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This week’s roundup of some of the latest 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 illness, such as cigarette smoking makes cells more vulnerable to the virus. and how longer lasting immunity could be in COVID-19 patients than previously thought.
Childhood MMR vaccine can help prevent severe COVID-19
People whose immune systems have responded strongly to a measles-mumps-rubella (MMR) vaccine may be less likely to become seriously ill if they are infected with the coronavirus, new data suggest. The MMR II vaccine, manufactured by Merck and licensed in 1979, works by activating the immune system to produce antibodies.
Researchers reported 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 so-called vaccine-produced IgG antibodies directed against mumps virus in particular, the less severe their symptoms are. People with the highest titers of mumps antibodies had asymptomatic COVID-19.
More research is needed to show that the vaccine prevents severe COVID-19. However, the new findings “could 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 World Organization. in Watkinsville, Georgia, in a statement.
“Most children receive their first MMR vaccination around 12-15 months of age and a second between 4 and 6 years old.”
Immune protection against severe reinfections appears to be lasting
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 resemble the coronavirus in different ways , the researchers say.
In a study of 185 patients, including 41 who had been infected more than six months earlier, scientists at the La Jolla Institute for 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 can 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 on 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,” study leaders Shane Crotty and Alessandro Sette said.
Cigarette smoking increases the vulnerability of cells to COVID-19
Exposure to cigarette smoke makes airway cells more vulnerable to coronavirus infections, UCLA researchers found.
They obtained airway lining cells from five individuals without COVID-19 and exposed some cells to cigarette smoke in test tubes. Then they 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 in Cell Stem Cell reported.
Single cell airway analysis showed that cigarette smoking 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 boring holes in these walls,” co-author Brigitte Gomperts told Reuters. “Smoking reduces natural defenses, which allows the virus to enter and take control of the cells.”
Researchers examine coronavirus-infected cells
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 balloon clusters. The virus also disrupts cellular systems responsible for secreting substances, researchers at Cell Host & Microbe reported.
It also rearranges the “cytoskeleton”, which gives the cells their shape and “acts as a rail system to allow the transport of various loads within the cell,” co-author Dr. Ralf Bartenschlager of the University of Heidelberg told Reuters. , in Germany.
When his team added drugs that affect the cytoskeleton, the virus had trouble making copies of itself, “which indicates that the virus needs to rearrange the cytoskeleton to replicate with high efficiency,” Bartenschlager said.
“Now we 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 the cells are dying so quickly.”
The Zika virus causes similar cellular changes, he said, so it may be possible to develop drugs for COVID-19 that work against other viruses as well.
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