COVID-19 roundup: Cold antibodies won't protect, heightened risk for cancer patients

This week's news roundup of some of the latest scientific studies on the coronavirus and efforts to find treatments and vaccines for COVID-19 addresses increased risk for certain groups of people, misconceptions about antibodies from colds and how neurological symptoms may not be caused directly by the virus.

COVID-19 increases risks for cancer patients

Cancer patients face poorer outcomes if they become infected with the coronavirus, a new study shows. However, undergoing recent cancer treatments did not make COVID-19 outcomes worse, so cancer therapies should not be delayed, the research team advises in a report published in the Journal of the National Cancer Institute.

The study involved nearly 23,000 patients with cancer who were tested for COVID-19 at U.S. Veterans Affairs health facilities nationwide. Roughly 1,800 (7.8%) had tested positive, with no effect of age on the likelihood of infection. COVID-19 rates were higher in patients with blood cancers (11%) than in those with solid tumors (8%).

Compared to patients who tested negative for the virus, COVID-19 patients had more hospitalizations, needed more intensive care, and needed more help with breathing. Death rates were 14% among cancer patients with COVID-19 and 3% in those without the virus.

Across the country, African American and Hispanic cancer patients had higher rates of COVID-19 infection than white cancer patients – 15%, 11% and 6%, respectively. They also had higher rates of hospitalization.

The real prevalence of COVID-19 among cancer patients remains uncertain, the researchers point out, because many have not been tested for the virus.

Common cold antibodies do not protect against COVID-19

Your immune system may be able to produce antibodies that recognize and fight off the coronaviruses that cause common colds, but those antibodies are not likely to protect against the coronavirus that causes COVID-19, new research shows.

At Rockefeller University in New York City, scientists studied blood samples collected and stored before the pandemic from people known to have had common colds in the past few months. In test-tube experiments, they found that each sample contained antibodies that could recognize and neutralize, or disable, at least one common cold coronavirus – and most could recognize multiple such viruses. But none of the samples had antibodies that could recognize and disable a virus that had been modified to look like the new coronavirus, carrying the spike protein that helps it infect healthy cells.

In a report published ahead of peer review on medRxiv, the researchers say that while there may be rare individuals with common cold antibodies that can also target the COVID-19 virus, their new data suggest those antibodies are not going to have much of an effect on the population as a whole.

COVID-19 neurological effects may reflect immune response

The new coronavirus might not be having major direct effects on the brain despite neurological issues that have been widely reported.

Researchers examined the brains of 43 COVID-19 patients who died in intensive care units, nursing homes, regular hospital wards, or at home. They found coronavirus proteins in the brain stem, but "little involvement" of the frontal lobe – the part of the brain important for movement, language and higher-level functioning. They also saw increases in brain cells called astrocytes, signaling the destruction of other nearby cells. Because critical illness itself can contribute to this finding, it is not clear that COVID-19 is the direct cause.

The presence of the virus was not associated with the severity of brain tissue changes, researchers said. All of the brains showed signs of "neuroimmune activation," meaning the immune system had been activated to respond to the infection in the brain.

Patients' neurological symptoms might be due to the body's immune response, rather than to direct central nervous system damage from the virus, the authors reported in The Lancet Neurology.

"We have started to define the immune reaction to SARS-CoV-2 virus in the brain," co-author Markus Glatzel of University Medical Center Hamburg-Eppendorf in German told Reuters. "We think that the neuroimmune reaction may be a factor explaining some of the neurological symptoms seen in COVID-19 patients."