Medical Bulletin 28/April/2023

Here are the top medical news for the day:

Post-COVID-19 conditions alter a person’s immune response: Study

When a person has an infection, the immune system typically responds by making antibodies that block germs from entering cells. Vaccines imitate an infection so that the body’s immune system knows to release certain antibodies when it comes across a virus. In both cases, the immune system eventually stops creating antibodies when the suspected infection is gone.

A new study by investigators from the Smidt Heart Institute at Cedars-Sinai suggests long COVID-19 might be caused by a dysfunction of the immune system.

The study, published in BMC Infectious Diseases, found that after people with long COVID-19 received the COVID-19 vaccine, they produced antibodies against the virus that causes COVID-19 for months longer than expected.

Reference:

Serological response to vaccination in post-acute sequelae of COVID,BMC Infectious Diseases,DOI: 10.1186/s12879-023-08060-y

Novel clinical tool for clonal hematopoiesis identifies high risk for clonal hematopoiesis patients

Clonal hematopoiesis (CH) is a recently characterized condition in which the genetic mutations associated with leukemia and other blood cancers are found in the blood of individuals without cancer. This pre-cancerous state is fairly common - for example, it’s present in roughly 15% of people over age 65 - but only a small percentage, around 4%, will go on to develop blood cancer. Because there is no robust, rigorous way to assess risk, clinicians have struggled to advise CH patients on what the future could hold.

A new clinical tool developed by a team of researchers led by the Dana-Farber Cancer Institute pinpoints which Clonal hematopoiesis patients are at highest risk for cancer progression. Their work was published this week in the New England Journal of Medicine Evidence.

Reference:

Prediction of Risk for Myeloid Malignancy in Clonal Hematopoiesis,NEJM Evidence

Researchers slow aging by engineering longevity in cells

Three years ago a group of University of California San Diego researchers deciphered essential mechanisms behind the aging process. After identifying two distinct directions that cells follow during aging, the researchers genetically manipulated these processes to extend the lifespan of cells.

As described April 28, 2023 in Science, they have now extended this research using synthetic biology to engineer a solution that keeps cells from reaching their normal levels of deterioration associated with aging. Cells, including those of yeast, plants, animals and humans, all contain gene regulatory circuits that are responsible for many physiological functions, including aging.

Reference:

Engineering longevity-Design of a synthetic gene oscillator to slow cellular aging,Science,DOI: 10.1126/science.add7631