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These protein particles are involved in intracellular and extracellular transport and are symbiotic in nature. Three criteria are, according to the scientific method needed to properly identify a virus. It must be isolated from a host cell. As of this has never been accomplished in humans. It must be biochemically characterized. The black and white electron microscopy that are seen Wikipedia are once again NOT the actual virus.

Many of the photos are colored indicating that they are the art work of designers, because electron microscopic photos always appear in black and white. No virus has been isolated. The photos actually show cells and typical endogenous particles in them.

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These particles are partially the cellular particles mentioned above and typical artifacts which means structures that accrue after inappropriate fixing and drying of the probes, while being prepared for the electron microscope. This is the scientific term for proteins from the blood that are clumped together, as is typical for coagulations. Typically, thereby round and also crystal structures accrue depending on the condition of the blood sample. The Ultimate Conspiracy. This book serves as a wonderful introduction to the virus question, GNM and so much more.

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Virus Mania by Torsten Engelbrecht. We need to look to the work of Dr. Hamer and the discovery of The Five Biological Laws. With AIDS, we simply need to break down the clinical picture by the individual biological conflicts and adaptive bodily response. Thrush is a biological conflict of being unable to swallow or spit something out, e.

Kaposi sarcoma relates to a dirtiness or soil conflict, e. A separation touch conflict is about wanting to or not wanting to separate i. Lymphoma reflects a self devaluation conflict, e. Low platelets CD4, T-Cells reflects a blood disorder conflict. An abnormal blood result. Upcoming SlideShare. Like this document?

Why not share! Embed Size px. Start on. Show related SlideShares at end. WordPress Shortcode. Full Name Comment goes here. Are you sure you want to Yes No. Be the first to like this. No Downloads. Views Total views. The coefficient for EBV infection was close to 0 in both models. The other independent predictors of shorter telomeres at follow-up were older age, male sex, and shorter LTL at baseline. Model 1 shows coefficients for separate regressions with individual infections.

In model 2, coefficients are mutually adjusted for the other infections. Serological evidence of exposure to multiple herpesviruses was also significantly associated with shorter LTL at follow-up Table 3. Figure 1 illustrates the pattern of mean change in LTL across the 2 time periods by the total number of infections for which an individual was seropositive. To explore whether one particular herpesvirus, such as CMV, was primarily driving these results, we explored all combinations of infection pairs and their association with LTL, illustrated in Table 3 and Figure 2.

Overall, there was evidence of an important role for CMV infection and some interaction effects with other herpesviruses. Coinfection with both HSV-1 and CMV showed the strongest association with shorter LTL, suggesting an interactive effect of seropositivity for both infections compared with only one. Table 3 also shows the remainder of coinfection pair-wise combinations, with some evidence for the importance of HHV-6 coinfection for the association between HSV-1 and LTL.

Because of previous findings of associations between CMV and telomerase activity in women only, we tested for interactions between sex and each infection, as well as burden of infection. No significant sex-infection interactions were found. Because inflammation is a hypothesized mechanism through which infections may affect telomere shortening, we also tested models adjusting for available markers of inflammation serum C-reactive protein, interleukin 6, and fibrinogen, measured at baseline.

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None of these inflammatory markers were associated with LTL shortening, and thus they did not mediate the associations between infections and LTL. Although LTL is correlated with many important aging-related outcomes, its determinants are not well understood. Persistent viral infections may be an important determinant of individual variation in LTL, but have not been extensively studied in vivo [ 11 , 12 ].

This study was the first to test the association of multiple highly prevalent persistent herpesvirus infections with prospective LTL in humans. These findings suggest an important role for these infections for understanding LTL dynamics.

There are several reasons why CMV, more than other pathogens, may contribute to telomere shortening. CMV infection is thought to be associated with a continuous low-grade reactivation, causing a highly characteristic differentiation among T cells that yields a robust expansion of T cells that down-regulate telomerase and exhibit short telomeres [ 35 ].

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The causality of this association was confirmed in the same study, showing that primary CMV infection among 19 renal transplant recipients coincided with a steep drop in lymphocyte LTL. Thus, the LTL decreases associated with CMV infection may driven in part be by a change in the cellular composition of the peripheral blood, the main cellular source of LTL determination, and not a direct cellular effect of telomere attrition.

Recent results from this sample found that greater cortisol responsivity to acute stressors predicted more rapid telomere attrition [ 36 ]. CMV can infect and replicate in human adrenocortical cells, thereby triggering steroidogenesis [ 37 ], which in turn has been shown to inhibit telomerase activity in CD4 and CD8 T cells [ 38 ]. Steptoe et al [ 39 ] previously reported an altered diurnal cortisol slope in healthy CMV-positive individuals, in which those who are infected exhibited a flatter decline over the day than those who are not infected.

Such a flattened secretion pattern of cortisol has repeatedly been associated with impaired immunity and enhanced inflammatory activity [ 40 , 41 ], which, in turn, may further promote elevated viral reactivation. Indeed, studies have suggested that cells exposed to glucocorticoids increased replication of HSV and CMV in vitro [ 42 ]. The mechanisms underlying the observed associations of HSV-1 and HHV-6 and telomere shortening are not known and should be replicated and explored in future work. The lack of an association of EBV with shorter LTL, in contrast to the other herpesvirus infections, is consistent with fundamental differences in how these viruses modulate the host immune system, with dramatic expansion of T cells with short telomeres not seen in EBV as in CMV [ 18—20 ].

A major strength of this study is that our findings come from a well-characterized longitudinal population cohort, in contrast to the previous small clinical sample used to explore CMV and lymphocyte LTL [ 11 ].

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The prospective assessment of LTL over 3 years and data on the serostatus to multiple herpesviruses at baseline is also novel. Previous cross-sectional work showed that CMV seropositivity was associated with lower levels of telomerase in women [ 26 ], but this did not seem to generalize to shorter LTL in that sample. Future work should test whether CMV plays a role, at least in part, in the association between LTL and the onset of chronic disease, especially vascular disease. Results from a small clinical study found that, among patients with coronary heart disease, LTL in CD8 cytotoxic T cells was shorter in CMV-positive than in CMV-negative patients, and this LTL shortening was correlated with a decrease in left ventricular function, suggesting a role for CMV in the coevolution of coronary heart disease and immunosenescence [ 43 ].

Our findings of an association between higher CMV IgG and shorter telomeres warrants further investigation, particularly given epidemiological evidence that higher CMV IgG is associated with increased risk of mortality [ 44 ], weaker vaccine response [ 29 ], and lower levels of psychological well-being [ 45 ]. Strong and consistent associations have also been observed between stress and increased herpesvirus IgG [ 46 ].

Given the evidence that chronic stress contributes to shorter telomeres [ 47 ], our results could have implications for understanding the pathways through which psychosocial factors affect cellular aging. The role of stress-related reactivation of herpesviruses as a mediator of stress and telomere dynamics should be further explored. Our study has several limitations.

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LTL was measured in peripheral blood mononuclear cells, and values may differ in lymphocyte subpopulations. Future flow cytometric analysis of cell subpopulations would allow better mechanistic understanding of how infections decrease LTL. Measures were also made with 2 different PCR machines at baseline and follow-up, but though this may affect comparisons of absolute values, it did not affect the relative results shown here, as indicated by identical findings with standardized measures of LTL.

Furthermore, our results are virtually identical when we use only follow-up LTL data, providing further assurance that changes in LTL measurement methods are not driving our results.

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Because IgG antibodies reflect any past exposure, it is not known when these herpesviruses were acquired, though it is likely that many were acquired early in life, given the concentration of risk factors for early exposure to these infections [ 48 ]. Furthermore, although shorter LTL has been shown to increase the risk of experimentally induced upper respiratory tract infections in younger adults [ 7 ], the we infections analyzed were not associated with LTL at baseline, reducing the risk that reverse causality from shorter LTL to increased risk of infection was driving the observed associations.

In conclusion, our results suggest large and significant associations between highly prevalent persistent herpesvirus infections and telomere shortening in humans. The magnitude of the association for CMV seropositivity was equal to almost half an SD in LTL, or the equivalent of 12 years of chronological age as estimated in this sample.

In contrast, previously identified risk factors for cross-sectional LTL, including smoking, obesity, SES, and inflammatory markers, were not associated with LTL attrition in this sample, suggesting that infection history may be a more robust predictor of LTL than these prior commonly identified risk factors.