In this week's roundup, the latest scientific research on the coronavirus and efforts to find treatments and vaccines suggest that lower COVID-19 risks are seen after weight-loss surgery and that coronavirus can trigger kidney scarring.
Coronavirus infection during pregnancy does not appear to affect infants' brain function, but the pandemic itself may be having an impact, a study published on Tuesday in JAMA Pediatrics suggests.
Researchers in New York City tracked 255 full-term infants born during the pandemic, including 114 whose mothers had COVID-19 during pregnancy. When the babies were six months old, the researchers saw "absolutely no effect of maternal infection with (COVID-19)" on neurodevelopment, said Dr. Dani Dumitriu of Columbia University and New York State Psychiatric Institute. But overall, compared with 62 infants born before the pandemic, the babies born during the health crisis had slightly lower scores on tasks involving large muscles, tasks requiring small muscle movements and personal interactions. The findings do not necessarily mean these infants will suffer long-term consequences, Dumitriu said. Assessments at six months are poor predictors of long-term outcomes, she added.
If additional research confirms that birth during the pandemic negatively impacts neurodevelopment, she said, "because this is such an early time point there are lots of opportunities to intervene and get these babies onto the right developmental trajectory."
The coronavirus can directly damage the kidneys by initiating a cascade of molecular events that leads to scarring, new laboratory research found. The resulting scar tissue could have long-term impacts on survivors' kidney function, according to a report published in Cell Stem Cell.
The researchers exposed tiny replicas of kidneys to the COVID-19 virus in test tubes. They found the virus could infect multiple types of kidney cells and trigger "a molecular switch" that starts the scarring process. The findings suggest that high rates of kidney function decline seen in a separate study of more than 90,000 COVID-19 survivors might be due to scarring of the kidney by the virus, the researchers said.
Jitske Jansen of Radboud University Medical Center in The Netherlands said in a statement that her team had found another "piece of the puzzle showing the deleterious effects the virus can have in the body."
Weight-loss surgery may reduce the risk of severe COVID-19 even if the infected person is still obese after losing weight, according to a report in JAMA Surgery.
Researchers studied 20,212 obese adults, including 5,053 who had undergone bariatric surgery before the pandemic and lost a substantial amount of weight. On average, the people in the surgery group, while still technically obese, weighed about 44 pounds (20 kg) less than study participants who had not undergone the surgery. Although the two groups had similar rates of COVID-19 infection at about 9%, infected patients with prior weight-loss surgery had a 49% lower risk of hospitalization, a 63% lower risk of need for supplemental oxygen, and a 60% lower risk of becoming critically ill or dying compared to the non-surgery group. Obesity is well known to be a risk factor for poor COVID-19 outcomes, but as the study was not a randomized trial it cannot prove weight-loss surgery caused the better outcomes. Still, the authors said, patients who underwent weight-loss surgery were likely healthier when they became infected.
The results "support the reversibility of the health consequences of obesity" for patients with COVID-19, coauthor Dr. Steven Nissen of the Cleveland Clinic said in a statement. "This study suggests that an emphasis on weight loss as a public health strategy can improve outcomes during the COVID-19 pandemic ... That is a very important finding considering that 40% of Americans have obesity. "
Months after recovering from COVID-19, survivors have elevated levels of antibodies that can mistakenly attack their own organs and tissues, even if they had not been severely ill, according to new findings.
Among 177 healthcare workers who had recovered from confirmed coronavirus infections contracted before the availability of vaccines, all had persistent autoantibodies, including ones that can cause chronic inflammation and injury of the joints, skin and nervous system. "We would not normally expect to see such a diverse array of autoantibodies elevated in these individuals or stay elevated for as long six months after full clinical recovery," said Susan Cheng of the Cedars-Sinai Smidt Heart Institute in Los Angeles. Patterns of elevated autoantibodies varied between men and women, the researchers reported on Thursday in the Journal of Translational Medicine.
"We don't yet know how much longer, beyond six months, the antibodies will stay elevated and/or lead to any important clinical symptoms," Cheng said. "It will be essential to monitor individuals moving forward." Her team is investigating whether autoantibody elevations are linked with persistent symptoms in people with long COVID and planning to study autoantibody levels after infections with newer variants of the virus.
The effects of antibodies produced by the immune system's "memory B cells" against the omicron variant of the coronavirus, while weakened, could still be significant, researchers believe.
Once the body learns to recognize COVID-19, either after infection or vaccination, B cells generate fresh antibodies against the virus if there are not already enough antibodies circulating in the blood that can neutralize it. In a study reported on bioRxiv ahead of peer review, researchers analyzed the strength of more than 300 antibodies produced by memory B cells obtained from vaccinated volunteers, including some who had a prior COVID-19 infection.
"Omicron seemed to evade a very large share of the memory B cells pool," researchers said, adding that it "seems to still be efficiently recognized by 30% of total antibodies and close to 10% of all potent neutralizing antibodies," said Matthieu Mahevas and Pascal Chappert of Universite de Paris in a joint email. Memory B cells' robust ability to proliferate and produce antibodies might compensate "in less than two days" for those antibodies' reduced effectiveness, they speculate.
In combination with other immune system components, particularly T cells, the effects of B cells likely help to explain why most vaccinated individuals who become infected do not become sick enough to require hospitalization, they said.
Along with spike mutations that help the coronavirus break into cells, mutations that change how the virus behaves inside the cells are a big factor in why some variants have been more transmissible, researchers have discovered.
The findings, published in Nature, show that scientists "have to start looking at mutations outside the spike," which has so far been the main focus of vaccines and antibody drugs, said Nevan Krogan of the University of California, San Francisco. Studying the alpha variant, his team found a mutation at a non-spike site that causes infected cells to ramp up their production of a protein called Orf9B. Orf9b in turn disables a protein called TOM70 that cells use to send signals to the immune system. With higher levels of Orf9B disabling TOM70, the immune system does not respond as well and the virus can better evade detection, the researchers said.
Referring to the increase in Orf9B, Krogan said, "It's rare that mutations 'turn up' a protein. It's a very sneaky thing for this virus to do." The same mutation was identified on delta, "and sure enough, almost the same mutation is on omicron," he said, which suggests they may have similar effects on the immune system. The new information could spur development of drugs that target the interaction of Orf9b and TOM70.
