Does Omicron cause less lung damage?

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Does Omicron cause less lung damage than Delta? David Paul Morris/Bloomberg via Getty Images
  • Animal studies and experiments involving 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 may be more effective at infecting the upper respiratory tract than the Delta variant, potentially explaining its increased contagiousness.
  • The ability of the Omicron variant to evade neutralizing antibodies may also be responsible for its increased transmissibility.

Early reports following the emergence of the Omicron variant suggest that the variant is more likely to cause less severe disease than previous SARS-CoV-2 variants.

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 potential reason for this reduction in disease severity.

However, the milder illness due to Omicron infection could also be the result of a person’s enhanced immunity, acquired due to vaccination or previous SARS-CoV-2 infections.

Although increased immunity may influence disease severity, studies in animals and lab-grown cells suggest that mutations carried by the Omicron variant made it less effective at infecting the lungs than the variant. Delta. This could explain the less severe disease caused by the Omicron variant.

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

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

Severe illness due to wild-type SARS-CoV-2 and previous variants often involves infection and inflammation of the lungs.

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

Scientists conducted experiments using animal models and laboratory lung cell cultures to characterize Omicron’s ability to infect the airways and cause serious illness.

This includes a to study carried out at the University of Hong Kong which used human lung cells cultured in the laboratory, to analyze the ability of the Omicron variant to infect the lungs. These cells were cultured from lung tissue removed during lung processing. As a rule, this fabric is discarded.

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

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

There is a link between infection with Delta and other variants and weight loss in hamsters and mouse after 1 week, with some data suggesting a correlation between increased virus levels in the respiratory tract and weight loss.

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

Additionally, these studies found that hamsters infected with Omicron had higher or similar virus levels, compared to wild-type SARS-CoV-2 and the Delta variant in the upper respiratory tract. In contrast, the researchers observed lower levels of virus in the lower respiratory tract after infection with the Omicron variant, compared to the Delta variant.

In sum, these studies show that Omicron may be less effective at infecting the lungs. Significantly, these animal studies show that infection with Omicron results in lower levels of inflammation and damage to the lungs.

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

Medical News Today speak with Dr. Scott Roberts, 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 as well as other variants and therefore leads to fewer patients admitted with pneumonia who require oxygen. and fans.”

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

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

A potential reason for the less severe lower respiratory tract infection by Omicron in the present studies could be changes in the ability of this variant to enter lower respiratory tract cells.

The Omicron variant features 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 required before fusion of the viral membrane with the human cell membrane can occur.

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

Studies using cells grown in the laboratory to suggest this mutations in Omicron’s spike protein have impaired its ability to enter human cells using TMPRSS2.

These studies showed that the Omicron variant is less efficient at infecting lab-cultured lung cells expressing TMPRSS2 than the Delta variant.

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

The ACE2 receptor and TMPRSS2 are expressed at higher levels in cells from the human lower respiratory tract than in cells from the upper respiratory tract. This could potentially explain why the Omicron variant may be less effective at infecting the lower respiratory tract and causing severe disease.

The interaction of the SARS-CoV-2 spike protein and TMPRSS2 is also implicated 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 help reduce the severity of lower respiratory tract infections due to COVID-19.

These results come from cell cultures and animal studies. Therefore, human studies are needed to establish that such a change in Omicron is responsible for its reduced ability to infect lung cells.

DTM speak with Dr. Peter Kasson, a professor at the University of Virginia at Charlottesville. He said:

“The Omicron variant is interesting in that it appears to swap preferences for the entry route with Delta and previous variants. As a result, it is less efficient at infecting lung cells but more efficient at infecting many cells. upper respiratory tract.

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

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

Studies conducted at the start of the pandemic show a association between SARS-CoV-2 levels in the upper respiratory tract and increased transmission.

The faster replication of Omicron in the upper respiratory tract may therefore explain its increased contagiousness.

“[These studies] give rise to appealing speculation that increased replication in upper respiratory tract tissues may contribute to increased transmissibility, potentially both by increasing exhaled viral load and decreasing the number of viral particles needed to infect, although, to my knowledge, this has not been definitively demonstrated,” explained Dr Kasson.

The increased contagiousness 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 COVID-19 vaccines were designed to induce an immune response against the spike protein of the wild-type SARS-CoV-2 strain.

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

A to study conducted by researchers at the MRC-University of Glasgow Center for Virus Research in the UK showed that the Omicron variant can evade neutralization by antibodies in individuals immunized with the AstraZeneca COVID-19 vaccine. This could be another reason for the high transmissibility of the Omicron variant.

Although scientists need to do more research before they can draw any solid conclusions, the characteristics of this new variant are slowly being revealed.

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.

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