming from France, the UK, and Iran. In these countries, doctors and bureaucrats are opposed to the panic and hysteria around SARS-CoV-2. In France, we can cite prof. Didier Raoult. In the UK, we can cite Boris Johnson and many bureaucrats from the UK’s health authority. In Iran, both doctors and bureaucrats should be opposed to the panic and hysteria. Yet, there are high mortality rates that are being reported by these countries.
To understand what explains high mortality rates in some countries and low mortality rates in other countries, notably in Germany and in the US, we need to look at the tests that are used to detect SARS-CoV-2 and at other possible causes.
In the US, in 5 months, 23 thousand people died from seasonal flu (from pneumonia and other complications). Do we now count those deaths as COVID?
In the meantime, here are some data on the clinical characteristics of the patients with COVID-19 from China from the study Wei et al., 2020 (25):
Reference intervals for white blood cells for comparison with the levels in the patients with COVID-19.
SARS-CoV-1 (2002-2004 SARS) virus is believed to be extinct. How come SARS-CoV-2 is so similar but more contagious? (March 24, 2020).
Sheahan et al., 2006 (22):
(The 2002-2004) SARS CoV is extinct.
Brigitte A.Wevers, Lia van der Hoek, 2009 (22):
In February 2003, a newly emerged HCoV, which originated from a wild animal reservoir, was demonstrated to be the etiologic agent of this syndrome. 11 Of all HCoVs described thus far, SARS-CoV causes the most severe clinical symptoms. Of interest, SARS rarely is detected in young chil- dren, and if so, it seems to follow a less aggressive clinical course. 40 The strongest predictor of poor disease outcome appears to be an advanced age (older than 60 years).
Analysis: The 2002-2004 SARS-CoV-1 and the 2019 SARS-CoV-2 both spontaneously “emerged” from animals. Yet, they are almost identical. How come?
2002-2004 SARS (“SARS-CoV-1”) fatality rate (death rate) was 10%. In the US, seasonal flu among the CONFIRMED cases has the SAME fatality rate, 10% (March 25, 2020).
Brigitte A.Wevers, Lia van der Hoek, 2009 (22):
The first case of SARS, a severe lower respiratory tract illness with a mortality rate of 10%, emerged in November 2002 in Fushan City, China. 38 Subsequently, SARS spread rapidly throughout eastern Asia and to 28 other regions around the world, causing 774 deaths in 8098 infected individuals.
We wrote about the data on other common coronaviruses mortality rates from the French study by Didier Raoult and his group (10). The overall mortality rate was 1.3%. However, as we also already showed earlier in this article, seasonal flu kills 10% of the confirmed cases in the US according to the CDC.
Given the above, we need to investigate if COVID-19 and seasonal flu mortality statistics are a result of testing or statistical artifacts.
COVID-19 fatality rates (death rates) as of March 25, 2020. Italy – 9.51%, Germany – 0.43%, the US – 1.12%, South Korea – 1.33%.
The “Italian Corona Virus” is 22 times deadlier than the “German Corona Virus”. This needs to be explained.
The source for the Total fatality rates calculated below was the March 24, 2020 report of the WHO (21).
Why does Italy keep showing an almost 10% COVID-19 death rate? (March 25, 2020).
As of March 25, 2020, COVID-19 case fatality rate, or death rate, in Italy remains at 9.51%. What is the reason for such a high rate? Are hospitals using inappropriate treatments?
Protect yourself from the Global Propaganda Ministry. Recommended sources of information on society and politics: David Knight at The David Night Show.
David Knight is not always right but, in general, gives a correct interpretation of the events.
David Knight on Chloroquine on a social network:
Which makes it all the more amazing that govt & media would keep silent about #stemcells curing #COVID19 in 100% of patients in Wuhan trial Not just a cure, but REVERSAL of damage to lungs So many agendas in play by #DeepState #chloroquine.
SARS-CoV utilizes angiotensin converting enzyme 2 (ACE2) to infect host cells. What is ACE2? (March 24, 2020).
Brigitte A Wevers & Lia van der Hoek, 2010 (19):
To infect its target host cells, SARS-CoV utilizes ACE2, the RAS component now known to orchestrate protection from acute lung failure/ARDS.
Varagic et al., 2014 (20):
Angiotensin converting enzyme 2 (ACE2) has emerged as a key player in the pathophysiology of hypertension and cardiovascular and renal disease due to its pivotal role in metabolizing vasoconstrictive/hypertrophic/proliferative angiotensin II into favorable angiotensin-(1–7).
Similar to ACE, ACE2 is a plasma membrane-bound ectoenzyme, although soluble forms in plasma and urine are also found. ACE2 metabolizes Ang I and Ang II into Ang-(1–9) and Ang-(1–7) respectively with higher preference for Ang II degradation.
COVID-19 fatality rate among health workers in China was 0.3%. In Wuhan, 63% of health workers were infected. (March 23, 2020).
Wu Z., 2020 (16):
Health care personnel infected
Total in China: 3.8% (1716 of 44 672) and
63% in Wuhan (1080 of 1716).
Jason Oke, Carl Heneghan (17):
1716 case were health workers (3.8%), 254 cases (14.8%) were classified as severe or critical and 5 health workers (0.3%) died.
The Infection Rate Fatality (IFR) differs from the CFR in that aims to estimate the fatality rate in all those with infection: the detected disease (cases) and those with an undetected disease (asymptomatic and not tested group).
Researchers from the UK estimated that the “infection fatality rate” (IFR) for SARS-CoV-2 was 0.2% as of March 22, 2020.
Jason Oke, Carl Heneghan (17):
Our current best assumption, as of the 22nd March, is the IFR is approximate 0.20% (95% CI, 0.17 to 0.25). To estimate the IFR, we used the estimate from Germany’s current data 22nd March (93 deaths 23129) cases); CFR 0.40% (95% CI, 0.33% to 0.49%) and halved this for the IFR of 0.20% (95% CI, 0.17% to 0.25%) based on the assumption that half the cases go undetected by testing and none of this group dies.
The masses embraced toxic chloroquine and hydroxychloroquine (March 23, 2020).
Hydroxychloroquine retinal toxicity is far more common than previously considered (7.5% if taken more than 5 years).
Yusuf et al., 2017 (18):
Hydroxychloroquine and chloroquine (CQ) have been associated with irreversible visual loss due to retinal toxicity. Hydroxychloroquine retinal toxicity is far more common than previously considered; an overall prevalence of 7.5% was identified in patients taking HCQ for greater than 5 years, rising to almost 20% after 20 years of treatment.
Systemic toxicity Hydroxychloroquine.
Yusuf et al., 2017 (18):
The manufacturer lists reported adverse events attributed to HCQ therapy.12 They suggest caution in patients with known hepatic or renal dysfunction, or drugs known to compromise function of these organs. HCQ has been reported to cause severe hypoglycaemia in patients with diabetes taking hypoglycaemic drugs, and rarely, bone marrow suppression or skeletal muscle weakness12 There have been reports of fulminant hepatic failure in patients with no pre-existing liver disease soon after the initiation of HCQ treatment.29, 30 It is considered that <1% of patients taking conventional doses of HCQ suffer elevation of liver enzymes on serum evaluation, and taken together, these reported cases are considered to represent idiosyncratic drug reactions.
The most severe adverse effects associated with high doses of chloroquine.
Gerriets, 2019 (15):
The most severe adverse effects associated with high doses of chloroquine include retinal toxicity, long and subtle symptoms of reduced visual acuity, diplopia, and bilateral loss of vision.[11] High doses have also been shown to cause severe psychiatric issues, such as paranoia, hallucinations, and suicidal ideations.[12]
– Dermatological reactions include pruritus and photosensitivity.
– Retinopathy will typically present with the inability to focus between near and far objects.
– Neuropathy can include seizures, paranoia, and hallucinations.
When administered intramuscularly, chloroquine has been shown to cause potentially lethal hypotension.[13]
Chloroquine retinopathy can result in a devastating permanent loss of vision
Raines et al., 1989 (14):
Chloroquine retinopathy can result in devastating loss of vision. To date (TNNM: 1989), there are no effective and reliable methods of detecting the toxicity at an early stage when retinopathy may be reversible. Chloroquine is deposited in the retinal pigment epithelium, which forms part of the blood-retinal barrier (BRB). By vitreous fluorophotometry we have shown that there is breakdown of the BRB in chloroquine retinopathy. However, in asymptomatic patients who had received varying amounts of hydroxychloroquine (up to 1067 g), the BRB remained intact.
Of the 31 patients receiving chloroquine alone, 6 developed retinal toxicity (19%).
Finbloom et al., 1985 (13):
We assessed the frequency of retinal toxicity in patients receiving either chloroquine or hydroxychloroquine and factors which may predict patient susceptibility to toxicity. The overall frequency of retinopathy was 6% (7 of 110 patients). Of the 31 patients receiving chloroquine alone, 6 developed toxicity (19%). In contrast, of the 66 patients receiving hydroxychloroquine, none developed retinopathy. Retinopathy was associated with greater age and with greater accumulative doses of chloroquine. Thus, hydroxychloroquine can be used safely with minimal risk of toxicity.
Prof. Didier Raoult (Marseille, France): Prevent hospital outbreaks that eventually foster larger community epidemics.
Raoult et al., 2020 (4):
The first pillar for interventions is to preserve the healthcare system. The implementation of infection control measures within hospitals is crucial to protect healthcare workers, maintain adequate work force levels and to prevent hospital outbreaks that eventually foster larger community epidemics.
Ng et al., 2008-2014 (11):
Memory T cell responses targeting the SARS coronavirus persist up to 11 years post-infection.
Raoult et al., 2020 (4):
Most of the SARS-CoV-2 infections need no therapy, and overtreatment of patients without current or future medical needs should be avoided.
Marseille hospital network AP-HM tests the cases where respiratory viruses are suspected. The group of Didier Raoult, already cited in this article, investigated the mortality rates of the four common coronaviruses and compared them to the mortality rate of SARS-CoV-2, the virus that causes COVID-19.
During 2019, 21 662 samples were tested. Among these, 770 samples were positive for coronavirus, with eight deaths (mortality rate 1%). This mortality rate is is NOT statistically different from COVID-19 the mortality rate in OCDE (“developed”) countries. E.g., COVID-19 mortality rate in South Korea as of March 3rd, 2020, was 0.6%.
Roussel et al., 2020 (9):
Assistance Publique-Hôpitaux de Marseille (AP-HM) covers all public hospitals in Marseille, including four university hospitals: La Timone Hospital, Conception Hospital, North Hospital and South Hospital; this corresponds to 3400 beds and 125 000 admissions each year [23]. The IHU Méditerranée Infection diagnostic laboratory tests all samples from AP-HM in which respiratory viruses are suspected.
In 2016, there were 594 000 deaths in France; 59.2% of these deaths occurred in a care establishment [25]. In the same year, AP-HM reported 2854 deaths. As such, it can be estimated that approximately 0.8% of deaths in care establishments in France died in AP-HM hospitals. This estimate provides an approximation of the number of people affected by a pathogen in France according to the number of people who died each year at AP-HM hospitals.
From 1 January 2013 to 31 December 2019, 21 662 samples were tested by the IHU Méditerranée Infection diagnostic laboratory. Among these, 770 samples were positive for coronavirus, with eight deaths (mortality rate 1%). Among identified coronaviruses, 63 were identified as HKU1 (one death, mortality rate 1.6%), 74 were identified as NL63 (two deaths, mortality rate 2.7%), 92 were identified as E229 (one death, mortality rate 1.1%) and 160 were identified as OC43 (four deaths, mortality rate 2.5%). Three hundred and eighty-one coronaviruses, diagnosed before 2017, were not assigned to any of these four strains.
Roussel et al., 2020 (9):
Four common human coronaviruses (HKU1, NL63, OC43 and E229) cause 10–20% of respiratory infections worldwide and are present in all continents. Mortality is poorly assessed.
Roussel et al., 2020 (9) provide a table with mortality data on the four common human coronaviruses from different studies. We can see that the mortality rates are quite high and range from 1.5% to 15%.
In OECD countries. the mortality rate for SARS-CoV-2 (1.3%) is not significantly different from that for common coronaviruses identified at the study hospital in France (0.8%; P=0.11).
The problem of SARS-CoV-2 is probably overestimated, as 2.6 million people die of respiratory infections each year compared with less than 4000 deaths for SARS-CoV-2 at the time of writing.
Confinement of infected patients with uninfected patients resulted in rapid infection of the uninfected.
Roussel et al., 2020 (9):
(SARS-CoV-2) is incontestably contagious, as a quasi-experimental study on the Diamond Princess cruise ship showed that confinement of infected patients with uninfected patients resulted in rapid infection of the uninfected patients, leading to 700 additional cases on board.
COVID-19 death rates: Germany – 0.2%, Spain – 5%??? (March 22, 2020).
The data on the number of cases and mortality of COVID-19 from the World Health Organization website (8):
Let us calculate the death rate for the confirmed cases of COVID-19 for Germany and Spain as “total deaths”/”total cases”.
Germany: 45/18323=0.0025=0.25%
Spain: 1002/19980= 0.05=5%
Analysis:
1. “The Spanish Corona virus” would be 25 times more deadly than “The German Corona virus”.
2. Seasonal flu in the US kills 10% of the confirmed cases according to the CDC and thus is 50 times deadlier than the “German Corona Virus”.
The CDC says 7 days of quarantine for the infected is enough. Is it an act of sabotage? (March 22, 2020).
2.5% of the infected will develop symptoms 11.5 days after infection according to the study by Laurer et al., 2020 (9). Why then the CDC instructs to discontinue the quarantine 7 days after a positive test? Lauer et al., 2020 (9):
The median incubation period was estimated to be 5.1 days (95% CI, 4.5 to 5.8 days), and 97.5% of those who develop symptoms will do so within 11.5 days (CI, 8.2 to 15.6 days) of infection. These estimates imply that, under conservative assumptions, 101 out of every 10 000 cases (99th percentile, 482) will develop symptoms after 14 days of active monitoring or quarantine.
The CDC encourages the asymptomatic infected to discontinue their quarantine after 7 days while 30% of them can still develop symptoms.
Moreover, if we look at the graph from the study by Lauer et al., 2020 (9), we can see that as much as 30% of the infected can develop symptoms 7 days after infection. This means that the CDC guidance encourages the asymptomatic infected to discontinue the quarantine while 30% of them can still develop symptoms.
An asymptomatic carrier of SARS-CoV-2 may have infected people during a period of 21 days.
The study by Bai et al., 2020 (12), describes a case where an asymptomatic carrier of SARS-CoV-2 may have infected people during a period of 21 days, from January 1st to January 31, 2020. See the graph below.
The virus survives in the body for 20 days or longer and there is asymptomatic transmission. So, why people who are confirmed carriers of SARS-CoV-2 are advised to discontinue the quarantine 7 days after a positive test?
Discontinuation of Home Isolation for Persons with COVID-19 (Interim Guidance) by the Centers for Disease Control and Prevention (7):
Individuals with laboratory-confirmed COVID-19 who have not had any symptoms may discontinue home isolation when at least 7 days have passed since the date of their first positive COVID-19 diagnostic test and have had no subsequent illness.
The previous horrible deadly global “Corona Virus Pandemic” in 2002-2003 killed only 774 around the world (March 21, 2020).
Pyrc et al., 2007 (6):
The SARSCoV pandemic took 774 lives around the globe and infected more than 8000 people in 29 countries.
Analysis: The previous horrible deadly Corona Virus Pandemic killed 774 people around the globe in 2 years. Seasonal flu killed 22 thousand people in the US alone between September 2019 and March 2020.
Pyrc et al., 2007 (6):
The 4 human coronaviruses HCoV-229E, HCoVOC43, HCoV-NL63 and HCoV-HKU1 cause mild respiratory illnesses when compared to SARS, but these infections are involved in 10 – 20 % of hospitalizations of young children and immunocompromised adults with respiratory tract illness.
Coronaviruses received relatively little attention as human pathogens, as they were considered to be common cold viruses. Inoculation of HCoV-229E and HCoV-OC43 in healthy volunteers revealed that infection with these viruses causes common cold, but more severe lower respiratory tract infections (LRTI) were observed in infants and immunocompromized persons
Lectins inhibit replication of SARS-CoV.
Pyrc et al., 2007 (6):
The S protein of coronaviruses is highly glycosylated. This carbohydrate shield may be used as a target for compounds specifically binding to sugar moieties, e.g. lectins, thus coating the protein and blocking the interaction with the receptor. Plant lectins are known to inhibit the infection of viruses that contain a glycosylated envelope such as human immunodeficiency virus type 1, cytomegalovirus and human T-cell leukemia virus type I [46-48]. The mannose-specific plant lectins derived from Galanthus nivalis (Common Snowdrop), Hippeastrum hybrid (Amaryllis) and Allium porrum (leek) inhibit replication of SARS-CoV and feline coronavirus [49,50]. These lectins indeed block the S – receptor interaction as inhibition is observed at a very early stage of replication [49].
Inhibitors of vacuolar acidification, like the anti-malarial drug Chloroquine, inhibit SARS-CoV entry in cells.
Pyrc et al., 2007 (6):
A second step of coronavirus cell entry is the virion fusion with the host cell membrane and release of the virion core with the RNA genome into the cytoplasm. Depending on the virus species, the fusion can occur directly on the cell surface or may require internalization into the endosome [37]. Treatment with inhibitors of vacuolar acidification like ammonium chloride, chloroquine (an anti malaric drug, approved for use in humans) or bafilomycin A, demonstrated that HCoV-229E and SARS-CoV require the endosomal pathway for entry.
Use of steroids to treat SARS-CoV.
Pyrc et al., 2007 (6):
Proinflammatory cytokines released by stimulated macrophages in the alveoli play a prominent role in SARS pathogenesis, resulting in cytokine dysregulation [193,194]. During the SARS-CoV outbreak in 2003 several patients received anti-inflammatory corticosteroids that may reduce the damaging effect of the local inflammatory response.
However, other studies show lack of direct effect of steroid treatment in SARS patients [194,199,200]. It is also worth mentioning that immunosupression caused by steroid treatment may increase the danger of secondary infections, in fact occasionally increasing the mortality in SARS patients [201].
Incompetent bureaucracy is the main threat (March 21, 2020).
Our civilization may perish if the current system of appointing bureaucracy remains. An end of a civilization is not unusual, but this time, humanity may disappear with the civilization.
Despite catastrophic consequences, incompetent bureaucrats and elected officials worldwide insist on maintaining the total shutdown.
An update on the correct terminology: the virus was named SARS-CoV-2, the disease caused by this virus was named COVID-19 (March 21, 2020).
Wu et al., 2020 (1):
The (TNNM: International Committee on Taxonomy of Viruses) ICTV has designated the virus as SARS-CoV-2; in addition, the WHO has released the official name of the disease caused by this virus, which is COVID-19.
“In Italy, there are only two deaths ascertained so far due to Covid-19” (March 20, 2020).
Jon Rappoport, a moral authority, analyst and journalist from the US, published on his website the opinion of the president of the Italian National Institute of Health. Rome, 13 March 2020, Agenzia Nova: “Coronavirus: ISS [Italian National Institute of Health]: in Italy there are only two deaths ascertained so far due to Covid-19” (Italian, English)
The president of the Italian National Institute of Health Silvio Brusaferro (March 13, 2020): “In Italy there are only two deaths ascertained so far due to Covid-19”.
Rome, 13 March 2020, Agenzia Nova (5):
“There may be only two people who died from coronavirus in Italy, who did not present other pathologies. This is what emerges from the medical records examined so far by the Higher Institute of Health, according to what was reported by the President of the Institute [Istituto Superiore di Sanità (ISS), Italian National Institute of Health], Silvio Brusaferro, during the press conference held today at the Civil Protection in Rome. ‘Positive deceased patients have an average of over 80 years – 80.3 to be exact…The majority of these people are carriers of chronic diseases. Only two people were not presently carriers of [other non-COV] diseases’, but even in these two cases, the examination of the files is not concluded and therefore, causes of death different from Covid-19 could emerge. The president of the ISS has specified that ‘little more than a hundred medical records’ have so far come from hospitals throughout Italy.”
“…At present, in fact, the authorities are unable to distinguish those who died from the virus, from those who, on the other hand, are communicated daily to the public, but who were mostly carriers of other serious diseases and who, therefore, would not have died from Covid-19. In response to a question from ‘Agenzia Nova’, in fact, Brusaferro was unable to indicate the exact number of coronavirus deaths. However, the professor clarified that, according to the data analyzed, the vast majority of the victims ‘had serious [non-COV] pathologies and in some cases the onset of an infection of the respiratory tract can lead more easily to death.’ To clarify this point, and provide real data, ‘as we acquire the folders we will go further. However, the populations most at risk are fragile, carriers of multiple diseases’.”
Non-SARS-like corona viruses are endemic globally (March 20, 2020).
Some Physiological Literacy on corona viruses.
There are (at least) 4 other corona viruses that are endemic (regularly found) globally.
Raoult et al., 2020 (4):
The clinical features of low pathogenic non-SARS CoV infections are undistinguishable from those found in patients with influenza virus.
Raoult et al., 2020 (4):
Four human CoVs (HCoVs), the non-severe acute respiratory syndrome (SARS)-like HCoVs (namely HCoV 229E, NL63, OC43, and HKU1), are globally endemic and account for a substantial fraction of upper respiratory tract infections.
The propensity for nosocomial (TNNM: a disease originating in a hospital ) spreading (TNNM: of the “non-SARS-like” coronaviruses) and the dominant role played by symptomatic patients in the spreading of the infection are supported by basic virology.
CoVs, such as CoV-NL63, SARS-CoV-1 and SARS-CoV-2, use a specific receptor, angiotensin converting enzyme 2 (ACE2), a type I transmembrane metallocarboxypeptidase with homology to ACE, which is expressed in human airway epithelial cells, lung parenchyma, heart, lung, kidney and intestinal tract.
Raoult et al., 2020 (4):
As of Feb 29, 2020, there have been 83,652 laboratory confirmed cases of COVID-19, with 2791 deaths (3.4% mortality). Outside China, there have been 4691 cases reported from 51 countries with 67 deaths.
Analysis: COVID-19 death rate outside China: 67/4691=1.4%
This is as of March 2, 2020, based on Raoult (4) paper.
Is it smart to rush to a hospital “to test for Corona virus” (March 20, 2020)?
Raoult et al., 2020 (4):
Similar to other CoVs, it is now evident that health care services play an important role in the amplification of SARS-CoV-2 local epidemics.
Italy: The epidemic started in a hospital.
Raoult et al., 2020 (4):
a large proportion of the primary clusters reported form Lombardy were actually linked to an emergency department where a symptomatic case was received on February 16th (currently the whole hospital building is on quarantine).
South Korea: The epidemic started in hospitals.
Raoult et al., 2020 (4):
the current COVID-19 spreading in South Korea has been largely fostered by several hospital outbreaks, the most recent of which occurred in a hospital in Cheongdo county, where COVID-19 spread within the psychiatric unit.
Make the World think again (March 20, 2020).
Someone posted the right slogan on January 29, 2020, before the “Corona virus” psychosis took over the world.
The UK bureaucrats stand out favorably: no total shutdown in the UK. The “Globalists” do not like this (March 20, 2020).
Researcher Gabor Erdosi reads and believes the stories put out by a filthy Globalist TV-tabloid “Sky News”. What the article on the Sky News website really means is that “the Globalists” are not happy that the UK did not sabotage itself into a total shutdown. UK health bureaucrats stand out favorably.
Seasonal flu mortality is 10% of the cases confirmed through testing. COVID-19 kills only 1.6% of the confirmed cases (March 19, 2020).
The Gateway Pundit, a publication, accused the Ethiopian head of the WHO of grossly exaggerating COVID-19 death rates.
The Gateway Pundit’s own calculation is of interest. It appears that seasonal flu kills 10% of the cases confirmed through testing, while COVID-19 kills only 1.6% of confirmed cases.
The Gateway Pundit as retrieved from their article (2):
A look at the numbers:
** Tedros Adhanom Ghebreyesus used the actual number of deaths due to coronavirus divided by confirmed cases to get his 3.4% mortality rate number (from last week -since that time the mortality rate based on currentreported numbers is near 4%).** Tedros Adhanom Ghebreyesus then compared the actual coronavirus mortality rate to an estimated flu mortality rate of 0.1% — The US flu mortality rate is based on an estimated 22,000 deaths divided by an estimated 36 million flu cases giving a 0.1% mortality rate.
** Tedros Adhanom Ghebreyesus compared known numbers for coronavirus (3.4 percent mortality rate) but did not include the estimated number of those infected who are asymtomatic. This number is likely in the tens of thousands and could be in the millions! There is no way of knowing right now. One study released this week revealed that 6 of 7 people infected by coronavirus are asymptomatic! They do not know they are infected!
** Tedros Adhanom Ghebreyesus then compared the known numbers of 206,845 cases of coronavirus to the millions of estimated annual cases of flu cases. Again he does not include the asymtomatic cases, the 6 of 7 people infected who do not suffer severe symptoms.
** If asymtomatic cases are included in Ghebreyesus’s calculation the actual mortality rate of the coronavirus is somewhere between 0.2% to 0.8% or lower.
The Gateway Pundit is right: In the US, seasonal flu killed 10% of the confirmed cases this year according to the CDC (March 19, 2020).
The CDC writes on its website (3):
CDC estimates that so far this season there have been at least 38 million flu illnesses, 390,000 hospitalizations and 23,000 deaths from flu.
In the US, according to the CDC, the cumulative number of positive cases of influenza A and B between September 29, 2019, and through March 14, 2020, “week 11”, was 231,654.
The number of deaths divided by the number of confirmed positive cases: 23,000/231,654=10%.
The virus genotype used to develop a PCR test came from a single patient from Wuhan (March 18, 2020).
Wu, 2020 (1):
The patient studied was a 41-year-old man with no history of hepatitis, tuberculosis or diabetes.
The Wuhan Center for Disease Control and Prevention revealed that the patient worked at a local indoor seafood market.
Elevated levels of C-reactive protein (41.4 mg l−1 of blood; reference range, 0–6 mg l−1) were observed and the levels of aspartate aminotransferase, lactic dehydrogenase and creatine kinase were slightly elevated in blood chemistry tests.
Wu, 2020 (1):
To investigate the possible aetiological agents associated with this disease, we collected bronchoalveolar lavage fluid (BALF) and performed deep meta-transcriptomic sequencing. The clinical specimen was handled in a biosafety level 3 laboratory at Shanghai Public Health Clinical Center. Total RNA was extracted from 200 μl of BALF and a meta-transcriptomic library was constructed for pair-end (150-bp reads) sequencing using an Illumina MiniSeq as previously described4,6,7,8. In total, we generated 56,565,928 sequence reads that were de novo-assembled and screened for potential aetiological agents. Of the 384,096 contigs assembled by Megahit9, the longest (30,474 nucleotides (nt)) had a high abundance and was closely related to a bat SARS-like coronavirus (CoV) isolate—bat SL-CoVZC45 (GenBank accession number MG772933)—that had previously been sampled in China, with a nucleotide identity of 89.1%
The viral load in the BALF sample was estimated by qPCR to be 3.95 × 108 copies per ml (Extended Data Fig. 4).
SARS-CoV-2 can use human ACE2 as a receptor for cellular entry.
WHCV (TNNM: i.e. SARS-CoV-2 ) may efficiently use human ACE2 as a receptor for cellular entry.
Wu, 2020 (1).
In summary, the high similarities of the amino acid sequences and predicted protein structures of the RBD domains of WHCV and SARS-CoV suggest that WHCV may efficiently use human ACE2 as a receptor for cellular entry, which could potentially facilitate human-to-human transmission.
Although SARS-like coronaviruses have been widely identified in mammals including bats since 2005 in China10,26,27,28, the exact origin of human-infected coronaviruses remains unclear. Here we describe a new coronavirus—WHCV—in the BALF from a patient who experienced severe respiratory disease in Wuhan, China. Phylogenetic analysis suggests that WHCV is a member of the genus Betacoronavirus (subgenus Sarbecovirus) that has some genomic and phylogenetic similarities to SARS-CoV1, particularly in the RBD of the spike protein. These genomic and clinical similarities to SARS, as well as its high abundance in clinical samples, provides evidence for an association between WHCV and the ongoing outbreak of respiratory disease in Wuhan and across the world. Although the isolation of the virus from only a single patient is not sufficient to conclude that it caused these respiratory symptoms, our findings have been independently corroborated in further patients in a separate study.
All the findings, including the genomic sequence of the new (?) SARS-CoV-2 virus, are obtained on several pieces of sequencing equipment from Qiagen, Agilent Technologies, TaKaRa, Illumina.
Selected references:
1. Wu F, Zhao S, Yu B, et al. A new coronavirus associated with human respiratory disease in China. Nature. 2020;579(7798):265–269. doi:10.1038/s41586-020-2008-3
2. https://www.thegatewaypundit.com/2020/03/breaking-exclusive-the-coronavirus-fatality-rate-reported-by-the-media-is-completely-inaccurate-the-actual-rate-is-less-than-the-flu-media-lying-again/) Retrieved on March 19, 2020.
3. https://www.cdc.gov/flu/weekly/index.htm
Retrieved on March 20, 2020.
4. Raoult D, Zumla A, Locatelli F, Ippolito G, Kroemer G. Coronavirus infections: Epidemiological, clinical and immunological features and hypotheses. Cell Stress. 2020;Published 2020 Mar 2. doi:10.15698/cst2020.04.216
5. ttps://www.agenzianova.com/a/5e6bcf1da7fbe3.23491954/2851060/2020-03-13/coronavirus-iss-in-italia-i-decessi-accertati-finora-per-causa-del-covid-19-sono-solo-due
Accessed on March 20, 2020.
6. Pyrc K, Berkhout B, van der Hoek L. Antiviral strategies against human coronaviruses. Infect Disord Drug Targets. 2007;7(1):59–66. doi:10.2174/187152607780090757
7. https://www.cdc.gov/coronavirus/2019-ncov/hcp/disposition-in-home-patients.html
“Discontinuation of Home Isolation for Persons with COVID-19 (Interim Guidance).”
Accessed on March 22, 2020.
8. Coronavirus disease 2019 (COVID-19) Situation Report – 61.
https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200321-sitrep-61-covid-19.pdf?sfvrsn=6aa18912_2
Accessed March 22, 2020.
9. Lauer SA, Grantz KH, Bi Q, et al. The Incubation Period of Coronavirus Disease 2019 (COVID-19) From Publicly Reported Confirmed Cases: Estimation and Application [published online ahead of print, 2020 Mar 10]. Ann Intern Med. 2020;M20-0504. doi:10.7326/M20-0504
10. Yanis Roussel, Audrey Giraud-Gatineau, Marie-Thérèse Jimeno, Jean-Marc Rolain, Christin eZandotti, Philippe Colson, DidierRaoult. “SARS-CoV-2: fear versus data.” International Journal of Antimicrobial Agents, Available online 19 March 2020, 105947, In Press, Journal Pre-proof. https://doi.org/10.1016/j.ijantimicag.2020.105947
11. Ng OW, Chia A, Tan AT, Jadi RS, Leong HN, Bertoletti A and Tan YJ (2016). Memory T cell responses targeting the SARS coronavirus persist up to 11 years post-infection. Vaccine 34(17): 2008-2014. doi: 10.1016/j.vaccine.2016.02.063
12. Bai Y, Yao L, Wei T, Tian F, Jin DY, Chen L and Wang M (2020). Presumed Asymptomatic Carrier Transmission of COVID-19. JAMA. doi: 10.1001/jama.2020.2565
13. Finbloom DS, Silver K, Newsome DA, Gunkel R. Comparison of hydroxychloroquine and chloroquine use and the development of retinal toxicity. J Rheumatol. 1985;12(4):692–694.
14. Raines MF, Bhargava SK, Rosen ES. The blood-retinal barrier in chloroquine retinopathy. Invest Ophthalmol Vis Sci. 1989;30(8):1726–1731.
15. Goel P, Gerriets V. Chloroquine. [Updated 2019 Dec 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551512/
16. Wu Z, McGoogan JM. Characteristics of and Important Lessons From the Coronavirus Disease 2019 (COVID-19) Outbreak in China: Summary of a Report of 72 314 Cases From the Chinese Center for Disease Control and Prevention. JAMA. Published online February 24, 2020. doi:10.1001/jama.2020.2648
17. Jason Oke, Carl Heneghan. An article on a website of The Centre for Evidence-Based Medicine which is a part of the Nuffield Department of Primary Care Health Sciences at the University of Oxford.
https://www.cebm.net/global-covid-19-case-fatality-rates/
Accessed on March 23, 2020.
18. Yusuf IH, Sharma S, Luqmani R, Downes SM. Hydroxychloroquine retinopathy. Eye (Lond). 2017;31(6):828–845. doi:10.1038/eye.2016.298
19. Brigitte A Wevers & Lia van der Hoek. Renin–angiotensin system in
human coronavirus pathogenesis. Future Virol. (2010) 5 (2), 145–161
20. Varagic J, Ahmad S, Nagata S, Ferrario CM. ACE2: angiotensin II/angiotensin-(1-7) balance in cardiac and renal injury. Curr Hypertens Rep. 2014;16(3):420. doi:10.1007/s11906-014-0420-5
21. Coronavirus disease 2019 (COVID-19) Situation Report – 64 by WHO.
https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200324-sitrep-64-covid-19.pdf?sfvrsn=703b2c40_2
Accessed March 25, 2020.
22. Brigitte A.Wevers, Lia van der Hoek. Clin Lab Med 29 (2009) 715–724 doi:10.1016/j.cll.2009.07.007
23. Sheahan T., Deming D., Donaldson E., Pickles R., Baric R. (2006) Resurrection of an “Extinct” SARS-CoV Isolate GD03 from LATE 2003. In: Perlman S., Holmes K.V. (eds) The Nidoviruses. Advances in Experimental Medicine and Biology, vol 581. Springer, Boston, MA
24. Xu et al., Viruses 2020, 12, 244; doi:10.3390/v12020244
25. Wei, Xiao-Shan and Wang, Xuan and Niu, Yi-Ran and Ye, Lin-Lin and Peng, Wen-Bei and Wang, Zi-Hao and Yang, Wei-Bing and Yang, Bo-Han and Zhang, Jian-Chu and Ma, Wan-Li and Wang, Xiao-Rong and Zhou, Qiong, Clinical Characteristics of SARS-CoV-2 Infected Pneumonia with Diarrhea (2/26/2020). Available at SSRN: https://ssrn.com/abstract=3546120 orhttp://dx.doi.org/10.2139/ssrn.3546120
26. Yuen KS, Ye ZW, Fung SY, Chan CP, Jin DY. SARS-CoV-2 and COVID-19: The most important research questions. Cell Biosci. 2020;10:40. Published 2020 Mar 16. doi:10.1186/s13578-020-00404-4
27. Wu, J.T., Leung, K., Bushman, M. et al. Estimating clinical severity of COVID-19 from the transmission dynamics in Wuhan, China. Nat Med(2020). https://doi.org/10.1038/s41591-020-0822-7
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