This week’s review of some of the latest scientific studies on coronavirus and efforts to find treatments and vaccines for COVID-19 explores how childhood vaccination could be key in preventing serious diseases, how cigarette smoke makes cells more susceptible to the virus, and how long-lasting immunity could exist. in patients with COVID-19 than previously thought.
The pediatric MMR vaccine may help prevent severe COVID-19
People who have had a strong immune response to the measles-mumps-rubella (MMR) vaccine may be less likely to become seriously ill if they are infected with the coronavirus, new data show. The MMR II vaccine, manufactured by Merck and licensed in 1979, works by triggering the immune system to produce antibodies.
The researchers reported on Friday in mBio that among the 50 patients with COVID-19 under the age of 42 who received MMR II as children, their titer – or level – of so-called vaccine-produced IgG antibodies is higher. especially viruses, the less severe their symptoms. Subjects with the highest mumps antibody titer 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 than adults, as well as a much lower mortality rate,” said co-author Jeffrey Gold, president of the World Organization in Watkinsville, Georgia. statement.
“Most children vaccinate their first MMR around 12 to 15 months and the second from 4 to 6 years.”
Immune protection against severe reinfection appears to be permanent
Regardless of their detectable antibody levels, most COVID-19 survivors are likely to have permanent protection against severe COVID-19 if re-infected, thanks to other components of the body’s immune response that are remembered by coronaviruses in different ways, the researchers say.
In a study of 185 patients, including 41 infected more than six months earlier, researchers 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 a month ago, they reported in a paper published on bioRxiv before the 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 extended periods of time,” study leaders Shane Crotty and Alessandro Sette said.
Cigarette smoke increases the vulnerability of cells to COVID-19
Exposure to cigarette smoke makes airway cells more vulnerable to coronavirus infection, UCLA researchers have found.
They were given air-lined cells from five people without COVID-19 and some cells were exposed to cigarette smoke in test tubes. All cells were then exposed to the coronavirus.
Compared to non-smoke-exposed cells, smoke-exposed cells were two or even three times more likely to become infected with the virus, researchers at Cell Stem Cell reported.
Analysis of individual airway cells showed that cigarette smoke reduced the immune response to the virus.
“If you think of airways like the high walls that protect the castle, smoking cigarettes is like creating holes in those walls,” co-author Brigitte Gomperts told Reuters. “Smoking reduces the natural defenses, and this allows the virus to enter and take over the cells.”
Researchers are investigating 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.
Integrating multiple imaging techniques, they saw the virus create “virus copying factories” in cells that look like balloon clusters. The virus also disrupts the cellular system responsible for secreting the substance, researchers at Cell Host & Microbe reported.
Furthermore, it reorganizes the “cytoskeleton,” which gives cells shape and “serves as a railway system that allows the transport of various loads within the station,” co-author Dr. Ralf Bartenschlager of the University of Heidelberg told Reuters.
When his team added drugs that affect the cytoskeleton, the virus had trouble making copies of it, “which indicates to us that the virus needs to reorganize the cytoskeleton so that it can reproduce with high efficiency,” Bartenschlager said.
“We now have a much better idea of how SARS-CoV-2 changes the intracellular architecture of an infected cell and that will help us understand why cells die so quickly.”
The Zika virus causes similar changes in cells, he said, so it could be possible to develop drugs for COVID-19 that work against other viruses as well.