Reduced telomere length has been associated with aging as well as
Van de Berg et al. measured the relationship between telomere length in T cells and CMV infection. They report that one year post primary CMV infection, that is during the latent phase, the cells exhibited shorter telomeres.
We would like to propose an explanation for the observed relationship between latent CMV infection and reduced telomere length. The explanation is based on the theory presented by Hanan Polansky in 2003 in his book on Microcompetition.
Many viruses contain an
After establishing a latent infection, the viral
of the complex to cellular genes. As a result, the cellular genes express abnormal levels of their proteins.
Those that are stimulated by the GABP∙p300 complex produce fewer proteins, and those that are suppressed by the complex produce more proteins. The abnormal levels of these cellular proteins cause a disease. Polansky used the term «Microcompetition» to describe the relationship between viral and cellular regulatory elements.
Many common viruses that establish latent infections have a strong
These viruses include the
results from a few studies. Liu et al. showed that the CMV promoter/enhancer, which includes the
Slobedman and Mocarski showed that during latency, an infected cell harbors about 10 copies of CMV [5]. Now, let us multiply 10 copies by
Yu et al. reported that GABP directly regulates genes involved in telomere maintenance. Specifically, they determined the telomere repeat binding factor 2 (Terf2) gene to be a
A number of studies have reported an association between short telomeres and increased risk for vascular diseases. Spyridopoulos et al. mention that individuals with shorter telomeres in leukocytes carry a higher risk for dying of cardiovascular disease [9]. A study by Van der Harst et al. that showed that telomere length is shorter in patients with congestive heart failure. Spyridopoulos et al. reported that the most pronounced degree of telomere shortening was in their
studies also suggest that shortened telomeres are associated with diabetes [10]. CMV infection is also associated with an increased risk for CHD [11]. Mendy et al. reported that CMV infection increased the risk of mortality from diabetes [12]. It is also interesting that in his book, Polansky explains how microcompetition between a latent virus, such as CMV, and certain cellular genes, could cause most major diseases. These genes include the tissue factor (TF), CD18, and CD49d, which are suppressed by GABP.
According to the theory, microcompetition between CMV and these genes for GABP, increases their transcription, and increases the risk of atherosclerosis, stroke, and autoimmune diseases, including diabetes.
In their study, van de Berg et al. reported a correlation between T cell telomere length and T cell differentiation after infection with CMV, proposing an indirect causal relationship between latent CMV infection and the shortening of telomere length. We believe there is a direct causal relationship between latent CMV infection and reduced telomere length via GABP transcription factor deficiency, according to the Microcompetition Theory. Furthermore, we believe that microcompetition and
factor deficiency is important since most people harbor a latent viral infection.
For instance, more than 90%-95% of people are infected with the EBV [13]. Seroprevalence of CMV is greater than 70–80% by the age of 50 [14]. HSV type 1 has an estimated seroprovalence of greater than 90% in many nations [15]. Therefore, most people struggle with microcompetition, and are at risk for a transcription factor deficiency, and the diseases that are triggered by such deficiency, including heart disease and autoimmune disease.
http://www.degruyter.com/view/j/med.2015.10.
