This week’s summary of some of the latest scientific studies on the coronavirus and efforts to find treatments and vaccines for COVID-19 explore how childhood immunizations could be essential to prevent serious illness, how cigarette smoke makes which cells are more vulnerable to the virus and how there might be longer lasting immunity 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 suggests. The MMR II vaccine, manufactured by Merck and licensed in 1979, works by causing the immune system to produce antibodies.
Researchers reported in mBio on Friday that among 50 COVID-19 patients under the age of 42 who received MMR II as children, plus their titers – or levels – of so-called IgG antibodies produced by the vaccine and directed against mumps were high. viruses in particular, the less severe their symptoms. People with the highest anti-mumps antibody titers had asymptomatic COVID-19.
More research is needed to prove that the vaccine prevents severe COVID-19. Still, the new findings “may explain why children have a much lower rate of COVID-19 cases 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.
“The majority of children receive their first MMR vaccine around the age of 12 to 15 months and a second from 4 to 6 years old. “
Immune protection against severe re-infections seems long-lasting
Regardless of their detectable antibody levels, most COVID-19 survivors are likely to have lasting protection against severe COVID-19 if re-infected, through other components of the body’s immune response. who remember the coronavirus in different ways, 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 of Immunology in California found that several branches of the immune system – not just antibodies – recognized the coronavirus for at least eight months.
For example, the so-called memory B cells capable of recognizing the virus and producing antibodies to fight it were more abundant six months after infection than one month, they reported in an article published on bioRxiv before the peer review.
The new findings “suggest that the immune system can remember the virus for years, and that most people can be protected from severe COVID-19 for a substantial amount of time,” said study officials Shane Crotty and Alessandro Sette.
Cigarette smoke increases cell vulnerability to COVID-19
Exposure to cigarette smoke makes cells in the airways more vulnerable to infection with the coronavirus, UCLA researchers have found.
They obtained lining cells from the airways of five people without COVID-19 and exposed some of the 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.
Analysis of individual cells in the respiratory tract 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 those walls,” co-author Brigitte Gomperts told Reuters. “Smoking reduces the natural defenses, which allows the virus to enter and take control of the 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 several imaging techniques, they saw the virus create “virus copy factories” in cells that look like clumps of balloons. The virus also disrupts the cellular systems responsible for secreting substances, the researchers reported in Cell Host & Microbe.
In addition, it rearranges the ‘cytoskeleton’, which gives cells their shape and ‘serves as a rail system to allow the transport of various cargoes within the cell,’ said co-author Dr Ralf Bartenschlager of the ‘University of Heidelberg, Germany, to Reuters.
When his team added drugs that affect the cytoskeleton, the virus struggled to reproduce, “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 would be possible to develop drugs for COVID-19 that work against other viruses as well.