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The coronavirus family are a diverse group of viruses that infect various animals and are typically known to cause respiratory infections of varying severity in humans.
Among all pathogenic viruses, as well as all RNA-duplicating viruses, the coronavirus family are large. Many are 125 nm in diameter, but more important are their genomes, which house nearly 30,000 genetic bases. Each virus also has a genomic proofreading mechanism, which renders many kinds of drugs like ribavirin ineffective. Ribavirin aims at weakening viruses like hepatitis C by inducing mutations, but these changes will be detected by the proofreading mechanism of coronaviruses. Coronaviruses have another ability that gives them a deadly advantage: they often undergo recombination, criss-crossing chunks of RNA with other coronaviruses—and if these two coronaviruses are distant-enough relatives of each other, this could mean the formation of novel and deadly viruses that could infect new cell types or even other species.
First in 2002 and 2012, respectively, two zoonotic coronaviruses had made their names infamous by causing fatal respiratory illnesses: severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). In 2019, the current pandemic has been caused by a different, novel strain originating in in the city of Wuhan, China, known as SARS-CoV-2, the “2” designating the second, evolved appearance of SARS-CoV. This coronavirus disease 2019 (COVID-19) caused by this novel strain has proven itself to be highly transmissible, beating its older relatives in both the number of infections and the distance covered. Unlike MERS-CoV or SARS-CoV, the novel coronavirus is able to easily reach the lungs, as well as efficiently infect cells in the lungs. Whether it starts in the throat or the nose, SARS-CoV-2 is capable of swiftly infecting important lung cells, making the disease it causes highly transmissible. SARS-CoV-2 has one other ability that sets it apart from its genetic relative, SARS-CoV: it can infect and actively reproduce in the upper respiratory tract—this, its relative could not do, proving why COVID-19 has been as dangerous as it has shown itself to be.
Once SARS-CoV-2 enters the lungs, it acts in a similar way to other respiratory viruses. Much like SARS-CoV, as well as influenza, it infects and destroys the alveoli, tiny sacs that help transport oxygen into the bloodstream. As the cellular barrier in between the alveoli and the blood vessels break down, fluids from the vessels can leak and block oxygen from getting into the blood stream. Immune aid that come to the scene often make matters worse by over-reacting—this can then cause excessive inflammation and tissue damage that may be fatal.
Tthe over-action of the immune system in response to SARS-CoV-2, like the “cytokine storm,” is one predominant way that COVID-19 has often led to organ failure and death. Damage to regions other than the lungs, like the kidney, liver, and spleen, have also been reported—indicating that SARS-CoV-2 is well-capable of traveling through the blood and causing havoc throughout the body.
Undeniably, these are genuinely concerning features about the virus and the disease responsible for the current pandemic, but learning about them, recording them, and adapting to them, are even more important, now more than ever.
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