Will We Need COVID-19 Vaccines Every Year? Although the jury is still out, a study out of Charité – Universitätsmedizin Berlin suggests that the answer is yes for a few years, but may be unnecessary after a few years post-pandemic.
Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.
Will We Need COVID-19 Vaccines Every Year?
Although the jury is still out, a study out of Charité – Universitätsmedizin Berlin suggests that the answer is yes for a few years, but may be unnecessary after a few years post-pandemic. The researchers compared the evolution of endemic common cold coronaviruses with influenza viruses. Influenza viruses make such rapid mutations that flu shots need to be updated every year. SARS-CoV-2 is not an influenza virus, but a coronavirus. The rise of more infectious SARS-CoV-2 variants has made it likely that at least for a few years, updates will be required. The investigators focused on the two longest-known coronaviruses, 229E and OC43, evaluating changes in the spike gene in samples collected over about 40 years. They published their research in the journal Virus Evolution.
Based on the mutations they observed and mapped and then compared these phylogenetic trees to that of H3N2, a well-known influenza subtype that is particularly good at evading the human immune response, they were able to calculate the likelihood of the SARS-CoV-2 mutating so fast and thoroughly that yearly shots would be required. They found that all three they compared had a pronounced ladder-like shape.
“An asymmetrical tree of this kind likely results from the repeated replacement of one circulating virus variant by another which carried a fitness advantage,” said Wendy K. Jo, first author of the study. “This is evidence of ‘antigenic drift,’ a continuous process involving changes to surface structures which enable viruses to evade the human immune response. It means that these endemic coronaviruses also evade the immune system, just like the influenza virus. However, one also has to look at the speed with which this evolutionary adaptation happens.”
Which they did, and found that the influenza virus gathered 25 mutations per 10,000 nucleotides per year, while the coronaviruses had about six in the same timeframe—or about four times slower than the influenza virus. SARS-CoV-2 appears to change at a rate of about 10 mutations per 10,000 nucleotides per year.
“As far as SARS-CoV-2 is concerned, this is good news,” said Christian Drosten, director of the Institute of Virology and a researcher at the German Center for Infection Research (DZIF).
The Link Between Obesity and Depression
Although there is an association between obesity and depression and anxiety, the link wasn’t well understood. Researchers at Baylor College of Medicine recently identified and characterized a novel neural circuit that appears to explain the link. The neural circuit mediates the reciprocal control of obesity and depression, at least in mice. The mice that consumed a high-fat diet became obese, but also became anxious and depressed. When the research team genetically or pharmacologically corrected the defective brain circuit, the mice became less anxious and depressed and later lost excess body weight. One unexpected result was that the weight loss was not the result of a lack of appetite, but a change in the mice’s food preference.
How Astrocytes Fix Damage in the Brain
Investigators with Charité – Universitätsmedizin Berlin described how a type of glial cell, called astrocytes, plays a role in protecting surrounding brain tissue after damage. They become part of a defense mechanism called reactive astrogliosis, which helps form scars, and contains inflammation and controls tissue damage. Astrocytes are also able to ensure the nerve cells survive that are located immediately next to the tissue injury, which preserves the function of neuronal networks. The mechanism was the protein drebrin, which controls astrogliosis. Astrocytes require drebrin to form scars and protect the surrounding tissue. Drebrin controls the reorganization of the actin cytoskeleton, an internal scaffold that maintains astrocyte mechanical stability.
Specific Brain Signature Tied to Vulnerability to Addiction
Researchers at the Institut de Neurosciences de la Timone (CNRS/Aix-Marseille Universite), working in rats, found they could predict which rats would become cocaine addicts based on a brain signature. They observed abnormal activity in a specific part of the brain called the subthalamic nucleus, only in the rats that went on to become addicted. They also believe that it is possible to decrease the compulsive cocaine-addictive behavior, in rats, at least, by stimulating the subthalamic nucleus.
Repurposed Arthritis Drug Appears to Prevent Scleroderma Lung Infection
Investigators at Michigan Medicine’s Scleroderma Program found that by repurposing tocilizumab (Genentech’s Actemra), an FDA-approved anti-inflammatory medication used to treat rheumatoid arthritis, they could prevent lung disease in patients with systemic sclerosis, if it was detected early enough. Systemic sclerosis is an autoimmune disease that causes tightening and thickening of the skin and can affect internal organs and the lung—lung disease is the leading cause of death in scleroderma patients. They did, however, find there was a window of opportunity for specific patients where the drug can halt or prevent irreversible lung damage, but it does require early diagnosis.
Why COVID-19 Infection Rate is So High
Scientists out of Lehigh University quantified the interaction between the SARS-CoV-2 virus’s spike protein and the ACE2 receptors in human cells that the spike protein uses to enter the cells. Other studies had indicated that the interaction between the virus’s spike protein and ACE2 receptors were stronger than the interaction between the structurally identical spike protein of SARS-CoV-1, the virus that causes SARS, and the same ACE2 receptors. So the question was, why is COVID-19 more infectious? They published their research in the Biophysical Journal.
What they found was a previously unknown interaction between ACE2 glycans, which are sugar groups attached to the surface of proteins, and the SARS-CoV-2 spike. This seems to be the cause of the stronger virus-cell interaction and may partially explain the higher infection rate compared to SARS-CoV-1.
“It is possible that this newly-discovered interaction with ACE2 glycans could be a contributing factor to the higher rates of COVID-19 than the structurally similar SARS-CoV-1, which has a weaker interaction,” said X. Frank Zhang, an associate professor in Bioengineering and Mechanical Engineering & Mechanics at Lehigh. “Our hope is that researchers may be able to use this information to develop new strategies to identify, prevent, treat and vaccinate against COVID-19.”
