Ah ma forse non ha stato il vaccino
What if the virus behind COVID-19 did more than just infect cells, but also altered them in a way that could worsen heart disease? A recent study explores this question by investigating how the spike protein of SARS-CoV-2, the virus causing COVID-19, contributes to heart failure through a process called cellular senescence (when cells lose the ability to replicate themselves). The study uncovers how this viral protein can provoke long-lasting changes in heart cells, even in the absence of active viral infection, shedding light on the complex aftermath of COVID-19.
The findings appear in the journal PLOS Pathogens (
https://doi.org/10.1371/journal.ppat.1012291).
In this groundbreaking research, scientists discovered that the spike protein of SARS-CoV-2, even without the presence of the virus itself, can cause heart cells to become superglued together into into larger structures known as syncytia. These globs of cells go into a state of cellular senescence, where the cells stop dividing and begin to secrete inflammatory molecules. This senescent state is characterized by changes that can exacerbate heart failure, a condition already associated with increased risk and severity in COVID-19 patients.
The study demonstrated that these syncytia (cell globs) are not only prevalent in tissues during active infection but can also persist in the body long after the virus is gone. This lingering presence of viral proteins can continually activate immune responses, leading to chronic inflammation and potentially worsening heart conditions. The research highlights a crucial mechanism by which COVID-19 may contribute to long-term cardiovascular problems, providing a biological basis for some cases of long COVID.
The authors of the study clarify that the syncytial senescence triggered by the SARS-CoV-2 spike protein is not a result of COVID-19 mRNA vaccines. These vaccines, including those by Pfizer and Moderna, have been engineered to include mutations that stabilize the spike protein in a prefusion state, thereby preventing it from causing the cell fusion seen with the wild-type virus spike protein.
What makes this discovery of the harmful effects of the wild viral spike protein particularly significant is its potential implications for treating heart failure in COVID-19 survivors. The researchers found that certain drugs, including those that inhibit a protein called WNK1, can mitigate the harmful effects of these senescent cells. By targeting the metabolic dysfunction and inflammation caused by the syncytia, these treatments could offer a new way to protect heart health in those affected by the virus.
This study emphasizes the importance of recognizing the long-term health impacts of COVID-19, particularly on the heart. It highlights the need for continued vigilance and medical monitoring of individuals who have recovered from the virus, as well as the potential for developing targeted therapies to address post-viral complications. Understanding these mechanisms is crucial for improving care and outcomes for patients dealing with the lingering effects of COVID-19, underscoring the importance of research in guiding future public health strategies.
