The following is a roundup of some of the latest scientific studies on the novel coronavirus and efforts to find treatments and vaccines for COVID-19, the illness caused by the virus.
Childhood vaccine may help prevent severe COVID-19
People whose immune systems responded strongly to a measles-mumps-rubella (MMR) vaccine may be less likely to become severely ill if they are infected with the new coronavirus, new data suggest. The MMR II vaccine, manufactured by Merck and licensed in 1979, works by triggering 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 the MMR II as children, the higher their titers, or levels, of so-called IgG antibodies produced by the vaccine and directed against the mumps virus in particular, the less severe their symptoms.
People with the highest mumps antibody titers had asymptomatic COVID-19.
More research is needed to prove 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,” co-author Jeffrey Gold, president of World Organisation, in Watkinsville, Georgia, said in a statement. “The majority of children get their first MMR vaccination around 12 to 15 months of age and a second one from 4 to 6 years of age.”
Cigarette smoke increases cell vulnerability to COVID-19
Exposure to cigarette smoke makes airway cells more vulnerable to infection with the new coronavirus, UCLA researchers found.
They obtained airway-lining cells from five individuals 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 the smoke, smoke-exposed cells were two- or even three-times more likely to become infected with the virus, the researchers reported on Tuesday in Cell Stem Cell. Analysis of individual airway cells showed the cigarette smoke reduced the immune response to the virus.
“If you think of the airways like the high walls that protect a castle, smoking cigarettes is like creating holes in these walls,” co-author Brigitte Gomperts told Reuters. “Smoking reduces the natural defences and this allows the virus to enter and take over the cells.”
AstraZeneca’s COVID-19 vaccine shows promise in elderly
AstraZeneca and Oxford University’s experimental COVID-19 vaccine produced strong immune responses in older adults in a mid-stage trial, researchers reported on Thursday in The Lancet. Late-stage trials are underway to confirm whether the vaccine protects against COVID-19 in a broad range of people, including those with underlying health conditions.
The current study involved 560 healthy volunteers, including 240 age 70 or over.
Volunteers received one or two doses of the vaccine, made from a weakened version of a common cold virus found in chimpanzees, or a placebo. No serious side effects were reported.
Participants older than 80, frail patients, and those with substantial chronic illnesses were excluded, according to an editorial published with the study.
“Frailty is increasingly understood to affect older adults’ responses to vaccines,” the editorialists write. “A plan for how to consider frailty in COVID-19 vaccine development is important.”
Researchers look into cells infected with new 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-copying factories” in cells that look like clusters of balloons.
The virus also disrupts cellular systems responsible for secreting substances, the researchers reported on Tuesday in Cell Host & Microbe. Furthermore, it reorganises the “cytoskeleton,” which gives cells their shape and “serves like a railway system to allow the transport of various cargos inside the cell,” coauthor Dr. Ralf Bartenschlager of the University of Heidelberg, Germany told Reuters.
When his team added drugs that affect the cytoskeleton, the virus had trouble making copies of itself, “which indicates to us that the virus needs to reorganise the cytoskeleton in order to replicate with high efficiency,” Bartenschlager said. “We now have a much better idea how SARS-CoV-2 changes the intracellular architecture of the infected cell and this will help us to understand why the cells are dying so quickly.”
The Zika virus causes similar cell changes, he said, so it might be possible to develop drugs for COVID-19 that also work against other viruses.