As it turned out, the revived viruses not only accelerate and complicate aging in each individual cell, but also “infect with aging” neighboring ones, affecting entire organs and tissues.
The aging of the body is associated with the deterioration of its physiological state and the manifestation of a number of chronic diseases.
Despite many years of research into this process, many molecular changes and underlying mechanisms remain poorly understood.
Cellular aging is the most characteristic feature of aging and related diseases, in which programmed epigenetic changes play an important role.
These changes occur under the influence of external environmental factors and affect which genes and how they work.
Thus, an external source of stress can cause an irreversible stop of the cell cycle (the life of a cell from division to division) and lead to its death.
And it is practically unknown what role mobile elements of the genome, retrotransposons, play in these processes.
Retrotransposons (or endogenous retroviruses) are a relic of an ancient retroviral infection that struck our ancestors, fixed in their genome in the course of evolution.
Today, such insertions of genes from ancient viruses make up about eight percent of the entire human genome.
Naturally, retrotransposons are not preserved in their original form: as a result of evolutionary pressure, they accumulate mutations that usually prevent their replication (reproduction), transposition (movement) in the genome and the synthesis of proteins associated with them.
An international team of researchers from China and the United States is interested in the youngest subfamily of human endogenous retroviruses HERVK (HML-2).
Scientists have found that in aging human cells, these retroviruses regain their ability to produce proteins needed to create retrovirus-like particles (RVLPs).
Therefore, under stress, as soon as the cell cycle stops and the “supervision” of retrotransposons weakens, hundreds of copies of the HERVK virus contained in the human genome begin to synthesize RNA, DNA and proteins of viral particles.
Accumulation of viral genetic material in cells triggers an innate immune response, causing inflammatory responses and accelerating cellular aging.
Moreover, after the death of one cell, the released RVPCs can effectively transmit aging signals to other cells nearby, as well as to other organs and tissues, using the bloodstream.
Thus, this leads to an avalanche-like aging of “infected” young cells.
However, as it turns out, these processes can be interrupted: researchers have developed and tested several effective intervention strategies to inhibit the reactivation of endogenous retroviruses and eliminate viral particles.
Each of these strategies blocks different stages of the virus life cycle in order to alleviate and slow down the aging of tissues and the whole organism.
Thus, the work opens up great opportunities for creating a scientific method for assessing aging and developing therapeutic strategies to alleviate the aging process and related diseases.
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