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This week’s summary of some of the most recent scientific studies on the coronavirus and efforts to find treatments and vaccines for COVID-19 explore how childhood vaccination could be essential to prevent serious diseases, how cigarette smoke makes cells are more vulnerable to the virus and how you could do it. be longer lasting immunity in COVID-19 patients than previously thought.
Childhood MMR Vaccine May Help Prevent Severe COVID-19
People whose immune systems responded strongly to a measles, mumps and rubella (MMR) vaccine may be less likely to become seriously ill if infected with the coronavirus, new data suggests. The MMR II vaccine, manufactured by Merck and licensed in 1979, works by activating the immune system to produce antibodies.
Researchers reported on Friday in mBio that among 50 COVID-19 patients under the age of 42 who had received MMR II as children, the higher their titers, or levels, of the so-called IgG antibodies produced by the vaccine and directed against the mumps. viruses in particular, the less severe are its symptoms. People with the highest mumps antibody titers had asymptomatic COVID-19.
More research is needed to show that the vaccine prevents severe COVID-19. Still, the new findings “may explain why children have a much lower COVID-19 case rate than adults, as well as a much lower death rate,” said co-author Jeffrey Gold, president of the Organization. World Cup in Watkinsville, Georgia, in a statement.
“Most children receive their first MMR vaccine around 12 to 15 months of age and the second between 4 and 6 years of age.”
Immune protection against severe reinfection appears durable
Regardless of their detectable antibody levels, most COVID-19 survivors are likely to have lasting protection against severe COVID-19 if they are reinfected, thanks to other components of the body’s immune response that are reminiscent of different coronavirus. ways, say the researchers.
In a study of 185 patients, including 41 who had been infected more than six months previously, scientists at the La Jolla Institute of Immunology in California found that multiple branches of the immune system, not just antibodies, recognized the coronavirus for at least eight months .
For example, so-called memory B cells that could recognize the virus and produce antibodies to fight it were more abundant six months after infection than one month, they reported in a paper published in bioRxiv before peer review.
The new findings “suggest that the immune system can remember the virus for years, and most people can be protected from severe COVID-19 for a considerable time,” said study leaders Shane Crotty and Alessandro Sette.
Cigarette smoke increases cellular vulnerability to COVID-19
Exposure to cigarette smoke makes cells in the airways more vulnerable to infection with the coronavirus, UCLA researchers found.
They obtained cells that line the airways of five people without COVID-19 and exposed some of the cells to cigarette smoke in test tubes. They then exposed all the cells to the coronavirus.
Compared to cells not exposed to smoke, cells exposed to smoke were two or even three times more likely to be infected with the virus, the researchers reported in Cell Stem Cell.
Analysis of individual cells in the airways showed that cigarette smoke reduced the immune response to the virus.
“If you think of the airways as the high walls that protect a castle, smoking cigarettes is like creating holes in these walls,” co-author Brigitte Gomperts told Reuters. “Smoking reduces natural defenses and this allows the virus to enter and take over cells.”
Researchers examine cells infected with coronavirus
Cells infected with the new coronavirus die within a day or two, and researchers have found a way to see what the virus is doing to them.
By integrating multiple imaging techniques, they saw the virus create “virus copy factories” in cells that look like clumps of balloons. The virus also disrupts cellular systems responsible for secreting substances, the researchers reported in Cell Host & Microbe.
In addition, it rearranges the “cytoskeleton,” which shapes cells and “serves as a rail system to allow the transport of various charges within the cell,” co-author Dr. Ralf Bartenschlager of the University of Heidelberg told Reuters, Germany.
When his team added drugs that affect the cytoskeleton, the virus had trouble making copies of itself, “which tells us that the virus needs to rearrange the cytoskeleton in order to replicate with high efficiency,” Bartenschlager said.
“We now have a much better idea of how SARS-CoV-2 changes the intracellular architecture of the infected cell and this will help us understand why cells die so quickly.”
The Zika virus causes similar cellular changes, he said, so it might be possible to develop drugs for COVID-19 that also work against other viruses.
