COVID-19 summary: Cold antibodies do not protect, increased risk for cancer patients


This week’s round-up of some of the latest scientific studies on the coronavirus and efforts to find treatments and vaccines for COVID-19 looks at the increased risk for certain groups of people, misunderstandings about cold antibodies, and how neurological symptoms may not be direct that are causing virus.

COVID-19 increases the risk for cancer patients

Cancer patients have worse outcomes when they contract the coronavirus, a new study shows. However, recent cancer treatments have not worsened COVID-19 results, 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 included nearly 23,000 cancer patients tested for COVID-19 in U.S. Veterans Affairs health facilities nationwide. Approximately 1,800 (7.8%) had tested positive with no age affecting the likelihood of infection. COVID-19 rates were higher in patients with blood cancer (11%) than in patients with solid tumors (8%).

Compared to patients who tested negative for the virus, COVID-19 patients had more hospitalizations, needed more intensive care and more help with breathing. The death rate was 14% in cancer patients with COVID-19 and 3% in patients 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 actual prevalence of COVID-19 in cancer patients remains uncertain, the researchers say, as many have not been tested for the virus.

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 colds. However, these antibodies are unlikely to protect against the coronavirus that causes COVID-19, new research shows.

At Rockefeller University in New York, scientists looked at blood samples collected and stored prior to the pandemic from people known to have had colds in recent months. In test tube experiments, they found that each sample contained antibodies that could recognize and neutralize or deactivate at least one cold coronavirus – and most were able to detect several such viruses. But none of the samples had antibodies that could recognize and deactivate a virus that had been modified to look like the new coronavirus and contained the spike protein that helps infect healthy cells.

In a report released prior to the peer review on medRxiv, the researchers say that while there are rare people with cold antibodies who can also target the COVID-19 virus, their new data suggests these antibodies are not will have a great effect on the population as a whole.

The neurological effects of COVID-19 can mirror the immune response

The new coronavirus may not have a significant direct impact on the brain, despite major neurological problems that have been widely reported.

The 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” in the frontal lobe – the part of the brain that is important for movement, language and higher-level functions. They also saw an increase in brain cells called astrocytes, which signals the destruction of other nearby cells. Since critical illness itself can contribute to this finding, it is not clear that COVID-19 is the direct cause.

The presence of the virus wasn’t linked to the severity of the changes in the brain tissue, the researchers said. All of the brains showed signs of “neuroimmune activation,” which means that the immune system was activated to respond to the infection in the brain.

The patients’ neurological symptoms may be due to the body’s immune response rather than direct damage to the central nervous system by the virus, the authors reported in The Lancet Neurology.

“We have started to define the immune response to the SARS-CoV-2 virus in the brain,” said co-author Markus Glatzel from the University Medical Center Hamburg-Eppendorf to Reuters. “We believe the neuroimmune response may be a factor explaining some of the neurological symptoms seen in COVID-19 patients.”


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