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home:diseases:hiv_and_aids [02.17.2019] – [at this time there are no AIDS patients on the Marshall Protocol] sallieq | home:diseases:hiv_and_aids [09.14.2022] (current) – external edit 127.0.0.1 | ||
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====== HIV and AIDS ====== | ====== HIV and AIDS ====== | ||
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===== Introduction ===== | ===== Introduction ===== | ||
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- | HIV uses the VDR to recognize its own LTR promoter region in order to transcribe its own genome, thus taking over the VDR.(({{pubmed> | + | HIV uses the VDR to recognize its own LTR promoter region in order to transcribe its own genome, thus taking over the VDR.(({{pmid> |
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There is no evidence that supplemental vitamin D helps HIV or AIDS patients. | There is no evidence that supplemental vitamin D helps HIV or AIDS patients. | ||
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Of note, we observed that patients with low vitamin D levels displayed a reduced CD4/CD8 ratio (P ¼ 0.03, Table 1), which is usually a sign of increased immune activation in HIV-infected patients receiving effective ART [16]. We also analyzed CD38 expression on the surface of memory CD8+ T cells as a robust marker of immune activation. Although there was substantial interindividual variability, | Of note, we observed that patients with low vitamin D levels displayed a reduced CD4/CD8 ratio (P ¼ 0.03, Table 1), which is usually a sign of increased immune activation in HIV-infected patients receiving effective ART [16]. We also analyzed CD38 expression on the surface of memory CD8+ T cells as a robust marker of immune activation. Although there was substantial interindividual variability, | ||
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Pathogens are able spread effectively in an immunocompromised environment. This means it's possible that AIDS patients pick up substantial pathogen loads. It is further possible that it is these Th1 pathogens, which kill patients. Viral co-infections (including Epstein-Barr virus, Human Herpes Virus 6, etc.) are found in all the diseases the Marshall Protocol treats, but the viruses are not believed to bethe proximate cause of disease. | Pathogens are able spread effectively in an immunocompromised environment. This means it's possible that AIDS patients pick up substantial pathogen loads. It is further possible that it is these Th1 pathogens, which kill patients. Viral co-infections (including Epstein-Barr virus, Human Herpes Virus 6, etc.) are found in all the diseases the Marshall Protocol treats, but the viruses are not believed to bethe proximate cause of disease. | ||
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+ | Mycobacterium avium-intracellulare infection and immunoblastic sarcoma in a fatal case of AIDS. (({{pmid> | ||
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===== CD38 ===== | ===== CD38 ===== | ||
- | CD38 plays a role in effective containment of mycobacteria within granulomata and polarization of Th1 immune responses against Mycobacterium avium. (({{pubmed> | + | CD38 plays a role in effective containment of mycobacteria within granulomata and polarization of Th1 immune responses against Mycobacterium avium. (({{pmid> |
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- | The role of CD38 as a signaling molecule is suggested by the observation that CD38 triggering is involved in T cell costimulation, | + | The role of CD38 as a signaling molecule is suggested by the observation that CD38 triggering is involved in T cell costimulation, |
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- | CD38 expression in HIV-1-infected individuals | + | In mature germinal center B cells, CD38 delivers rescue signals that protect cells from apoptosis and upregulate Bcl-2 (a molecule associated with antiapoptotic effects) in a manner similar to that observed with triggering of CD40, which is known to deliver costimulatory signals to the B cell . In purified T cells, CD38 signaling induces production of high levels of interleukin (IL) 6, granulocyte-macrophage colony-stimulating factor, interferon γ, and IL-10 and low levels of IL-4 and IL-2 (i.e., a cytokine profile shared by T helper 1 and 2 cells) . |
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+ | CD38 expression in HIV-1-infected individuals: | ||
As in most viral infections, HIV-1 infection causes activation of B and T cells (both CD4 and CD8 cells), which consequently upregulates the surface expression of CD38 and other activation markers. CD38 upregulation can be detected on uninfected cells, indicating that this expression is not caused by direct infection. | As in most viral infections, HIV-1 infection causes activation of B and T cells (both CD4 and CD8 cells), which consequently upregulates the surface expression of CD38 and other activation markers. CD38 upregulation can be detected on uninfected cells, indicating that this expression is not caused by direct infection. | ||
===== Research on children ===== | ===== Research on children ===== | ||
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+ | An observational study of children vertically infected with human immunodeficiency virus type 1 (HIV-1) was performed to determine the role of CD38 expression in CD8+ T cells as prognostic marker of virological failure in children receiving HAART. | ||
- | CD38 Expression in CD8+ T Cells Predicts Virological Failure in HIV Type 1–Infected Children Receiving Antiretroviral Therapy | + | We studied 42 children who were receiving |
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- | Infection with HIV-1 induces lymphoid activation, resulting in an increase in T cell activation–associated antigens, such as CD38 [1–3]. Also, CD38 could represent HIV-1–specific or cytokine-activated cells [4–6]. | + | |
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- | It has also been shown that the initiation of antiretroviral therapy | + | |
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- | Children with AIDS had higher CD8+CD38+ MFI values than did children without AIDS (mean ± SEM, 15.83 ± 1.15 vs. 11.54 ± 0.92; P = .008). Also, the CD8+CD38+ percentage was higher in children with AIDS (mean ± SEM, 70.53% ± 2.88%) than in children without AIDS (mean ± SEM, 61.67% ± 3.47%; P = .054). | + | |
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- | In the present study, we confirmed that CD8+CD38+ T cell count is a marker of immune activation and that this expression | + | |
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- | The increase in the CD8+CD38+ T cell count has been associated with elevated VLs in HIV-1–infected children [2] and adults [28]. Tilling et al. [13] monitored | + | |
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- | However, increased CD38 expression in CD8+ T cells obtained from patients with Epstein-Barr virus infection and other infections has been reported [33, 34]. The CD8+CD38+ T cell count may represent a sensitive marker for the early prediction of occurrence of infectious diseases in HIV-1–infected | + | |
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- | In conclusion, in this study, we demonstrate—to our knowledge, for the first time—that CD8+CD38+ T cell count is a good long-term prognostic marker of therapeutic failure in HIV-1–infected | + | |
+ | Children with CD38 values in CD8+ T cells that were higher than the median had a higher incidence and relative risk of virological failure than did those with values lower than the median. In conclusion, we demonstrate for the first time that CD8+CD38+ T cell count is a good prognostic marker of therapeutic failure in HIV-1–infected children. | ||
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===== Notes and comments ===== | ===== Notes and comments ===== | ||
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his HIV-positive patients, even if they are not deficient. | his HIV-positive patients, even if they are not deficient. | ||
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Indeed, a third study here confirmed the risk of bone loss among those with HIV. | Indeed, a third study here confirmed the risk of bone loss among those with HIV. | ||
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* Legacy content | * Legacy content | ||
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- | http:// | + | ===== References =====</ |
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