The 2019 novel coronavirus (2019-nCoV) has been formally named ‘severe acute respiratory syndrome coronavirus 2’ (SARS-CoV-2) with its associated illness being labeled ‘coronavirus disease 2019’ (COVID-19) [1]. The SARS-CoV-2 outbreak marks the third coronavirus outbreak in two decades [2]. Coronaviruses derive their name from the characteristic covering of their surface by peplomers that resembles a solar or stellar corona [3].
SARS-CoV-2 has an average incubation period of about 5 days, and is mainly transmitted through respiratory droplets, with direct contact and aerosol transmission being lesser routes [4] [5]. Common symptoms include cough, fever, shortness of breath, and fatigue, but sore throat, headache, dizziness, nausea, and diarrhea may also be seen [6]. Evidently, coronaviruses can persist on inanimate surfaces for up to nine days, but they can be inactivated with disinfectants containing ethanol or hydrogen peroxide [7]. SARS-CoV-2 is a positive-sense, single-stranded RNA virus that falls under the Betacoronavirus genus and is closely related to two SARS-related coronaviruses found in Chinese rufous horseshoe bats [8]. The genetic information of positive-sense RNA viruses can be quickly translated in the nuclei of host cells by ribosomes, and coronaviruses house the largest known RNA genomes [9]. Genomic investigations suggest that SARS-CoV-2 could have originated in a seafood market in Wuhan or the nearby Wuhan Institute of Virology [10]. Yu et al. have proposed that the virus was imported from outside the market, with the market only having catalyzed its spread [11]. Pradhan et al. discovered four insertion sequences in the SARS-CoV-2 genome that are not present in any other coronavirus yet match what can be found in two key proteins of HIV-1 (human immunodeficiency virus type 1) [12]. This finding has generated suspicion of genetic engineering as the researchers concluded that the natural acquisition of these insertions is highly unlikely. A combination of the two antiretroviral drugs lopinavir and ritonavir (normally used to combat HIV-1) being efficacious against SARS-CoV-2 lends support to the genetic engineering origin of SARS-CoV-2 [13]. Relatedly, chloroquine and hydroxychloroquine (both antimalarial drugs) have also been used successfully in the treatment of COVID-19 [14]. According to the work of Xu et al., SARS-CoV-2 has a strong binding affinity to the angiotensin-converting enzyme 2 (ACE2) receptor in humans, which drives entry of the virus into host cells so that replication can take place [15]. ACE2 is highly expressed in the alveolar cells of the lungs and the enterocytes of the small intestine, which is why SARS-CoV-2 gains access to the body most easily through the respiratory and gastrointestinal routes [16]. Just a few days ago, Hoffmann et al. reported that SARS-CoV-2 also relies on spike protein priming by TMPRSS2 (transmembrane protease serine 2) for entry into cells [17]. The coexpression of ACE2 and TMPRSS2 in pneumocytes (cells that line the alveoli in the lungs) apparently allows for a cleaving of the SARS-CoV-2 spike protein which then diminishes viral recognition by neutralizing antibodies as SARS-CoV spike protein fragments can serve as antibody decoys [18]. SARS-CoV-2 can also hide from the immune system by downregulating gene expression related to antigen presentation [19]. Inflammation and damage to the lungs may also be worsened by the induction of ACE2 ectodomain shedding by SARS-CoV-2, which has been associated with acute lung injury and hindered lung function [20]. Interestingly, evidence exists for a higher level of ACE2 expression in the bodies of East Asian populations compared with non-Asian populations [21] [22]. Once the viral RNA is released into the cytoplasm, host cell machinery is used to replicate the genome, after which virion-housing vesicles fuse with the plasma membrane to release and spread the virus [23]. In the cohort study of Yang et al., lymphocytopenia (low white blood cell count), possibly caused by pyroptosis, occurred in over 80% of the critically ill patients [24]. Because lymphocytopenia is prominent in critically ill subjects with SARS-CoV infection, the severity of lymphocytopenia may reflect the severity of SARS-CoV-2 infection [25]. Antigen presentation in response to SARS-CoV-2 exposure should stimulate the crafting of virus-specific antibodies, but if T cell hyperactivation takes place, a cytokine storm can be triggered and inadvertent injury to lung tissue can result, potentially leading to ARDS and ultimately death (ARDS is the main cause of death in COVID-19) [26] [27]. Older patients are statistically more likely to develop ARDS (acute respiratory distress syndrome) from viral pneumonia than those of a younger age [28]. Is there a connection between the incidence of pneumonia and air quality in Wuhan? Absolutely there is. As Qian et al. have expressed in their 2007 examination, “There are approximately 4.5 million residents in Wuhan who live in the city core area…where air pollution levels are higher and pollution ranges are wider than the majority of cities in the published literature” [29]. In 2012, Liu et al. found a significant association between ambient air pollution in Wuhan and daily respiratory disease mortality (this includes pneumonia) [30]. In 2017, Ren et al. found “Strong evidence of an association between [nitrogen dioxide] and daily respiratory disease mortality among men or people older than 65 years,” and concluded “There was a positive association between air pollutants and respiratory disease mortality in Wuhan, China. Both time-series and case-crossover analyses consistently reveal the association between three air pollutants and respiratory disease mortality” [31]. In 2013, Chen et al. studied the seasonal variation between ambient particulate matter and daily mortality in Wuhan and discovered that particulate matter pollution was greatest in the winter seasons, which matched the peaks in total mortality over a three-year period [32]. Qian et al. also discerned that the effects of three air pollutants on respiratory mortality was greatest during the winter seasons in Wuhan [33]. The outbreak of SARS-CoV-2 in Wuhan began in December of last year did it not? Next, the link between COVID-19 and 5G demands examination. China has made the deployment of 5G technology a national priority, and Wuhan has been chosen as a primary 5G hub with thousands of base stations already in place, making Wuhan one of the most electropolluted cities on the planet [34]. And a score of 5G antennas have been installed in the new hospitals built to treat patients with COVID-19 [35]. Behind China, South Korea and Italy have two of the highest number of SARS-CoV-2 cases in the world, and both have been heavily implementing 5G [36]. And let’s note that almost every single Italian COVID-19 fatality has been tied to a previous medical condition, and the average age among these fatalities is greater than the average life expectancy in the United States [37]. Additionally, Iran is an epicenter for the rollout of 5G and has had more reported deaths from COVID-19 than any other country in the world outside of China as of the writing of this article [38]. Digging deeper, mountains of research show the detrimental effects of man-made electromagnetic field irradiation on immune function, but specifically we know that millimeter waves or radiation from the extremely high frequency band (this band is used by 5G systems) can significantly disturb the activity of peripheral blood neutrophils [39]. We also know that neutrophils are important for controlling viral infections, and that their improper or prolonged activation can “lead to detrimental effects to the host and can even cause severe disease, including pneumonia and acute respiratory distress syndrome,” as explained by Galani and Andreakos in 2015 [40] [41] [42]. Drescher and Bai corroborate the above in their 2013 paper, stating that the unbalanced recruitment of neutrophils “may cause severe damage to the targeting tissues or organs during influenza and other viral infections” [43]. More specifically, it is known that oxidative stress can increase the infectivity of coronaviruses, as can abnormal calcium influx from the activation of voltage-dependent calcium channels by EMFs [44] [45] [46]. What this tells us is that exposure to very discordant EMFs can greatly weaken the immune system and make the body much more vulnerable to opportunistic infections [47]. Furthermore, pneumonia can be exacerbated by aberrant calcium influx (which 5G radiation can trigger), and because calcium channel blockers can reduce the severity of pneumonia, we can say that 5G radiation can both promote the development and worsen the severity of pneumonia [48]. And there is no denying that the eruption of COVID-19 paralleled the rapid construction of Wuhan’s 5G network. I’ve discussed the evil of 5G in another article, but let’s just mention here that many experiments do not account for pulsing and carrier signal modulation and therefore do not accurately reflect the very adverse and systemic effects of wireless radiation [49]. Let me also mention that millimeter waves activate voltage-dependent calcium channels in the body and excessive activation of these channels can promote fear conditioning, which is being clearly evinced around much of the world right now [50]. Now, most individuals who have contracted SARS-CoV-2 have presented with mild symptoms that resolved without problem, and many exhibited no symptoms at all [51]. And the toll of COVID-19 stands weakly compared to influenza, for in 2018, Iuliano et al. reported an estimate of between 291,243 and 645,832 for the number of annual influenza-associated deaths globally [52]. As of March 14, just under 5,400 deaths from COVID-19 have been tallied, the majority of which are from China. Turning to pneumonia, in 2011, Ruuskanen, Lahti, Jennings, and Murdoch reported that roughly 200 million cases (this bears repeating, 200 million cases!) of community-acquired viral pneumonia occur every year [53]. I feel it is safe to say that few folks were panicking over pneumonia before it began being associated with a coronavirus by every media outlet. We must also keep in mind that much of the data and testing for SARS-CoV-2 infection is unreliable, knowledge of which is making its way through the grapevine [54]. In corroboration, Zhuang et al. reported that approximately half of the results from nucleic acid testing currently being used in China might be false positives [55]. So what can we do to naturally oppose COVID-19? Firstly, the SARS-CoV-2 3a protein can trigger apoptosis via the mitochondrial death pathway where cytochrome c is released into the cytosol [56]. This disruption of mitochondrial dynamics by SARS-CoVs can cripple signaling within the innate immune system which helps SARS-CoVs evade immune responses and increases their infectivity [57]. Thankfully, vitamin C can do a great job of deflecting the apoptotic cascade and thus the virus-induced death of cells [58]. And this is why vitamin C has been and is continuing to be heavily used in China to successfully treat COVID-19 patients [59] [60] [61]. Of course, this information is being suppressed to instill fear and promote the false belief that nothing can be done for COVID-19 outside of vaccination. In fact, so much stigma and panic has been generated that many innocent Wuhan citizens have been the targets of violent attacks by vigilantes in the region [62]. And the CDC knows better than anyone that fear sells vaccines. Continuing, in 2017, To et al. found that many RNA viruses can block the signaling for type 1 interferon production, which is important because type 1 interferons help defend the body against viral infection [63]. In response, alpha-lipoic acid, sulforaphane, and spirulina may counter this blocking and boost the making of type 1 interferons, enhancing the antiviral response [64] [65] [66]. Zinc and selenium may help quell inflammation in the lungs induced by viral infection and slow the rate at which an infecting virus mutates, respectively [67] [68]. These nutrients could then aid in thwarting acute respiratory distress syndrome (ARDS). Furthermore, beta-glucan and elderberry have demonstrated effectiveness in protecting against RNA viruses [69] [70]. Cinnamomum cassia has demonstrated effectiveness against HIV-1, and curcumin has exhibited notable anti-SARS-CoV activity [71] [72]. And it seems that quercetin can help block the entry of SARS-CoV into host cells [73]. From the Chinese pharmacopeia, Stephania tetrandra, Salvia miltiorrhiza, Lycoris radiata, and Ganoderma lucidum have all shown strong antiviral abilities against coronaviruses [74] [75] [76] [77]. Houttuynia cordata has demonstrated significant inhibitory effects on SARS-CoV, while astragalus and resveratrol have done the same with other coronaviruses [78] [79] [80]. Essential oil-wise, the diffusing of peppermint and thyme could be helpful in preventing the spread of SARS-CoV-2 [81]. To conclude this article I would like to quickly bring us back to looking at things from a higher perspective, and ask that we please all do each other a favor and stop obsessing over propaganda from CNN and elsewhere. Instead, go for a walk, read a good book, and maybe eat an orange or two. We’re gonna be fine. Solar coronas illustrate that light always prevails over darkness – all we have to do is let love in. References:
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AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
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