In humans, Omicron appears to be highly contagious, but causes less symptoms than other variants. Why is it so?

How does it interact with host cells and the immune system?

Answering these questions could help lead to better drugs or vaccines, as well as provide clues about whether the new coronavirus will continue to change and new variants emerge.

In a recent report by the British "Nature" magazine, four mysteries about Omicron were solved.

  Why is the communication ability so strong?

  Omicron's rapid spread is due in large part to its possession of dozens of mutations that distinguish it from previous variants and allow it to evade the host's antibodies, especially those that interact with The spike protein on the periphery of the virus binds to neutralizing antibodies that prevent the virus from entering the cell.

This means that although many people already have broad immunity to early versions of the new coronavirus, Omicron has more hosts to choose from than the delta variant.

In addition, certain characteristics of Omicron itself may also make it highly contagious.

  In terms of viral transmission, one idea is that this variant produces higher concentrations of viral particles in the nasal cavity, so an infected person exhales more virus with each exhalation, but scientists do not agree on this.

  A study of human lung and bronchial tissue by virologist Michael Chang's team at the University of Hong Kong supports this speculation.

Their data suggest that Omicron is replicating faster in the upper respiratory system than all previous SARS-CoV-2 variants.

Research by the team of virologist Wendy Buckley at Imperial College London found that Omicron replicated faster than Delta in cultured nasal cells.

  But some studies reported that immune-compromised hamsters had fewer Omicron virus particles in their lungs than previous variants, and none of them were infectious.

Some studies in humans have shown that Omicron produces the same or lower concentrations of infectious virus particles in the upper respiratory tract than delta.

  Buckley thinks that the strength of Omicron's spread may be related to how it enters cells.

Early versions of the new coronavirus relied on the cellular receptor ACE2 to bind to cells and the TMPRSS2 cellular enzyme to break down its spike protein, allowing the virus to enter cells.

But Omicron has essentially given up on TMPRSS2, which cells swallow whole and burrows into small intracellular vesicles called endosomes.

  Many cells in the nose make ACE2, not TMPRSS2, which may help Omicron to kick in after being inhaled, before it reaches the lungs and other organs that commonly express TMPRSS2, Buckley said. This can partly explain why Omicron's ability to spread is so strong.

  Why are the symptoms not serious?

  Omicron appears to be weaker than previous variants in terms of hospitalization and mortality.

But given that many people have developed some level of immunity through vaccination or previous infection, scientists wanted to know to what extent it "weakened" because many people's immune systems were already able to deal with the virus; in How much is because of the virus itself.

  Scientists at Case Western Reserve University School of Medicine in Cleveland differentiated between the two factors by studying first-time infections in children younger than 5 years old (those who had not yet been vaccinated), from emergency room visits, admissions to the intensive care unit or intensive care unit and respiratory distress. Judging from the demand of the aircraft, the symptoms of infection with Omicron are milder than that of Delta.

In another study, South African scientists analyzed the risk of hospitalization and death among adults in the early stages of Omicron infection, and 25% of the factors that reduce the severity of symptoms of superficial infection were due to the nature of the virus itself.

  What made Omicron's "fangs" "blunt"?

Michael's team found that although the variant replicated faster in the upper respiratory system, it was less able to replicate in lung tissue.

Studies in rodents have found less inflammation and damage to the lungs from Omicron infection.

In humans, Omicron has less ability to multiply or cause damage in the lungs, leading to fewer cases of severe pneumonia and breathing difficulties, and a higher number of cases of nasal colds.

  Another reason for the reduced severity of symptoms of infection with Omicron may be its inability to fuse individual lung cells into larger syncytia, as was the case with previous SARS-CoV-2 variants, Buckley said.

Some scientists believe the aggregates can trigger symptoms or help the virus spread.

  How to deal with Omicron?

  One of the body's key "weapons" against pathogens is a molecule called interferon, which is produced by cells when they detect an invading virus.

Interferons tell infected cells to strengthen their defenses, and they send warning signals to uninfected neighboring cells to strengthen their defenses, too.

  Previous variants avoided or inhibited many of the effects of interferon.

Some studies suggest that while Omicron loses some of its advantages, it is better at resisting the effects of interferons.

  The researchers are also studying the part of the virus that draws the attention of T cells.

The viral proteins recognized by T cells appear to be unchanged in Omicron compared to previous variants—good news, because while T cells are slower to respond to recurring threats than antibodies, they once Get started and it can be very effective, helping to stop the symptoms of the infection from getting worse.

  Understanding which parts of the SARS-CoV-2 virus rarely mutate and activate T-cell responses could help scientists develop new vaccines that induce T cells to fight current and future virus variants.

  What will happen next?

  The data so far suggest that omicrons can be highly contagious early in infection, but when they try to spread beyond the upper respiratory tract, or are blocked by interferons, the number of viruses and their ability to infect other cells or people decreases. decline rapidly.

  While the severity of the symptoms of Omicron infection has been substantially reduced, most experts believe it will not be the final variant.

  Jesse Broom, an evolutionary virologist at the Hutchinson Cancer Research Center in the United States, said that there may be two scenarios in the future: One scenario is that Omicron continues to mutate, producing a worse Omicron+ mutation. The other is the emergence of a new, unrelated variant of Omicron.

  Scientists are concerned about the second scenario, which suggests the virus is so adaptable that "it had more than one evolutionary selection", said Lucy Thorne, a virologist at University College London.

With dozens of variants, Omicron has more room to evolve than the others, many of which are weaker but bloom everywhere.

In addition, scientists suspect that Omicron may infiltrate more species and then spread back to humans again, posing new dangers.