The SARS-CoV-2 Genome
Coronaviruses have the largest genomes of animal RNA viruses, ranging from 26 - 32 kilobases (kb). This size may be attributable to these viruses' ability to correct errors that are common in genomic replication. This proof-reading ability is not common amongst viruses and helps prevent rapid accumulation of deleterious mutations. Despite this feature, mutations do still arise and can be used to track virus spread and evolution.
SARS-CoV-2 is an enveloped, positive-sense, single-stranded ribonucleic acid virus (ssRNA+) with a genome encoding for about ten genes. Some of these genes encode for polyproteins. Polyproteins are large proteins, that once translated, are divided into multiple smaller proteins. The result is a genome which encodes for an estimated 25-29 different viral proteins in all. Four structural proteins, between five and nine accessory proteins, and sixteen non-structural proteins formed from two polyproteins in the ORF1ab gene.
SARS-CoV-2 Origins & Nucleotide Identity to Other Coronaviruses
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"SARS-CoV-2 is a member of the genus Betacoronavirus, subgenus Sarbecovirus of the family Coronaviridae. The genomes of multiple SARS-CoV-2 isolates derived from the first COVID-19 patients in Wuhan, China shared 99.98- 99.99% nucleotide identity, suggesting that the virus had only emerged recently in humans. SARS-CoV-2 is most closely related to coronaviruses isolated from bats within China called SARS-related coronaviruses (SARSr-CoVs)" (1). The most similar SARSr-CoVs to SARS-CoV-2 are Bat RaTG13-CoV and Bat RmYN02-CoV, both of which come from horseshoe bats in the Yunnan province of China. In comparison SARS-CoV-2 shares only 80% nucleotide identity with SARS-CoV which is responsible for the 2003 pandemic, and roughly 50% nucleotide sequence identity with other currently circulating coronaviruses such as MERS-CoV and common cold causing coronaviruses.
The degree of divergence between SARS-CoV-2 and other known coronaviruses is sufficient evidence to refute any claim of release (deliberate or accidental) from a lab space. Coupled with the genetic makeup of the virus, this degree of divergence also lends itself to the improbability of the already entirely unsupported claim that SARS-CoV-2 is an artificially constructed pathogen.
How Does SARS-CoV-2 Compare to Influenza Genetically?
Influenza viruses are an entirely different family of RNA viruses. They tend to have much smaller genomes (~14kb) with several strands of RNA rather than a single strand. Additionally, flu viruses lack any form of proof-reading ability. This causes influenza mutation rates (~3e-5) to be much higher on a site per cycle basis than most coronaviruses (~1e-6) (2). Flu viruses also generate different entry proteins. This results in varied manners of infecting human cells (3). Influenza viruses have Hemaglutinin epitopes rather than Spike protein epitopes which help them to latch onto and enter host cells.
Influenza viruses are an entirely different family of RNA viruses. They tend to have much smaller genomes (~14kb) with several strands of RNA rather than a single strand. Additionally, flu viruses lack any form of proof-reading ability. This causes influenza mutation rates (~3e-5) to be much higher on a site per cycle basis than most coronaviruses (~1e-6) (2). Flu viruses also generate different entry proteins. This results in varied manners of infecting human cells (3). Influenza viruses have Hemaglutinin epitopes rather than Spike protein epitopes which help them to latch onto and enter host cells.
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