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Truth About CoronaVirus #Covid19

Everyone who thinks coronavirus is harmless or doesn’t matter should rethink that opinion immediately. This is an extremely dangerous pathogen with wide spreading implications, including neurological impairment, brain, lung, heart & reproductive damage. There are now two recognized strains of the disease. The L strain is more infectious and severe than the ancestral S strain:

The SARS-CoV-2 epidemic started in late December 2019 in Wuhan, China, and has since impacted a large portion of China and raised major global concern. Herein, we investigated the extent of molecular divergence between SARS-CoV-2 and other related coronaviruses. Although we found only 4% variability in genomic nucleotides between SARS-CoV-2 and a bat SARS-related coronavirus (SARSr-CoV; RaTG13), the difference at neutral sites was 17%, suggesting the divergence between the two viruses is much larger than previously estimated. Our results suggest that the development of new variations in functional sites in the receptor-binding domain (RBD) of the spike seen in SARS-CoV-2 and viruses from pangolin SARSr-CoVs are likely caused by mutations and natural selection besides recombination. Population genetic analyses of 103 SARS-CoV-2 genomes indicated that these viruses evolved into two major types (designated L and S), that are well defined by two different SNPs that show nearly complete linkage across the viral strains sequenced to date. Although the L type (∼70%) is more prevalent than the S type (∼30%), the S type was found to be the ancestral version. Whereas the L type was more prevalent in the early stages of the outbreak in Wuhan, the frequency of the L type decreased after early January 2020. Human intervention may have placed more severe selective pressure on the L type, which might be more aggressive and spread more quickly. On the other hand, the S type, which is evolutionarily older and less aggressive, might have increased in relative frequency due to relatively weaker selective pressure. These findings strongly support an urgent need for further immediate, comprehensive studies that combine genomic data, epidemiological data, and chart records of the clinical symptoms of patients with coronavirus disease 2019 (COVID-19).

The disease has an R0 of around 6.6, which means 1 person infects that many other people, on average. There are also super-spreader incidents where one person can infect dozens of others. One person on average infects at least 6.6 other people.

The Novel Coronavirus, 2019-nCoV, is Highly Contagious and More Infectious Than Initially Estimated.

The novel coronavirus (2019-nCoV) is a recently emerged human pathogen that has spread widely since January 2020. Initially, the basic reproductive number, R0, was estimated to be 2.2 to 2.7. Here we provide a new estimate of this quantity. We collected extensive individual case reports and estimated key epidemiology parameters, including the incubation period. Integrating these estimates and high-resolution real-time human travel and infection data with mathematical models, we estimated that the number of infected individuals during early epidemic double every 2.4 days, and the R0 value is likely to be between 4.7 and 6.6. We further show that quarantine and contact tracing of symptomatic individuals alone may not be effective and early, strong control measures are needed to stop transmission of the virus.

The median incubation period is around 5 days, but outliers of 24+ days have been seen. The ability of the virus to stay active on surfaces for up to 27 days is also a cause for significant concern.

As the outbreak of coronavirus disease 2019 (COVID-19) progresses, epidemiological data are needed to guide situational awareness and intervention strategies. Here we describe efforts to compile and disseminate epidemiological information on COVID-19 from news media and social networks.


In this population-level observational study, we searched, a health-care-oriented social network that is currently streaming news reports on COVID-19 from local and national Chinese health agencies. We compiled a list of individual patients with COVID-19 and daily province-level case counts between Jan 13 and Jan 31, 2020, in China. We also compiled a list of internationally exported cases of COVID-19 from global news media sources (Kyodo News, The Straits Times, and CNN), national governments, and health authorities. We assessed trends in the epidemiology of COVID-19 and studied the outbreak progression across China, assessing delays between symptom onset, seeking care at a hospital or clinic, and reporting, before and after Jan 18, 2020, as awareness of the outbreak increased. All data were made publicly available in real time.


We collected data for 507 patients with COVID-19 reported between Jan 13 and Jan 31, 2020, including 364 from mainland China and 143 from outside of China. 281 (55%) patients were male and the median age was 46 years (IQR 35–60). Few patients (13 [3%]) were younger than 15 years and the age profile of Chinese patients adjusted for baseline demographics confirmed a deficit of infections among children. Across the analysed period, delays between symptom onset and seeking care at a hospital or clinic were longer in Hubei province than in other provinces in mainland China and internationally. In mainland China, these delays decreased from 5 days before Jan 18, 2020, to 2 days thereafter until Jan 31, 2020 (p=0·0009). Although our sample captures only 507 (5·2%) of 9826 patients with COVID-19 reported by official sources during the analysed period, our data align with an official report published by Chinese authorities on Jan 28, 2020.


News reports and social media can help reconstruct the progression of an outbreak and provide detailed patient-level data in the context of a health emergency. The availability of a central physician-oriented social network facilitated the compilation of publicly available COVID-19 data in China. As the outbreak progresses, social media and news reports will probably capture a diminishing fraction of COVID-19 cases globally due to reporting fatigue and overwhelmed health-care systems. In the early stages of an outbreak, availability of public datasets is important to encourage analytical efforts by independent teams and provide robust evidence to guide interventions.

SARS-CoV-2 is spreading at alarming levels due to its ability to be airborne. This means anyone infected will infects many of whom they come in contact with, simply by breathing near them.

An emergent pneumonia outbreak originated in Wuhan City, in the late December 2019. The pneumonia infection has rapidly spread from Wuhan to most other provinces and other 24 countries. World Health Organization declared a public health emergency of international concern over this global pneumonia outbreak on 30th January 2020.

The typical clinical symptoms of the patients who suffered from the novel viral pneumonia were fever, cough, and myalgia or fatigue with abnormal chest CT, and the less common symptoms were sputum production, headache, hemoptysis, and diarrhea. This new infectious agent is more likely to affect older males to cause severe respiratory diseases. Some of the clinical symptoms were different from the severe acute respiratory syndrome (SARS) caused by SARS coronavirus (SARS-CoV) that happened in 2002–2003, indicating that a new person-to-person transmission infectious agent has caused this emergent viral pneumonia outbreak. Chinese researchers have quickly isolated a new virus from the patient and sequenced its genome (29,903 nucleotides). The infectious agent of this viral pneumonia happenening in Wuhan was finally identified as a novel coronavirus (2019-nCOV), the seventh member of the family of coronaviruses that infect humans. On 11th February 2020, WHO named the novel viral pneumonia as “Corona Virus Disease (COVID19)”, while the international Committee on Taxonomy of Viruses (ICTV) suggested this novel coronavirus name as “SARS-CoV-2” due to the phylogenetic and taxonomic analysis of this novel coronavirus.

Transmission routes of 2019-nCoV and controls in dental practice


A novel β-coronavirus (2019-nCoV) caused severe and even fetal pneumonia explored in a seafood market of Wuhan city, Hubei province, China, and rapidly spread to other provinces of China and other countries. The 2019-nCoV was different from SARS-CoV, but shared the same host receptor the human angiotensin-converting enzyme 2 (ACE2). The natural host of 2019-nCoV may be the bat Rhinolophus affinis as 2019-nCoV showed 96.2% of whole-genome identity to BatCoV RaTG13. The person-to-person transmission routes of 2019-nCoV included direct transmission, such as cough, sneeze, droplet inhalation transmission, and contact transmission, such as the contact with oral, nasal, and eye mucous membranes. 2019-nCoV can also be transmitted through the saliva, and the fetal–oral routes may also be a potential person-to-person transmission route. The participants in dental practice expose to tremendous risk of 2019-nCoV infection due to the face-to-face communication and the exposure to saliva, blood, and other body fluids, and the handling of sharp instruments. Dental professionals play great roles in preventing the transmission of 2019-nCoV. Here we recommend the infection control measures during dental practice to block the person-to-person transmission routes in dental clinics and hospitals.


An emergent pneumonia outbreak originated in Wuhan City, in the late December 2019. The pneumonia infection has rapidly spread from Wuhan to most other provinces and other 24 countries. World Health Organization declared a public health emergency of international concern over this global pneumonia outbreak on 30th January 2020.

The typical clinical symptoms of the patients who suffered from the novel viral pneumonia were fever, cough, and myalgia or fatigue with abnormal chest CT, and the less common symptoms were sputum production, headache, hemoptysis, and diarrhea. This new infectious agent is more likely to affect older males to cause severe respiratory diseases. Some of the clinical symptoms were different from the severe acute respiratory syndrome (SARS) caused by SARS coronavirus (SARS-CoV) that happened in 2002–2003, indicating that a new person-to-person transmission infectious agent has caused this emergent viral pneumonia outbreak. Chinese researchers have quickly isolated a new virus from the patient and sequenced its genome (29,903 nucleotides). The infectious agent of this viral pneumonia happenening in Wuhan was finally identified as a novel coronavirus (2019-nCOV), the seventh member of the family of coronaviruses that infect humans. On 11th February 2020, WHO named the novel viral pneumonia as “Corona Virus Disease (COVID19)”, while the international Committee on Taxonomy of Viruses (ICTV) suggested this novel coronavirus name as “SARS-CoV-2” due to the phylogenetic and taxonomic analysis of this novel coronavirus.

Characteristics of 2019 novel coronavirus

Coronaviruses belong to the family of Coronaviridae, of the order Nidovirales, comprising large, single, plus-stranded RNA as their genome. Currently, there are four genera of coronaviruses: α-CoV, β-CoV, γ-CoV, and δ-CoV. Most of the coronavirus can cause the infectious diseases in human and vertebrates. The α-CoV and β-CoV mainly infect the respiratory, gastrointestinal, and central nervous system of humans and mammals, while γ-CoV and δ-CoV mainly infect the birds.

Usually, several members of the coronavirus cause mild respiratory disease in humans; however, SARS-CoV and the Middle East respiratory syndrome coronavirus (MERS-CoV) explored in 2002–2003 and in 2012, respectively, caused fatal severe respiratory diseases. The SARS-CoV and MERS-CoV belong to the β-CoV. 2019-nCoV explored in Wuhan also belongs to the β-CoV according to the phylogenetic analysis based on the viral genome. Although the nucleotide sequence similarity is less than 80% between 2019-nCoV and SARS-CoV (about 79%) or MERS-CoV (about 50%), 2019-nCoV can also cause the fetal infection and spread more faster than the two other coronaviruses. The genome nucleotide sequence identity between a coronavirus (BatCoV RaTG13) detected in the bat Rhinolophus affinis from Yunnan Province, China, and 2019-nCoV, was 96.2%, indicating that the natural host of 2019-nCoV may also be the Rhinolophus affinis bat. However, the differences may also suggest that there is an or more intermediate hosts between the bat and human. A research team from the South China Agricultural University has invested more than 1 000 metagenomic samples from pangolins, and found that 70% pangolins contained β-CoV. One of the coronaviruses they isolated from the pangolins comprised a genome that was very similar with that from 2019-nCoV, and the genome sequence similarity was 99%, indicating that the pangolin may be the intermediate host of 2019-nCoV.

2019-nCoV possessed the typical coronavirus structure with the “spike protein” in the membrane envelope, and also expressed other polyproteins, nucleoproteins, and membrane proteins, such as RNA polymerase, 3-chymotrypsin-like protease, papain-like protease, helicase, glycoprotein, and accessory proteins. The S protein from coronavirus can bind to the receptors of the host to facilitate viral entry into target cells. Although there are four amino acid variations of S protein between 2019-nCoV and SARS-CoV, 2019-nCoV can also bind to the human angiotensin-converting enzyme 2 (ACE2), the same host receptor for SARS-CoV, as 2019-nCoV can bind to the ACE2 receptor from the cells from human, bat, civet cat, and pig, but it cannot bind to the cells without ACE2. A recombinant ACE2-Ig antibody, a SARS-CoV-specific human monoclonal antibody, and the serum from a convalescent SARS-CoV-infected patient, which can neutralize 2019-nCoV, confirmed ACE2 as the host receptor for 2019-nCoV. The high affinity between ACE2 and 2019-nCoV S protein also suggested that the population with higher expression of ACE2 might be more susceptible to 2019-nCoV. The cellular serine protease TMPRSS2 also contributed to the S-protein priming of 2019-nCoV, indicating that the TMPRSS2 inhibitor might constitute a treatment option.

The possible transmission routes of 2019-nCoV

The common transmission routes of novel coronavirus include direct transmission (cough, sneeze, and droplet inhalation transmission) and contact transmission (contact with oral, nasal, and eye mucous membranes). Although common clinical manifestations of novel coronavirus infection do not include eye symptoms, the analysis of conjunctival samples from confirmed and suspected cases of 2019-nCoV suggests that the transmission of 2019-nCoV is not limited to the respiratory tract, and that eye exposure may provide an effective way for the virus to enter the body.

In addition, studies have shown that respiratory viruses can be transmitted from person to person through direct or indirect contact, or through coarse or small droplets, and 2019-nCoV can also be transmitted directly or indirectly through saliva. Notably, a report of one case of 2019-nCoV infection in Germany indicates that transmission of the virus may also occur through contact with asymptomatic patients.

Studies have suggested that 2019-nCoV may be airborne through aerosols formed during medical procedures. It is notable that 2019-nCoV RNA could also be detected by rRT-PCR testing in a stool specimen collected on day 7 of the patient’s illness. However, the aerosol transmission route and the fecal–oral transmission route concerned by the public still need to be further studied and confirmed.

Possible transmission routes of 2019-nCoV in dental clinics

Since 2019-nCoV can be passed directly from person to person by respiratory droplets, emerging evidence suggested that it may also be transmitted through contact and fomites. In addition, the asymptomatic incubation period for individuals infected with 2019-nCov has been reported to be ~1–14 days, and after 24 days individuals were reported, and it was confirmed that those without symptoms can spread the virus. To et al. reported that live viruses were present in the saliva of infected individuals by viral culture method. Furthermore, it has been confirmed that 2019-nCov enters the cell in the same path as SARS coronavirus, that is, through the ACE2 cell receptor. 2019-nCoV can effectively use ACE2 as a receptor to invade cells, which may promote human-to-human transmission. ACE2+ cells were found to be abundantly present throughout the respiratory tract, as well as the cells morphologically compatible with salivary gland duct epithelium in human mouth. ACE2+ epithelial cells of salivary gland ducts were demonstrated to be a class early targets of SARS-CoV infection, and 2019-nCoV is likely to be the same situation, although no research has been reported so far.

Dental patients and professionals can be exposed to pathogenic microorganisms, including viruses and bacteria that infect the oral cavity and respiratory tract. Dental care settings invariably carry the risk of 2019-nCoV infection due to the specificity of its procedures, which involves face-to-face communication with patients, and frequent exposure to saliva, blood, and other body fluids, and the handling of sharp instruments. The pathogenic microorganisms can be transmitted in dental settings through inhalation of airborne microorganisms that can remain suspended in the air for long periods, direct contact with blood, oral fluids, or other patient materials, contact of conjunctival, nasal, or oral mucosa with droplets and aerosols containing microorganisms generated from an infected individual and propelled a short distance by coughing and talking without a mask, and indirect contact with contaminated instruments and/or environmental surfaces. Infections could be present through any of these conditions involved in an infected individual in dental clinics and hospitals, especially during the outbreak of 2019-nCoV (Fig. 1).


Airborne spread

The airborne spread of SARS-Cov (severe acute respiratory syndrome coronavirus) is well-reported in many literatures. The dental papers show that many dental procedures produce aerosols and droplets that are contaminated with virus. Thus, droplet and aerosol transmission of 2019-nCoV are the most important concerns in dental clinics and hospitals, because it is hard to avoid the generation of large amounts of aerosol and droplet mixed with patient’s saliva and even blood during dental practice. In addition to the infected patient’s cough and breathing, dental devices such as high-speed dental handpiece uses high-speed gas to drive the turbine to rotate at high speed and work with running water. When dental devices work in the patient’s oral cavity, a large amount of aerosol and droplets mixed with the patient’s saliva or even blood will be generated. Particles of droplets and aerosols are small enough to stay airborne for an extended period before they settle on environmental surfaces or enter the respiratory tract. Thus, the 2019-nCoV has the potential to spread through droplets and aerosols from infected individuals in dental clinics and hospitals.

Contact spread

A dental professional’s frequent direct or indirect contact with human fluids, patient materials, and contaminated dental instruments or environmental surfaces makes a possible route to the spread of viruses. In addition, dental professionals and other patients have likely contact of conjunctival, nasal, or oral mucosa with droplets and aerosols containing microorganisms generated from an infected individual and propelled a short distance by coughing and talking without a mask. Effective infection control strategies are needed to prevent the spread of 2019-nCoV through these contact routines.

Contaminated surfaces spread

Human coronaviruses such as SARS-CoV, Middle East Respiratory Syndrome coronavirus (MERS-CoV), or endemic human coronaviruses (HCoV) can persist on surfaces like metal, glass, or plastic for up to a couple of days. Therefore, contaminated surfaces that are frequently contacted in healthcare settings are a potential source of coronavirus transmission. Dental practices derived droplets and aerosols from infected patients, which likely contaminate the whole surface in dental offices. In addition, it was shown at room temperature that HCoV remains infectious from 2 h up to 9 days, and persists better at 50% compared with 30% relative humidity. Thus, keeping a clean and dry environment in the dental office would help decrease the persistence of 2019-nCoV.

China confirms aerosol spread of Covid-19, frontline medical workers need to wear right masks

The health authorities in China have found that Covid-19 can be spread through the air, or aerosol transmission, in cases where an individual is exposed to high concentrations of droplets in the air in a relatively closed environment for a sustained period of time.

This is why front line medical workers need to wear the right masks. This finding was announced on Wednesday (Feb 19).

The number of infected medical personnel in China bears witness to the new findings: 1,716 medical workers had been infected with Covid-19 as of Feb 14. Six have died from the disease.

As a mask is necessary in such an environment, definitely in a hospital taking in Covid-19 patients, the question is what type of mask offers the best protection.

According to Professor Joseph Kwan of the Hong Kong University of Science and Technology, respirators, commonly known as N95 masks, which fit the wearer’s face snugly and have built-in filters, provide far better protection than surgical masks.

“Respirators are designed to protect the user, because they want to keep the contaminants out,” he said, while surgical masks, “actually in the healthcare environment are meant to protect the patients”.

N95 respirator masks are now worn by all the medical staff after a trial at the Zhongnan Hospital in China. Since this was implemented, there have been no new cases of Covid-19 from among them.

SARS-CoV-2 is capable of asymptomatic transmission and it is practically impossible to stop the spread by contact tracing and minor quarantines. There are a multitude of asymptomatic carriers walking around:

Potential Transmission of SARS-CoV-2 from an Asymptomatic Carrier

Although questions remain, this interesting report raises the possibility of asymptomatic transmission of SARS-CoV-2.

The current outbreak of COVID-19 that began in Wuhan, China, has infected thousands of people, but questions remain about the infectivity, infectious period, and mechanisms of transmission.

In this study, investigators report a family cluster of five patients who likely acquired infection with SARS-CoV-2 (the virus causing COVID-19) from an asymptomatic 20-year-old woman who lives in Wuhan and traveled to Anyang, China (approximately 673 kilometers from Wuhan). In Anyang, she had contact with two persons over a 3-day period and with another three persons on the third day of this period. Four days later, one of the contacts became symptomatic; the other four contacts became symptomatic over the ensuing 9 days. The suspected index person tested negative for SARS-CoV-2 by RT-PCR 16 days after arriving from Wuhan but tested positive 2 days later; yet she remained asymptomatic and had no evidence of infiltrates on chest CT performed the day before and three days after testing positive. She also had no elevation of C-reactive protein or any laboratory abnormalities. The five contacts all developed symptoms consistent with COVID-19; four were women aged 42 to 57 years old. All had positive RT-PCR testing for SARS-CoV-2 within 1 day after hospital admission and multifocal ground-glass opacities on chest CT.

SARS-CoV-2 can enter the eye through the ocular surface. Any protective mask must be full-face. Half-face masks are insufficient:

On Jan 22, Guangfa Wang, a member of the national expert panel on pneumonia, reported that he was infected by 2019-nCoV during the inspection in Wuhan. He wore an N95 mask but did not wear anything to protect his eyes. Several days before the onset of pneumonia, Wang complained of redness of the eyes. Unprotected exposure of the eyes to 2019-nCoV in the Wuhan Fever Clinic might have allowed the virus to infect the body.

Infectious droplets and body fluids can easily contaminate the human conjunctival epithelium. Respiratory viruses are capable of inducing ocular complications in infected patients, which then leads to respiratory infection. Severe acute respiratory syndrome coronavirus (SARS-CoV) is predominantly transmitted through direct or indirect contact with mucous membranes in the eyes, mouth, or nose. The fact that exposed mucous membranes and unprotected eyes increased the risk of SARS-CoV transmission suggests that exposure of unprotected eyes to 2019-nCoV could cause acute respiratory infection.Thus, Huang and colleagues should have analysed conjunctival scrapings from both confirmed and suspected 2019-nCoV cases during the onset of symptoms. The respiratory tract is probably not the only transmission route for 2019-nCoV, and all ophthalmologists examining suspected cases should wear protective eyewear.

The virus attacks ACE2 receptors in cells. ACE2 stands for Angiotensin Converting Enzyme 2, and it’s part of the angiotensin-renin system that regulates vasoconstriction and vasodilation. This system is essential for your body to maintain the correct blood pressure. ACE2 receptors are found in many vital organs and reproductive tissues in the human body — Lungs, heart, kidneys, & brain. SARS-CoV-2 infection also has severely negative effects on male fertility. ACE2 receptors are found in the seminiferous ducts of the testis:

The Cardiac Implications of Novel Coronavirus

February 20, 2020 — The American College of Cardiology (ACC) released a clinical bulletin addressing the cardiac implications of the novel coronavirus (COVID-19, also referred to as SARS‐CoV‐2, 2019-nCoV and Wuhan Coronavirus). The key message to clinicians is that patients with underlying cardiovascular disease may have a potential increased risk if they contract coronavirus.

The bulletin provides background on the epidemic, which was first reported in late December 2019, and looks at early cardiac implications from case reports. It also provides information on the potential cardiac implications from analog viral respiratory pandemics and offers early clinical guidance given current 2019-nCoV uncertainty. 

The ACC lists the following points regarding early cardiac implications from case reports on Wuhan Coronavirus.

   • Early case reports suggest patients with underlying conditions are at higher risk for complications or mortality from COVID-19; up to 50 percent of hospitalized patients have a chronic medical illness.

   • 40 percent of hospitalized patients with confirmed COVID-19 patients have cardiovascular or cerebrovascular disease.

   • In a recent case report on 138 hospitalized COVID-19 patients, 19.6 percent of patients developed acute respiratory distress syndrome.

   • 16.7 percent of patients developed arrhythmia; 7.2 percent developed acute cardiac injury.

   • 8.7 percent of patients developed shock; 3.6% developed acute kidney injury.

   • Rates of complication were universally higher for ICU patients.

   • The first reported death was a 61-year-old male, with a long history of smoking, who succumbed to acute respiratory distress, heart failure and cardiac arrest.

   • Early, unpublished first-hand reports suggest at least some patients develop myocarditis.

SARS-CoV-2 can potentially cause lung fibrosis and chronic lung disease if not caught and treated with antivirals at an early stage. This has serious implications for treatment of patients who get infected with a different strain; their weakened condition may increase mortality.


SARS-CoV (a relative of SARS-CoV-2) has been shown to cause severe neural death (surprisingly without encephalitis) in transgenic mouse models.

Infection of humans with the severe acute respiratory syndrome coronavirus (SARS-CoV) results in substantial morbidity and mortality, with death resulting primarily from respiratory failure. While the lungs are the major site of infection, the brain is also infected in some patients. Brain infection may result in long-term neurological sequelae, but little is known about the pathogenesis of SARS-CoV in this organ. We previously showed that the brain was a major target organ for infection in mice that are transgenic for the SARS-CoV receptor (human angiotensin-converting enzyme 2). Herein, we use these mice to show that virus enters the brain primarily via the olfactory bulb, and infection results in rapid, transneuronal spread to connected areas of the brain. This extensive neuronal infection is the main cause of death because intracranial inoculation with low doses of virus results in a uniformly lethal disease even though little infection is detected in the lungs. Death of the animal likely results from dysfunction and/or death of infected neurons, especially those located in cardiorespiratory centers in the medulla. Remarkably, the virus induces minimal cellular infiltration in the brain. Our results show that neurons are a highly susceptible target for SARS-CoV and that only the absence of the host cell receptor prevents severe murine brain disease.

Recent information seems to suggest that SARS-CoV-2 can cause neurological symptoms and cerebrovascular disease, leading to loss of autonomic functions of the brain and, in the worst case, lingering brain damage.

OBJECTIVE: To study the neurological manifestations of patients with coronavirus disease 2019 (COVID-19). DESIGN: Retrospective case series SETTING: Three designated COVID-19 care hospitals of the Union Hospital of Huazhong University of Science and Technology in Wuhan, China. PARTICIPANTS: Two hundred fourteen hospitalized patients with laboratory confirmed diagnosis of severe acute respiratory syndrome from coronavirus 2 (SARS-CoV-2) infection. Data were collected from 16 January 2020 to 19 February 2020. MAIN OUTCOME MEASURES: Clinical data were extracted from electronic medical records and reviewed by a trained team of physicians. Neurological symptoms fall into three categories: central nervous system (CNS) symptoms or diseases (headache, dizziness, impaired consciousness, ataxia, acute cerebrovascular disease, and epilepsy), peripheral nervous system (PNS) symptoms (hypogeusia, hyposmia, hypopsia, and neuralgia), and skeletal muscular symptoms. Data of all neurological symptoms were checked by two trained neurologists. RESULTS: Of 214 patients studied, 88 (41.1%) were severe and 126 (58.9%) were non-severe patients. Compared with non-severe patients, severe patients were older (58.7 ± 15.0 years vs 48.9 ± 14.7 years), had more underlying disorders (42 [47.7%] vs 41 [32.5%]), especially hypertension (32 [36.4%] vs 19 [15.1%]), and showed less typical symptoms such as fever (40 [45.5%] vs 92 [73%]) and cough (30 [34.1%] vs 77 [61.1%]). Seventy-eight (36.4%) patients had neurologic manifestations. More severe patients were likely to have neurologic symptoms (40 [45.5%] vs 38 [30.2%]), such as acute cerebrovascular diseases (5 [5.7%] vs 1 [0.8%]), impaired consciousness (13 [14.8%] vs 3 [2.4%]) and skeletal muscle injury (17 [19.3%] vs 6 [4.8%]). CONCLUSION: Compared with non-severe patients with COVID-19, severe patients commonly had neurologic symptoms manifested as acute cerebrovascular diseases, consciousness impairment and skeletal muscle symptoms.

This could cause a significant portion of the population to have severe drops in cognitive function, intelligence, and IQ.

The action of SARS-Coronaviruses (which attack ACE2 pathways) can dysregulate the angiotensin system and cause cardiopulmonary damage and inflammation directly through this route:

Severe acute respiratory syndrome (SARS) is an emerging infectious viral disease characterized by severe clinical manifestations of the lower respiratory tract. The pathogenesis of SARS is highly complex, with multiple factors leading to severe injury in the lungs and dissemination of the virus to several other organs. The SARS coronavirus targets the epithelial cells of the respiratory tract, resulting in diffuse alveolar damage. Several organs/cell types may be infected in the course of the illness, including mucosal cells of the intestines, tubular epithelial cells of the kidneys, neurons of the brain, and several types of immune cells, and certain organs may suffer from indirect injury. Extensive studies have provided a basic understanding of the pathogenesis of this disease. In this review we describe the most significant pathological features of SARS, explore the etiological factors causing these pathological changes, and discuss the major pathogenetic mechanisms. The latter include dysregulation of cytokines/chemokines, deficiencies in the innate immune response, direct infection of immune cells, direct viral cytopathic effects, down-regulation of lung protective angiotensin converting enzyme 2, autoimmunity, and genetic factors. It seems that both abnormal immune responses and injury to immune cells may be key factors in the pathogenesis of this new disease.

A novel coronavirus was identified as the etiological agent of SARS. This virus (SARS-CoV) belongs to a family of large, positive, single-stranded RNA viruses. Nevertheless, genomic characterization showed that the SARS-CoV is only moderately related to other known coronaviruses. In contrast with previously described coronaviruses, SARS-CoV infection typically causes severe symptoms related to the lower respiratory tract. The virus has been isolated from several animals, including civet cats and raccoon dogs, although neither of these animals is regarded as the true source. Recently, certain bat species have been reported as potential natural reservoirs. SARS is transmitted to and among humans by direct contact, droplet, and airborne routes. Viral isolation from fecal and urinary samples suggests additional routes of transmission.

SARS has a characteristic clinical course. Patients present with flu-like symptoms including fever, chills, cough, and malaise. Approximately 70% of the patients subsequently suffer from shortness of breath and recurrent or persistent fever, whereas the remaining 30% show clinical improvement after the first week. Approximately 20 to 30% of patients require intensive care treatment including mechanical ventilation. Increased alanine aminotransferase, lactate dehydrogenase, thrombocytopenia, and lymphopenia have all been frequently detected in SARS patients. In patients younger than 60 years of age the estimated fatality rate amounts to 6.8% and in older patients attains an estimated 43%.

A number of complete and partial autopsies of SARS patients have been reported since the first outbreak in 2003. The predominant pathological finding in these cases was diffuse alveolar damage (DAD). This severe pulmonary injury of SARS patients is caused both by direct viral effects and immunopathogenetic factors. Many important aspects of the pathology and pathogenesis of SARS have not yet been fully clarified. Here, we offer a comprehensive overview of the morphological and histopathological findings present in different organs and cells. In addition, we summarize the most important mechanisms that may play a role in the seemingly complex pathogenesis of this new disease.

Major Pathological Findings in Various Organs and Tissue

Respiratory tractDiffuse alveolar damage with varying degrees of acute exudative features including edema and hyaline membranes, organization, and fibrosis. Macrophagic or mixed cellular infiltration, multinuclear giant cells, atypical reactive pneumocytes, and vascular injury. Positive in situ hybridization signals in pneumocytes, lymphocytes, and macrophages

Spleen and lymph nodes — Lymphocyte depletion in spleen and lymph nodes with architectural disruption. Splenic white pulp atrophy. Positive in situ hybridization signals in immune cells.

Digestive tractIntestines: no obvious pathological changes/nonspecific changes. Depletion of mucosal lymphoid tissue. Positive in situ hybridization signals in mucosal epithelial cells

Liver: no specific pathological changes. In some cases, necrosis and evidence of apoptosis

Urogenital tractKidneys: acute tubular necrosis, in varying degrees and other nonspecific features. Positive in situ hybridization signals in the epithelial cells of the distal tubules
Central nervous systemEdema and degeneration of neurons, several neurons in situ hybridization-positive
Bone marrowIn some cases, reactive hemophagocytosis
Skeletal MusclesMyofiber necrosis and atrophy, few regenerative myofibers
Adrenal glandNecrosis and infiltration of monocytes and lymphocytes
Thyroid glandDestruction of follicular epithelial cells, several apoptotic cells
TestesGerm cell destruction, apoptotic spermatogenetic cells
HeartEdema and atrophy of myocardial fibers

SARS-CoV-2 can cause myocarditis leading to myoglobin accumulation in the blood and renal failure. It can also directly attack several vital organs of the body:

What is most disturbing about this virus is that it can potentially target so many different kinds of tissues. If, for instance, it attacks ACE2 in the neurons and leads to brain death and seizures, it may lead to a cadaver that, upon examination by a coroner conducting an autopsy, may reveal hardly any lung pathology whatsoever. Any autopsy of COVID-19 victims must absolutely cover several areas of the body. Not just the lungs. The heart, kidneys, liver, and the brain, as well. All must be sectioned and examined closely.

There are so many different things that could cause the collapses that have been witnessed. Febrile seizures from fever, heart attacks due to myocarditis, or even fainting from hypoxia from pneumonia.

However, what has been most concerning about the collapses is the consistent presentation of the victim; the rigidity of the body and the seizures. You would think there would be postural variations. Someone having a heart attack would struggle, they would bend their knees. These people, their limbs stretch out straight, and they begin to seize or show the fencing sign. At first, it was suspected that cerebral vasculitis caused by the virus attacking blood vessels in the brain, or viral encephalitis attacking the brain tissue directly.

However, it was discovered that in transgenic mouse models (hACE2 mice), SARS-CoV can cause neuronal damage without apparent encephalitis.

Coronavirus does not just effect the respiratory system, it embeds itself into the central nervous system & has the potential to cause significant neurological impairment, brain damage, & cancer. This would be worse than HPV or HSV-1 (70%+ of population already infected).


As we now know, HPV is the cause behind many cancers, with roughly 90% of colon & cervical cancers being caused by the virus. This has been theorized for some time, as viruses infect a cell, exude an anti-inflammatory barrier to avoid immune detection, then proliferate into cancer.




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