An important topic IMO.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9361571/
"Dear Editor
Recently, in this journal, Wu et al. (1) and Gao et al. (2) have both indicated that host genetic variation related to COVID-19 might be associated to endometrial cancer. We here add evidence from gene expression analysis supporting that the connection of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and cancer could be more general, in line with several other viral infections that represent serious risks for carcinogenesis in humans. The SARS-CoV-2 has developed similar strategies to Epstein-Barr virus (EBV) and hepatitis B virus (HSV1) to control p53 by hijacking the protein via virus antigens, and ultimately leading to its degradation (3, 4). Specifically, the Nsp2 viral protein of the SARS-CoV-2 interacts with the prohibitin 1 and 2 (PHB1, PHB2) that are primarily located in the mitochondrion and play an essential role in maintaining mitochondrial DNA activity. Their depletion triggers a chain of cell responses that lead to a leakage of reactive oxygen species (ROS) to the nucleus and oxidative damage, that ultimately provokes the impairment of the transactivation of p53-dependent genes. In addition, the Nsp3 SARS-CoV-2 protein binds and activates the RING finger and CHY zinc finger domain-cotainin protein 1 (RCHY1) and E3 ubiquitin ligase, promoting p53 degradation (5). Therefore, SARS-CoV-2 has the ability to trigger external and internal apoptotic pathways of the host cells, facilitating its spread. Impairment of p53 could be seen as a strategy of the virus to take advantage of the cell pathways controlled by this protein for its own benefit during acute phase of infection, therefore evading host immune response and facilitating its replication (3). In this context, a reduced expression of p53 during the acute phase of infection is also a biomarker of severe disease.
Although it has not been demonstrated yet, it has been hypothesized that a long-term inhibition of p53 by the SARS-CoV-2 could be carcinogenic. The onco-suppressive protein p53 is a key player within the apoptotic signaling pathway and regulates the expression of about 500 target genes; therefore, it plays a role in cell cycle arrest, cell aging, cell death, etc. (6). We examine three gene expression datasets to demonstrate that p53 is downregulated during acute SARS-CoV-2 infection and long coronavirus-disease 19 (COVID-19); a long-term reduction of p53 could be interpreted as a risk factor in carcinogenesis."
Dietary suppression of MHC class II expression in intestinal epithelial cells enhances intestinal tumorigenesis
For what it's worth here's my own list of supplements to help prevent and treat sars-covid-2 infection:
Allicin May Promote Reversal of T-Cell Dysfunction in Periodontitis via the PD-1 Pathway
Abstract
"We evaluated the role of allicin in periodontitis using an in silico and in vitro design. An in silico docking analysis was performed to assess the plausible interactions between allicin and PD-L1. The cytokine profile of gingival crevicular fluid (GCF) samples obtained from periodontitis patients was estimated by cytometric bead array. CD3+ lymphocytes isolated from the peripheral blood were sorted and characterized using immunomagnetic techniques. Cultured and expanded lymphocytes were treated with the GCF samples to induce T-cell exhaustion. Optimum concentrations of allicin were added to exhausted lymphocytes to compare the expression of TIM-3 and LAG-3 gene expression at baseline and post-treatment. Allicin was found to bind to the PD-L1 molecule as revealed by the in-silico experiment, which is possibly an inhibitory interaction although not proven. GCF from periodontitis patients had significantly higher concentrations of TNF-α, CCL2, IL-6, IFN-γ, and CXCL8 than controls. GCF treatment of CD3+ lymphocytes from the periodontitis patients significantly increased expression of T-cell exhaustion markers TIM-3 and LAG-3. Allicin administration with GCF treatment resulted in significant lowering of the expression of exhaustion markers. Allicin may exert an immunostimulatory role and reverse immune-destructive mechanisms such as T-cell exhaustion."
Clinical implications of T cell exhaustion for cancer immunotherapy
Histone deacetylase inhibition up-regulates MHC class I to facilitate cytotoxic T lymphocyte-mediated tumor cell killing in glioma cells
The comparative weight of thymus gland was linearly (p ¼ .0004) and quadratically (p ¼ .0390) increased in birds fed diet plus BS. The relative weight of spleen linearly (p ¼ .0416) enhanced in BS groups than the control group (Table 7). It is worth noting that the highest comparative weights of thymus and spleen were recorded in birds fed diets supplemented with 1.5 g/kg diet. In contrast, BS supplementation to broiler diet numerically increased the relative weight of bursa compared with the untreated birds. In the current study, WBCs, monocytes % and lymphocytes % were insignificantly impacted by the Boswellia trail. While, heterocyst % was quadratically (p ¼ .0063) reduced in birds fed diet plus BS compared to the control (Table 7).
https://www.tandfonline.com/doi/pdf/10.1080/1828051X.2021.1875336
https://www.nature.com/articles/s41598-022-24053-4
In the population of US veterans, we show that Vitamin D2 and D3 fills were associated with reductions in COVID-19 infection of 28% and 20%, respectively [(D3 Hazard Ratio (HR) = 0.80, [95% CI 0.77, 0.83]), D2 HR = 0.72, [95% CI 0.65, 0.79]]. Mortality within 30-days of COVID-19 infection was similarly 33% lower with Vitamin D3 and 25% lower with D2 (D3 HR = 0.67, [95% CI 0.59, 0.75]; D2 HR = 0.75, [95% CI 0.55, 1.04]). We also find that after controlling for vitamin D blood levels, veterans receiving higher dosages of Vitamin D obtained greater benefits from supplementation than veterans receiving lower dosages.
How many lives could have been saved? I remember watching a program on BBC during the early stages of the pandemic, one of the guests suggested vitamin D and was treated with complete disregard by the BBC news anchor.
The Use of Natural Agents to Counteract Telomere Shortening: Effects of a Multi-Component Extract of Astragalus mongholicus Bunge and Danazol
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7168059/
"A link between telomere shortening and oxidative stress was found in aging people and patients with cancer or inflammatory diseases. Extracts of Astragalus spp. are known to stimulate telomerase activity, thereby compensating telomere shortening. We characterized a multi-component hydroethanolic root extract (HRE) of Astragalus mongholicus Bunge and assessed its effects on telomeres compared to those of danazol. Astragalosides I to IV, flavonoids, amino acids and sugars were detected in the HRE. Samples of peripheral blood lymphocytes with short telomeres from 18 healthy donors (mean age 63.5 years; range 32–86 years) were exposed to a single dose of 1 µg/mL HRE or danazol for three days. Telomere length and telomerase expression were then measured. Significant elongation of telomeres associated to a less toxicity was observed in lymphocytes from 13/18 donors following HRE treatment (0.54 kb (0.15–2.06 kb)) and in those from 9/18 donors after danazol treatment (0.95 kb (0.06–2.06 kb)). The rate of cells with short telomeres (<3 kb) decreased in lymphocytes from all donors after exposure to either HRE or danazol, telomere elongation being telomerase-dependent. These findings suggest that the HRE could be used for the management of age-related diseases."
Effects of AHCC on the Interaction between T and B Lymphocytes
https://digitalscholarship.tsu.edu/cgi/viewcontent.cgi?article=1004&context=theses
