Latent Cytomegalovirus Can Cause Transcription Factor Deficiency

The Latent Cytomegalovirus ( CMV ) Can Cause a Transcription Factor Deficiency and Disease Harmonizing to Microcompetition Theory

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Many surveies showed a positive association between Cytomegalovirus ( CMV ) seropositivity and all-cause mortality. We use Microcompetition theory to explicate how the latent CMV can do a written text factor lack, chronic disease, and mortality. Since most people harbor a latent virus, farther development of the Microcompetition theory is of import

The presence of Ig G ( IgG ) antibodies against a peculiar virus indicates that the virus is in the latent stage.1IgG antibodies against the Cytomegalovirus ( CMV ) are found in about 60 % of grownups in developed states, and virtually 100 % of grownups in developing states. Gkrania-Klotsaset Al.showed that persons with CMV seropositivity have higher all-cause mortality compared to clean persons.2They besides showed that an addition in the concentration of the CMV IgG antibodies increases all-cause mortality in septic persons. We would wish to suggest a mechanism that explains these observations. This mechanism has been described by Hanan Polansky in 2003 in his book on Microcompetition.3

Many viruses consist of an N-box, which is a nucleus binding sequence found in their promoters/enhancers. After set uping a latent infection, the viral N-boxes bind the cellular GABPa?™p300 written text composite. Since the composite is restricting, the viral N-boxes lessening the handiness of the complex to cellular cistrons. As a consequence, the cellular cistrons express an unnatural degree of their protein. Those that are stimulated by the GABPa?™p300 complex green goods fewer proteins, and those that are suppressed by the complex green goods more proteins. The unnatural degrees of these cellular proteins cause a disease. Polansky used the term “ Microcompetition ” to depict the relationship between viral and cellular regulative elements.

Many common viruses, which set up a latent infection, have a strong N-box in their promoters/enhancers. These viruses include the Epstein-Barr virus ( EBV ) , Cytomegalovirus ( CMV ) , Herpes Simplex Virus ( HSV ) , Varicella Zoster Virus ( VZV ) , Hepatitis B Virus ( HBV ) , Hepatitis C Virus ( HCV ) , and the Human Papillomavirus ( HPV ) . It is interesting that the CMV has the strongest promoter/enhancer known to science. In order to gauge the power of the CMV booster, we will unite the consequences from a few surveies. Liuet Al. showed that the CMV promoter/enhancer, which includes the N-box, is more than 150-fold more powerful than the booster of the cellular platelet-derived growing factor-b concatenation ( PDGF-b ) cistron.4Slobedman and Mocarski showed that during latency, an infected cell seaports about 10 transcripts of the CMV.5Now, allow us multiply 10 transcripts by 150-fold. We conclude that a latent infection with CMV has a similar consequence on the PDGF-b booster, and therefore, its written text, as the debut of 10 ? 150, or 1500 transcripts of extra PDGF-b cistrons into the cell. Adamet Al.showed that PDGF-b is susceptible to microcompetition with CMV.6Therefore, the Microcompetition theory suggests that a latent infection with CMV causes a lessening in PDGF-b written text followed by a lessening in the concentration of the PDGF-b protein in the latently infected cell, and finally disease.

In his book, Polansky explains how microcompetition between a latent virus, such as CMV, and certain cellular cistrons, can do most major diseases. These cistrons include the tissue factor ( TF ) , CD18, and CD49d, which are suppressed by GABP. Harmonizing to the theory, microcompetition between CMV and these cistrons for GABP, increases their written text, and increases the hazard of coronary artery disease, shot, and autoimmune diseases, such as lupus, diabetes, and psoriasis. In contrast, the retinoblastoma ( Rb ) and BRCA1 cistrons are transactivated by the GABP written text factor. Therefore, microcompetition between CMV and these cistrons for GABP, decreases their written text. Since Rb and BRCA1 are tumor suppressers, the lessening in their written text increases the hazard of malignant neoplastic disease.

The grounds that CMV is associated with increased hazard of major diseases, such as cardiovascular disease ( CVD ) , malignant neoplastic disease, physical damage, and cognitive diminution, and mortality is mounting. Simaneket Al.reported the highest jeopardy ratio ( HR ) for all-cause and CVD-related mortality among people who were both CMV seropositive and had high CRP degrees ( 1.60 and 1.71, severally ) .7In another survey, Wanget Al.determined the consequence of latent CMV infection on incident infirmity and mortality in immunocompetent older adult females and reported an increased prevalence of infirmity with higher CMV IgG concentrations ( 5.6 % among seronegative persons and 18.4 % among those in the highest quartile of CMV antibody concentration ) .8Finally, Lepilleret Al.reported a important addition in HCMV seroprevalence in the group dwelling of grownup patients with hepatocellular carcinoma ( HCC ) and cirrhosis compared to the group of grownup patients with cirrhosis but no HCC and the group of patients with neither HCC nor cirrhosis ( 74 % versus 54 % and 57 % , severally ) .9

This grounds promoted many scientists to propose an implicit in mechanism. Some suggested that societal want or redness might do the ascertained relationships. However, Gkrania-Klotsaset Al.reported that both conditions do non lend to the association between CMV and mortality. Another account centered on the negative consequence of CMV on telomere length. This consequence was observed by Van De Berget Al.10, and was mentioned in Gkrania-Klotsaset Al.It is interesting that a significant part of cistrons involved in telomere care are upregulated by GABP.11For illustration, Terf2, which is involved in telomere care, is transactivated by GABP. Hence, microcompetition with CMV decreases the concentration of GABP edge to Terf2, decreases its written text, and finally decreases telomere length.

We believe that microcompetition and viral-induced written text factor lack is really of import. Most people harbor a latent viral infection. For case, more than 90 % -95 % are infected with the EBV. Seroprevalence of CMV is greater than 70-80 % by the age of 50.12HSV type 1 has an estimated seroprovalence of greater than 90 % in many states.13Therefore, most people struggle with microcompetition, and are at hazard for a written text factor lack, and the diseases that are triggered by such lack, including malignant neoplastic disease, bosom disease, shot, and autoimmune disease.


1. Scheld MW, Whitley RJ, Marra CM. Infections of the Central Nervous System. Philadelphia: Wolters Kluwer Health ; 2014.

2. Gkrania-Klotsas Tocopherol, Langenberg C, Sharp SJ, Luben R, Khaw KT, Wareham NJ. Seropositivity and Higher Immunoglobulin G Antibody Levels Against Cytomegalovirus Are Associated With Mortality in the Population-Based European Prospective Investigation of Cancer-Norfolk Cohort. Clin Infect Dis. 2013 ; 56 ( 10 ) :1421-7.

3. Polansky H. Microcompetition with Foreign DNA and the Origin of Chronic Disease. New York: The Center for the Biology of Chronic Disease ; 2003.

4. Liu BH, Wang X, Ma YX, Wang S. CMV Enhancer/Human PDGF-Beta Promoter for Neuron-Specific Transgene Expression. Gene Therapy. 2004 ; 11:52-60.

5. Slobedman B and Mocarski ES. Quantitative Analysis of Latent Human Cytomegalovirus. Journal of Virology. 1999 ; 73:4806-12.

6. Adam GI, Miller SJ, Ulleras E, Franklin GC. Cell-Type-Specific Transition of PDGF-B Regulatory Elements via Viral Enhancer Competition: A Caution for the Use of Reference Plasmids in Transient Transfection Assays. Gene. 1996 ; 178:25-9.

7. Simanek AM, Dowd JB, Pawelec G, Melzer D, Dutta A, Aiello AE. Seropositivity to Cytomegalovirus, Inflammation, All-Cause and Cardiovascular Disease-Related Mortality in the United States. PloS One. 2011 ; 6 ( 2 ) : e16103.

8. Wang GC, Kao WHL, Murakami P, Xue QL, Chiou RB, Detrick B, McDyer JF, Semba RD, Casolaro V, Walston JD, Fried LP. Cytomegalovirus Infection and the Hazard of Mortality and Frailty in Older Women: A Prospective Observational Cohort Study. Am J Epidemiol. 2010 ; 171 ( 10 ) :1144-52

9. Lepiller Q, Tripathy MK, Di Martino V, Kantelip B, Herbein G. Increased HCMV seroprevalence in patients with hepatocellular carcinoma. Virol J. 2011 ; 8:485.

10. new wave de Berg PJ, Griffiths SJ, Yong SL, Macaulay R, Bemelman FJ, Jackson S, Henson SM, Berge IJ, Akbar AN, new wave Lier RA. Cytomegalovirus Infection Reduces Telomere Length of the Circulating T Cell Pool. J Immunol. 2010 ; 184:3417-23.

11. Yu S, Cui K, Jothi R, Zhao DM, Jing X, Zhao K, Xue HH. GABP controls a critical written text regulative faculty that is indispensable for care and distinction of haematopoietic stem/progenitor cells. Blood. 2011 ; 117 ( 7 ) :2166-78.

12. Reddehase MJ. Cytomegaloviruss: From Molecular Pathogenesis to Intervention. Volume 2. United Kingdom: Horizon Scientific Press ; 2013.

13. Bernstein DI, Bellamy AR, Hook III EW, Levin MJ, Wald A, Ewell MG et Al. Epidemiology, Clinical Presentation, and Antibody Response to Primary Infection With Herpes Simplex Virus Type 1 and Type 2 in Young Women. Clin Infect Dis. 2013 ; 56 ( 3 ) :344-51.

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