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Does Omicron Cause Less Lung Damage?

Does Omicron Cause Less Lung Damage?

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Does Omicron cause less damage to the lungs than Delta? David Paul Morris/Bloomberg via Getty Images
  • Animal studies and experiments with lab-grown cells suggest that the Omicron variant may have a reduced ability to infect the lungs compared to the Delta variant.
  • This could explain why the Omicron variant appears to cause less severe disease than the Delta variant.
  • These studies indicate that the Omicron variant could be more efficient at infecting the upper respiratory tract than the Delta variant, possibly explaining its increased infectivity.
  • The ability of the Omicron variant to escape neutralizing antibodies may also be responsible for its increased transmissibility.

Early posts after the rise of the Omicron variant suggest that the variant is more likely to cause less severe disease than earlier variants of SARS-CoV-2.

Sequencing of the Omicron genome suggested that this variant carries a large number of mutations, including on the spike protein. The large number of mutations carried by Omicron could be a possible reason for this reduction in disease severity.

However, the milder illness resulting from an Omicron infection can also be the result of a person’s increased immunity gained from vaccination or previous SARS-CoV-2 infections.

While an increase in immunity can influence the severity of the disease, studies in animals and cells grown in the lab suggest that the mutations carried by the Omicron variant have made it less efficient at infecting the disease. lungs than the Delta variant. This could explain the less severe disease caused by the Omicron variant.

The SARS-CoV-2 virus can affect both the upper and lower airways. The upper respiratory tract consists of the nose, sinuses, and throat, while the lower respiratory tract includes the trachea and lungs.

Mild illness or early SARS-CoV-2 infections are likely to be associated with upper respiratory tract symptoms, such as a running nose and a sore throat.

Severe disease due to wild-type SARS-CoV-2 and its earlier variants often includes the infection and inflammation of the lungs.

Inflammation can cause fluid to build up in the air sacs, or alveoli, in the lungs, reducing the lungs’ ability to carry oxygen to the blood.

Scientists have conducted experiments with animal models and laboratory cultures of lung cells to characterize Omicron’s ability to infect the respiratory tract and cause serious illness.

This includes a study conducted at the University of Hong Kong, using lab-grown human lung cells to analyze the ability of the Omicron variant to infect the lungs. These cells were cultured from lung tissue that had been removed from the lung during the treatment. Usually this tissue is thrown away.

In the study, Omicron replicated 70 times faster than Delta in the human bronchi, the tubes that connect the trachea to the lungs. However, it was less efficient at replicating in the lung tissue than Delta and the wild-type SARS-CoV-2.

Other research groups have compared the ability of the Omicron, Delta and other SARS-CoV-2 variants to cause disease in animal models, such as hamsters and mice.

There is an association between infection with the Delta and other variants and weight loss in hamsters and mice after 1 week, with some data suggests a link between elevated virus levels in the respiratory tract and weight loss.

However, several research groups have independently shown that absence of such weight loss in hamsters and mice after Omicron infection.

In addition, these studies found that the hamsters with Omicron infection showed higher or comparable levels of virus, compared to the wild-type SARS-CoV-2 and the Delta variant in the upper respiratory tract. In contrast, after infection with the Omicron variant, the researchers saw lower levels of the virus in the lower respiratory tract than with the Delta variant.

In summary, these studies show that Omicron may be less efficient at infecting the lungs. Significantly, these animal studies show that an Omicron infection results in lower levels of inflammation and injury to the lungs.

In accordance with this, there is growing evidence suggesting that people with Omicron infection are less likely require hospitalization or admission to the intensive care unit or mechanical ventilation than persons with the Delta variant.

Medical news today talked to dr. Scott Roberts, a professor of infectious diseases at the Yale School of Medicine in New Haven, CT. He said,

“A number of laboratory studies have now shown that the Omicron variant is less able to infect the lungs and other variants, resulting in fewer patients with pneumonia who need oxygen and ventilators.”

“We see [that] the majority of Omicron-infected patients have mild disease that is more localized in the upper respiratory tract and hospitalizations do not increase as rapidly as with previous variants,” Dr. Roberts added.

“However, the number of hospitalizations and deaths is lagging behind the total number of cases, and as our cases continue to rise and set daily records, we will ultimately have to wait several more weeks to get a full picture of the severity of the disease here, in the United States.”

One possible reason for Omicron’s less severe lower respiratory tract infection in the current studies could be changes in the ability of this variant to enter cells in the lower respiratory tract.

The Omicron variant carries a large number of mutations in the gene encoding the spike protein, which is expressed on the surface of the SARS-CoV-2 virus.

The SARS-CoV-2 spike protein binds to the ACE2 receptor expressed on lung cells and helps the virus enter the cell. The cleavage of the spike protein by an enzyme called TMPRSS2 present on the surface of human cells is necessary for the fusion of the virus membrane to the human cell membrane to occur.

The SARS-CoV-2 virus can also enter human cells via an alternative route. This pathway involves the engulfment of the virus by endosomes, which are membrane-bound sacs present in the cell.

studies using lab-grown cells suggest That mutations in the spike protein of Omicron have altered the ability to invade human cells using TMPRSS2.

These studies have shown that the Omicron variant is less effective at infecting lab-grown lung cells expressing TMPRSS2 than the Delta variant.

In contrast, Omicron is more effective than Delta at infecting cells that allow cell entry through the endosome pathway.

The ACE2 receptor and TMPRSS2 are expressed at higher levels in cells obtained from the lower respiratory tract of humans than in cells from the upper respiratory tract. This could possibly explain why the Omicron variant may be less effective at infecting the lower respiratory tract and causing serious illness.

The interaction of the SARS-CoV-2 spike protein and TMPRSS2 is also involved in mediating the fusion of infected human cells with adjacent uninfected cells.

The reduced ability of the Omicron spike protein to utilize the TMPRSS2 enzyme also limits its ability to infect adjacent cells. This could further contribute to the lower severity of lower respiratory tract infection due to COVID-19.

These results are from cell culture and animal studies. Therefore, studies in humans are needed to establish that such a change in Omicron is responsible for the decreased ability to infect lung cells.

MNT talked to dr. Peter Kasson, a professor at the University of Virginia at Charlottesville. He said:

“The Omicron variant is interesting because it appears to switch pathway preferences compared to Delta and earlier variants. As a result, it is less efficient at infecting lung cells, but more efficient at infecting many upper respiratory tract cells.” .”

“This correlates with the disease pattern seen in Omicron – while lower lung pathology is seen, upper respiratory tract disease is often more common,” he concluded.

In addition to causing less severe disease, the Omicron variety is also more transmissible. The animal and cell culture studies also suggest that Omicron may be more efficient at infecting the upper respiratory tract.

Studies conducted during the early phase of the pandemic show that Association between levels of SARS-CoV-2 in the upper respiratory tract and increased transmission.

Thus, the faster replication of Omicron in the upper respiratory tract may explain its increased infectivity.

“[These studies] give rise to attractive speculation that the increased replication in upper airway tissues may contribute to increased transmissivity, possibly both by increasing the exhaled viral load and the number of viral particles needed to infect, although this, to my knowledge, has not been definitively demonstrated,” explains Dr. Cash out.

The increased infectivity of the Omicron variant may also be due to its ability to evade detection by antibodies.

Previous SARS-CoV-2 infections and immunization with COVID-19 vaccines lead to the production of antibodies that neutralize the virus. These neutralizing antibodies tendency to predict the level of protection against SARS-CoV-2 infection.

The vaccines against COVID-19 are designed to elicit an immune response against the spike protein of the wild-type SARS-CoV-2 strain.

The presence of the mutations in the spike protein of the Omicron variant suggests that this variant can escape neutralization by antibodies.

A study led by researchers from the MRC-University of Glasgow Center for Virus Research in the United Kingdom has shown that the Omicron variant can escape neutralization by antibodies in individuals immunized with the AstraZeneca COVID-19 Vaccine. This could be another reason for the high portability of the Omicron variant.

Although scientists need to do more research before we can draw firm conclusions, the characteristics of this new variant are slowly becoming apparent.

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Anna Wintour

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