In this week's roundup, the latest scientific research on the coronavirus and efforts to find treatments and vaccines suggest that antibodies from vaccines, antibody drugs and those produced from past COVID-19 infections appear to be weaker against the omicron variant, that more frequent treatment may help patients on ventilators and that the omicron variant multiplies much faster in airway passages but much slower in lungs than delta, which may explain the new variant's faster spread but milder symptoms.
Evidence emerging from lab experiments reveals weaknesses of vaccines and antibody drugs against the omicron variant of the coronavirus.
In a study reported Wednesday on bioRxiv ahead of peer review, researchers at Columbia University found omicron “to be markedly resistant to neutralization” by antibodies in blood from recipients of vaccines from Pfizer/BioNTech, Moderna, Johnson & Johnson or Oxford/AstraZeneca or from survivors of COVID-19.
Next, they tested nine monoclonal antibodies that have been authorized for use and 10 that are still experimental. Neutralizing abilities of 18 of the 19 antibodies “were either abolished or impaired,” including ones already authorized for use, they said.
European researchers reported similar results in a separate paper, also posted on Wednesday on bioRxiv. “Omicron was totally or partially resistant to neutralization” by the nine monoclonal antibodies they tested and by antibodies in blood samples from 90 vaccine recipients and COVID-19 survivors.
Both teams also found that even in vaccine recipients who received a booster dose, and in survivors who received vaccines, antibodies had substantially diminished neutralizing power. In these individuals, the European group said, neutralizing antibody levels were 5 to 31 times lower against omicron than against delta.
Major differences in how efficiently omicron and other variants of the coronavirus multiply may help predict omicron's effects, researchers said on Wednesday.
Compared to the earlier delta variant, omicron multiplies itself 70 times more quickly in tissues that line airway passages, which may facilitate person-to-person spread, they said. But in lung tissues, omicron replicates 10 times more slowly than the original version of the coronavirus, which might contribute to less-severe illness.
A formal report of the findings is under peer review for publication and has not been released by the research team.
In a news release issued by Hong Kong University, study leader Dr. Michael Chan Chi-wai said, “It is important to note that the severity of disease in humans is not determined only by virus replication” but also by each person's immune response to the infection, which sometimes evolves into life-threatening inflammation.
Chan added, “By infecting many more people, a very infectious virus may cause more severe disease and death even though the virus itself may be less pathogenic. Therefore, taken together with our recent studies showing that the omicron variant can partially escape immunity from vaccines and past infection, the overall threat from the omicron variant is likely to be very significant.”
A new study considers why COVID-19 patients on mechanical ventilators have trouble breathing and how refining a common treatment could help save lives.
A thin layer of fluid called pulmonary surfactant lines the air sacs in the lungs, helping to keep the sacs from collapsing at the end of each exhalation. Surfactant was first found to be important in premature babies, who are born without enough surfactant.
The study, published this month in the American Journal of Respiratory and Critical Care Medicine, shows for the first time that COVID-19 patients on ventilators have less surfactant in their lungs than healthy people.
When researchers treated 10 adult patients with the same artificial surfactant used in preterm babies, the benefit of treatment wore off very quickly and patients needed repeat doses far more often than expected.
The virus that causes COVID-19 infects and kills the lung cells that produce surfactant, but these cells will recover in time once the infection is over, the researchers said. The new findings suggest that in the meantime, “multiple surfactant doses over a number of days will be required ... until the lungs start to make their own surfactant.”