Could senescent cells be the hidden trigger behind the loss of smell in Long COVID?

As many are aware, losing the sense of smell is a prevalent symptom for individuals experiencing Long COVID. Scientists have put forward several possible explanations for this phenomenon, which include a hyperactive sympathetic nervous system as well as the lingering presence of the virus in the body.

A recent publication by Tsuji et al. investigates an entirely different potential source for this sensory deficit, specifically looking at senescent cells residing in the olfactory mucosa.

To make sense of this, it helps to define what a senescent cell actually is. Senescence refers to a specific biological phase that cells can occasionally enter. People often compare this to a zombie-like status because the cells are neither dead nor completely functional. Instead of dividing to generate new healthy cells, they stop replicating altogether. Consequently, they can start to release inflammatory chemicals that disrupt the natural messaging systems of the body and impair the performance of neighboring healthy cells.

Even though this process sounds quite harmful, senescence might actually serve as a defensive strategy used by the body to prevent major future health issues like cancer. Whenever a particular cell suffers damage, it is highly undesirable for that cell to keep replicating. As a result, entering a senescent state acts as a biological roadblock, minimizing the dangerous consequences of keeping an old or defective cell in circulation.

Through their experiments, Tsuji et al. observed that the SARS-CoV-2 virus successfully triggered senescence within the fibroblasts of the olfactory mucosa in mice. The most fascinating part of this discovery was that these particular fibroblasts had never been directly infected by the virus themselves.

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