Viral Feedback
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Viral Feedback

What do we know about SARS-CoV-2, the causative agent of COVID-19?

SARS-CoV-2 is a virus, a parasitic molecule which needs to infect a cell to reproduce (Figure 1 and 2).

Figure 1: The blue dots are SARS-CoV-2 virus which causes COVID-19 as visualized by transmission electron microscopy. The insert is a CDC computer generated image of the coronavirus structure.

Viruses are very small (20–1000 nm), and typically only visible by electron microscopy. Viruses are propagated in a lab by infecting cell culture. The virus is visualized in the lab as empty spots on a lawn of cells similar to seeing a disease ring in a lawn of grass. A virus is a blueprint of DNA or RNA with proteins for invasion of the host cell and possibly an outer boundary of fat and proteins. A virus cannot produce more virus particles without infecting a living cell. The virus injects its blueprint into the host cell. The virus blueprint uses the host cell resources to make many more virus particles. After many copies of the virus are produced, the virus destroys the host cell by popping it.

Figure 2: Cartoon depiction of SARS-CoV-2 infection of human lung cell.

How does the human immune system stop the virus cycle?

The human immune system has three ways to stop a virus invasion: kill infected cells, stop the virus from replicating, and neutralize the virus. Cytotoxic cells kill and remove cells infected with the virus before the virus makes many copies and kills the infected cell. The immune system fights the virus cycle by producing interferon which stops the virus from making more copies. The immune system also produces antibodies, proteins which neutralize the virus so that it cannot infect further cells. Antibodies also make the virus stick together so that it is easier for the immune system to destroy the virus.

Why is COVID-19 a bigger deal than other coronaviruses when the world barely notices the others?

Coronaviruses have been around for a long time. They cause diseases ranging from just another form of the common cold to the deadly SARS disease outbreak of 2002. So why is this coronavirus so different and why did it cause such a devastating, worldwide pandemic when its close relatives did not? The answer is simple — COVID-19 combines the nastiest characteristics of all its cousins.

Common cold viruses infect the nose and throat. That is why your common cold causes a sore throat and stuffed-up sinuses. The proximity of your throat and sinuses to your mouth allows the virus to mingle in your saliva, and when you breath or talk the evaporated saliva carries virus particles into the air around you. This makes it quite easy for the virus to enter someone else’s body. Also, the common cold just does not make people as sick, so people are more likely to be out and about while they are contagious. The result: the common cold’s greatest talent is its ability to spread unchecked in a population.

SARS was a unique and particularly deadly variation of the coronavirus. It primarily infected victims’ lungs. The result was severe pneumonia and often death. However, because it was a lung infection SARS lacked the common cold’s powerful ability to spread. Lung infections often make the victim much sicker so the victim will tend to be resting at home or in a hospital before they infect many other people. The result: although SARS killed ~15% of its victims which is much higher compared to a typical flu or cold, it only killed 774 people worldwide.

COVID-19 combines the strengths of both common colds and SARS. Covid can infect the nose, throat, and lungs with ease. Typically the sickness begins in a mild form in the nose and throat. During this early period, COVID viruses are mingling with saliva as the victim breathes. The virus hasn’t yet reached the lungs, however, so the victim probably feels fine and is out doing their daily business, interacting with others and spreading the virus. After a few days the infection establishes a foothold in the lungs and moves to its more dangerous phase. It is at this point that people most often become seriously ill and shortly thereafter that hospitalizations and deaths occur. The combined deadliness of the SARS virus and the ease of spread of the common cold makes COVID-19 a unique threat.

Do we know how SARS-CoV-2 enters lung cells? The molecular target of SARS-CoV-2

COVID-19 (SARS-CoV-2) has a surface spike protein which binds to the angiotensin converting enzyme 2 (ACE2). The spikes are seen in the insert in Figure 1. ACE2 is present on the surface of many cells in the body but is concentrated in the lungs which makes the lungs a specific target of SARS-CoV-2.

Has SARS-CoV-2 been visualized?

SARS-CoV-2 virus particles were observed in cultured laboratory vero cells and patient tissues using transmission electron microscopy. More detailed visualization of SARS-CoV-2 binding domain bound to the lung receptor ACE2 was determined using x-ray crystallography. Transmission Electron Microscopy and Scanning Electron Microscopy of COVID-19 patient tissue visualized SAR-CoV-2 in the lungs, heart, and kidney.

How does SARS-CoV-2 compare to other coronaviruses?

The disease COVID-19 results from infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 is a coronavirus. Coronaviruses are characterized as round with 125 nm diameter and a spike covered surface. Replication is encoded by RNA instead of DNA. Though the less stable RNA molecule is used for replication which typically results in a faster mutation rate, coronaviruses do not mutate as fast as other RNA viruses such as HIV because of a genome proofreading mechanism. Several coronaviruses cause the common cold (HCoV 229E, NL63, OC43, and HKU1) which is a nuisance but not considered deadly. Other coronaviruses (SARS-CoV and MERS-CoV) are deadly. SARS-CoV caused severe acute respiratory syndrome in 2002 with ~15% case-fatality rate. Middle East respiratory syndrome coronavirus (MERS-CoV) caused 34% case-fatality rate in 2012. The protein sequences encoded by the SARS-CoV-2 virus and SARS-CoV virus are 76.47% identical. Homology of spike protein amino acid sequence (how similar are spikes on virus) between SARS-CoV-2 and common cold viruses is ~30%. For comparison, a human and a worm are roughly 30% identical in terms of protein sequences.

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