Is Covid-19 A Natural Disaster or A Man-Made Pandemic
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Abstract
The covid-19 virus is widely associated with being developed in Chinese laboratories as a war weapon. It is commonly believed to be either accidentally or intentionally released to the world’s population as a bioterrorism tool with unknown objectives. The virus has infected people globally in more than 200 countries resulting in more than 350 thousand deaths hence being declared a global pandemic by the world health organization. This literature, therefore, aims at determining whether covid-19 is a natural disaster or man-made pandemic through analysis of findings from recent research.
Since December 2019 when the first case of coronavirus was reported in Hubei province of china, many global governments have reported several cases and deaths resulting from the virus. As a result, many researchers have attempted to determine the origin of this deadly virus. In contradiction to the common belief that covid-19 was made in Chinese laboratory as a bioterrorism weapon, most research findings reveal that the virus is a natural disaster.
Upon the outbreak of the virus in Wuhan China, the genome of the covid-19 virus was sequenced by the scientists in china and the resulting data was shared across the world for extensive study. Kristian Andersen and other researchers adopted this data as a foundation of their research which widely pointed out various pieces of evidence that associates these various to natural processes of evolution. The pieces of evidence that support covid-19 being a natural disaster are discussed below.
Firstly, many studies reveal that the covid-19 virus contains a spiking protein that facilitates the hooking of the virus to the human body cells. The covid-19 spiking protein successfully hooks to ACE2 enzyme which is mandated to aid in regulating blood pressure and is normally present at the outer surface of human body cells. According to Andersen et al (2007), the efficient evolution in the binding of the covid-19 virus spiking protein to the cells of the human body is only possible through natural processes and selection rather than artificial production.
Secondly, the covid-19 molecular structure possesses significant differences from other known existing viruses. Nevertheless, covid-19 possess a close relationship to the coronavirus that is most common in animals such as bats instead of resembling other known human viruses that are usually associated with causing severe illness. This openly contradicts the concept of artificial engineering of the covid-19 virus.
Whereas the exact origin of the covid-19 virus not being known by many scientists and relevant global authorities, researchers through their studies possess a strong belief that the evolution of the virus may have originated from non-human hosts with bats being a high possibility (Chakraborty, 2020). A second theory presents pangolins as an intermediate host or a potential third party to the transmission of the virus to the human population. The third theory suggested by researchers relates to a non-pathogenic covid-19 version originating from animals to human beings where it eventually underwent evolution to its present state.
Finally, the artificial engineering of the covid-19 virus possesses no valid evidence in its support. The inconsistencies in covid-19 patients’ death and recovery data from china authorities become the only potential but unproven argument which may persuade the artificial engineering argument of the virus. In conclusion, the covid-19 virus is a highly infectious virus which spreads faster mostly through contact with contaminated surfaces and respiratory droplets. This has prompted the need for constant research concerning both its origin and possible preventions.
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References
Chakraborty, M. K. (2020). Novel Corona Virus Disease 19 (N COVID-19) Epidemic Origin, Symptoms & Precaution Measure. Purakala with ISSN 0971-2143 is a UGC CARE Journal, 31(8), 1395-1409.
Møller, M., Andersen, G., & Gjedde, A. (2007). Serotonin 5HT1A receptor availability and pathological crying after stroke. Acta neurologica scandinavica, 116(2), 83-90.