The Animal Origins of Coronavirus and Flu

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China is in the midst of an epidemic caused by an emerging strain of coronavirus. The World Health Organization formally named the disease. COVID-19, and the Coronavirus Study Group named the underlying virus severe acute coronavirus 2 respiratory syndromeor SARS-CoV-2. A group of patients with unusual pneumonia was first detected at the end of December, and the new coronavirus was officially identified as the reason on January 8. To date, it has caused more than 78,000 confirmed cases and 2,445 confirmed deaths, mainly in the Hubei province of China. It has been extended to 29 countries or territories so far, including the United States, which has 14 cases diagnosedand 21 additional cases in individuals who were transferred back to the US. UU. after infection. One US citizen has died from the virus in Wuhan, China. Naturally, the disease has left many questions in its wake.

Have we ever seen something like this before?

Yes. In fact, SARS-CoV-2 is the third novel pathogenic coronavirus to emerge in the last two decades. The first, discovered in 2003 and called SARS-CoV, caused SARS, a serious and atypical pneumonia. The second, MERS-CoV, emerged a decade later in the Middle East and caused a similar respiratory disease called the Middle East respiratory syndrome (MERS). Since its identification, 2,494 cases of MERS-CoV infection and almost 900 deaths have been documented. The SARS-CoV epidemic was larger but less deadly, with approximately 8,000 cases and almost 800 deaths.

Where do these viruses come from?

MERS-CoV and SARS-CoV seem to originate in animals, and the same is probably true for SARS-CoV-2. This makes them zoonosis, diseases that can jump between humans and other animals. MERS-CoV and SARS-CoV were originally bat viruses that spread to an intermediate animal (camel and civet cat, respectively), which then exposed humans to viruses. Genetic analysis of the SARS-CoV-2 sequences shows that their closest genetic relatives they appear to be bat coronaviruses, with the role of intermediate species possibly played by pangolin, an endangered species trafficked in China for its scales and meat. There are four coronaviruses that cause colds in humans, known as HCoV-229E, HCoV-NL63, HCoV-OC43 and HCoV-HKU1, and these also appear to have zoonotic origins.

How do these viruses achieve these jumps between species?

Although the details differ, the mechanism is based on the same fundamental premise: access and capacity. Can a virus reach the cells of its host? And can virus proteins recognize and bind structures, known as receptors, in those cells? If so, that is all that is needed: the virus can now enter the cell and begin to replicate, infecting the host.

Coronaviruses have become very expert in discovering how to use these receptors to enter their host cells. Viruses use a surface glycoprotein, a protein with attached sugars, called spike protein (S) to bind to host cells. (This protein gives the virus a crown appearance, which is where the "crown" in its name comes from). The part of the protein that makes the real junction, called the S1 subunit, can vary considerably, allowing the virus to bind to many different species of host mammals.

Most coronaviruses that infect humans appear to adhere to one of three host-specific receptors in mammalian cells. SARS-CoV and NL63 use a human receptor called angiotensin 2 converting enzyme (ACE2), MERS uses dipeptidyl peptidase 4 (DDP-4) and 229E uses aminopeptidase N (APN). All these proteins are present in the epithelial or superficial cells of the human airways, presenting easy targets for any virus in the air. Two recent studies from SARS-CoV-2 suggest that, as SARS-CoV, use ACE2 as a receiver.

Any other zoonoses that we should worry about?

While it is not necessarily a cause for concern, there is another virus that commonly emerges from animal reservoirs: influenza. Almost all known influenza viruses originate in water birds such as ducks, geese, terns, seagulls and related species. Many viruses pass from birds to other species (including humans). Often, the new species is a dead end; The bird flu virus can jump from birds to humans, for example, but not among humans. But occasionally, a new virus can also spread efficiently among people. We saw this more recently in 2009 with H1N1, a swine virus that has spread among humans and eventually caused a pandemic. And an H1N1 avian virus was responsible for the 1918 global pandemic.

To gain access to a host's cells, influenza uses its own viral glycoprotein, hemagglutinin (H). Like the coronavirus peak protein, H is a pointed-looking surface protein that stands out from the virus. It binds to the cells of the upper respiratory tract that have sialic acid residues: sugar chains attached to the ends of proteins and lipids. These sialic acids can occur in different forms, with different types of bonds (ways in which sialic acid atoms bind to sugar). Avian influences prefer a bond known as the α2,3 bond, in which sialic acid binds to galactose sugar through a specific carbon atom. This type of bond causes sialic acid and galactose to adhere directly. Human-adapted influenza viruses seem to prefer an α2.6 bond, which uses a different carbon atom and has a more curved appearance. It is believed that this preference for sialic acid is the main factor in determining which species a virus can infect, and limits the ability of purely avian influenza viruses to infect and spread in human populations.

What other factors influence which animal diseases can jump to humans?

Recent work has shown that the virus-host interaction can also be modified by host proteases, enzymes that break down proteins, so it is not just the spike protein composition that determines which hosts are vulnerable to which virus. These proteases can cut parts of the spike protein and alter the way it binds to host cells, so viruses that normally cannot infect human cells can do so after a protease treatment.

The role of intermediate species may also be more complex than scientists initially thought. The researchers initially suspected that such species were necessary for coronaviruses to move from primary reservoir species to humans. Perhaps the virus evolved and adapted to intermediate species, making it more efficient in binding to human cells. However, recent studies have shown that some bat coronaviruses can infect human cells without passing through an intermediate host, which means that a significant deposit of undiscovered coronaviruses may be lurking. Similarly, once we believed that pigs could serve as a "mixing vessel" where strains of avian influenza would be better adapted to mammals, since pigs appear to have sialic acids bound to α2.3 and α2.6 in the cells of your trachea, allowing human and bird strains to mix and produce new viruses adapted for humans. But while pigs can fulfill this function, we now know that such a mixture is not necessary and that avian viruses can infect humans without a pig intermediary.

Therefore, both virus species present a continuous challenge due to their diversity and their propensity to jumping hosts. In fact, that diversity probably allows these jumps in the first place, since a large and diverse population may be more likely to contain viruses that can bind to a variety of host receptors than a more homogeneous population. Because of this, coronaviruses and influenza have pandemic potential.

What can we do to protect ourselves?

First, stay safe by washing your hands and avoid touching your face and eyes, practices that help prevent infection with any of the viruses. You can get a virus by directly inhaling droplets loaded with viruses in the air or touching contaminated surfaces and infecting your nose and eyes, whose mucous membranes serve as entry sites.

Researchers develop flu vaccines every year, and scientists are working to achieve that holy grail of flu research, a universal vaccine that protects against all strains of the virus. With the coronavirus, we are not so far away. The sporadic nature of serious outbreaks means that funding and experience are minimal. Several laboratories are currently designing a vaccine against SARS-CoV-2, but it takes time to carry out clinical tests on animals and humans.

Researchers will also continue their surveillance of emerging influenza and coronaviruses, examining their genomes for signs of adaptation to humans. We may have arrived too late to catch the SARS-CoV-2, but we can still prepare for the next one.

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