Hanan Polansky, Adrian Javaherian

Reduced telomere length has been associated with aging and age-related diseases. Latent infection with the Cytomegalovirus (CMV) induces telomere shortening in the infected cells. Latent CMV infection may cause reduced telomere length via GABP transcription factor deficiency, according to the Microcompetition Theory. Microcompetition and viral-induced transcription factor deficiency is important since most people harbor a latent viral infection.

The latent cytomegalovirus decreases telomere length by microcompetition (PDF file)

3 thoughts on “Hanan Polansky, Adrian Javaherian

  1. shinichi Post author

    Latent CMV infection induces telomere shortening

    News-Medical.net
    Source: http://www.degruyter.com/

    http://www.news-medical.net/news/20150702/Latent-CMV-infection-induces-telomere-shortening.aspx

    Molecular, cellular and clinical changes that arise from an infection with a latent virus and result in a decrease in longevity.

    The telomeres are repetitive DNA sequences at each end of our chromosomes. Studies show that in every cell division, the telomere is shortened. As a result, the telomere limits the cell to a fixed number of divisions and a limited life span. An essential part of human cells they affect how our cells age – as people with longer telomeres live longer lives. Surprisingly, people who are infected with a latent virus, that is, an asymptomatic virus, have shorter telomeres. This is an important observation and a great mystery. Is the virus causing the telomere shortening, and how? And if this is the case, what does it mean in terms of the relationship between the latent viruses and longevity?

    Now, an article “The Latent Cytomegalovirus Decreases Telomere Length By Microcompetition” by Hanan Polansky and Adrian Javaherian, published in Open Medicine by De Gruyter Open, provides some answers to these questions. As it turns out, a certain gene, called telomere repeat binding factor 2 (Terf2), belongs to a complex of six telomere-associated proteins, termed shelterin. The protein produced by this gene protects the chromosome ends of the DNA from damage, and controls telomere maintenance by the telomerase enzyme. When does a cell produce the Terf2 protein? After receiving a signal that tells a transcription factor called GABP to bind the Terf2 gene. One can think of GABP as a finger that pushes the “ON” button on the Terf2 gene. Now consider a case where a latent virus called CMV infects the cell. As it turns out, the CMV virus also uses the GABP transcription factor to press the “ON” button on its own genes. When the CMV virus steals the GABP “fingers” from the Terf2 gene, there are no fingers left to press the “ON” button on the Terf2 gene, and the Terf2 gene fails to produce the Terf2 protein. What is the result of a shortage of Terf2 proteins? Short telomeres. In his book “Microcompetition with Foreign DNA and the Origin of Chronic Disease”, Dr. Polansky used the term Microcompetition to describe this event.

    Most people are infected with a latent virus. For instance, CMV is present in more than 70-80% of individuals by the age of fifty. A study by Gkrania-Klotsas et al. showed that individuals with signs of CMV have higher all-cause mortality compared to uninfected individuals. Polansky and Javaherian (both from The Center for the Biology of Chronic Diseasein Valley Cottage, NY) explain the molecular, cellular and clinical changes that result from a latent infection with the CMV and the consequent decrease in longevity.

    There are many implications of the Microcompetition theory. Not only does it suggest new targets for drug development, but it also puts forward new behavioral changes that may be taken on the part of the infected individual in order to decrease the chances of developing a major disease and increase longevity. A common misconception that only the active phase of a viral infection can cause harm proves inadequate, as the Microcompetition theory shows that the latent phase is the most dangerous one. These findings can be crucial to further research into viral infections.

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  2. shinichi Post author

    (sk)

    生物は細胞分裂をくりかえすと、染色体末端の塩基配列部位であるテロメア(telomere)が短くなっていき、これが短くなりきると死を迎えることになる。言い方を変えれば、テロメアの生成を行う酵素が体内で作られ続け、テロメアの長さが再び長くなれば、老化を防げるということになる。

    そうまでして長く生きたいのか。死にたくないという本能に従うのはいいとして、生きてなにをしようというのだろうか。

    髪はフサフサ、歯はピカピカ、膚はツルツル、眼はキラキラなんていう老人は、不自然で気持ち悪い。人は老いて死ぬ。それでいいではないか。

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