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What if the same genetic mutation was consistently correlated with the following issues?
Long Haul 
Hepatitis - severity of liver fibrosis 
tick-borne encephalitis virus infection 
ME CFS - regression analysis from 4,000 clinically diagnosed ME CFS database of 4,000
Reports of influenza severity in mexican population 
Mold Illness: IL-10 response is different for MDR Bacterial Infections (think mold colonization of MDR resistant Staph bacteria) versus non MDR Bacterial Infections.  Read the section at the very end of the blog article for this part.
Associated with Chrones Disease in Pediatrics 
Associated with IBD (Irritable Bowel Disease) 
Associated with Lupus 
I just tied IL-10 across: Long Haul, ME CFS, Lyme, Mold, Flue, Hepatatis......interested ?
Read more:). And not just IL-10, a specific mutation on a specific location on IL-10, for everything but Mold.
Would this be sort of interesting, interesting, or well, use your favorite string of 4 letter words.....
To be clear, i am not suggesting that this SNP alone causes the above, nor that it by itself is the only factor. Rather, lets all get curious about the role it could be playing in both the pathogensis of these viral / bacterial infections and the potential solutions......
IL - 10 Holds Much Interest To Me In Chronic Illness
Modulates gut inflammatory responses
Directly connected to IL-6, an inflammatory cytokine
Controls TNFA, an inflammatory cytokine
Inhibits a gene (CPOX) in the heme pathway
Is inhibited by the mycotoxins Citrin, and Gliotoxin
Is elevated by the mycotoxin Zearalanone
Helps regulate a number of immune functions and pathways
Is often found initially elevated in ME CFS, and then much lower later on in ME CFS
Modulated By Aryl Hydrocarbon Receptor (AHR)
AHR modulates SOOOOO many genes (NMDA receptors, Typtophan pathway (IDO1/2), and is master regulator of a number of immune functions, like IL-10
IL-10 modulates CD 8 cells, and Norepinephrine preferentially modulates memory CD8 T cell function . Norepenephrine is blocked by copper deficiency and overgrowth of pathogenic clostridia bacteria.
IL-10 can be modulated by viral IL-10 Homologs so they can survive and manipulate the host immune response. Think EBV especially, see more below.
IL-10 Induces JAK/Stat;
Different Virusues Up-Regulate IL-10 Enhancing Infection Via Immuno Suppression
IL-10 is a key player in the establishment and perpetuation of viral persistence
The Blockade of IL-10 by various cells to end viral persistence
Based on statistical regression analysis I requested, a researcher queried a genetic database of 4,000 clinically diagnosed ME CFS folks, and the most statistically relevant mutation was on............. IL-10.......and......this same mutation plays a role in recovery from hepatitis....
"IL10 −819T (rs1800871), −592A (rs1800872), and +504T (rs3024490) alleles were associated with treatment-induced hepatitis B surface antigen (HBsAg) seroclearance. Additionally, IL10 ATAC haplotype increased the chance of HBsAg loss and was significantly more frequent in patients with less liver injury. Moreover rs1800871TT, rs1518110TT, rs1800872AA, and rs3024490TT genotypes were identified as predictors of a lower FIB-4 score (<0.5)."
......what do you know, these same variants are in play in Long Haul.....just a coincidence:)
"Polymorphisms in the interleukin-10 (IL10) gene have been linked to the severity of the patients infected with the viral infections. This study aimed to assess if the IL10 gene polymorphisms rs1800871, rs1800872, and rs1800896 were linked to coronavirus disease 19 (COVID-19) mortality in different severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants in the Iranian population......The obtained finding indicated IL10 rs1800871 CC genotype in the Alpha variant and CT genotype in the Delta variant had a relationship with COVID-19 mortality; however, there was no association between rs1800871 polymorphism and the Omicron BA.5 variant. The COVID-19 mortality rate was associated with IL10 rs1800872 TT genotype in the Alpha and Omicron BA.5 variants and GT in the Alpha and Delta variants. The COVID-19 mortality rate was associated with IL10 rs1800896 GG and AG genotypes in the Delta and Omicron BA.5; nevertheless, there was no association between rs1800896 polymorphism with the Alpha variant. According to the obtained data, the GTA haplotype was the most common of haplotype in different SARS-CoV-2 variants. The TCG haplotype was related to COVID-19 mortality in the Alpha, Delta and Omicron BA.5 variants."
*****Same Variants in Play With tick-borne encephalitis virus infection*****
Elevated IL-10 & Covid
"Mortality of COVID-19 patients is caused by severe pneumonia and vital organ damage with the involvement of many proinflammatory mediators......
In support of this hypothesis, first, the inflammatory/immune-stimulating cytokines discussed in the previous text (IL-2Rα, IL-4, IL-7, IL-18, IFN-γ, GM-CSF, TNF-α, and chemokines IP-10 and CXCL9) are elevated in peripheral blood in severe/critically ill COVID-19 patients. Second, severe/critically ill COVID-19 patients bear circulating hyperactivated and proliferating cytotoxic CD8+ T cells despite a total reduction in peripheral CD8+ T-cell count. Furthermore, correlating with high serum IL-10 in severe/critically ill COVID-19 patients, the percentages of IFN-γ-producing effector CD4+ and CD8+ T cells can be increased in peripheral blood. Third, as COVID-19 disease progresses, exhausted PD-1+TIM3+CD8+ T cells in the peripheral blood of patients have been found to increase, and these correlate with serum IL-10 concentrations in COVID-19 patients, suggesting a role of IL-10 in T cell exhaustion, presumably via overactivation and proliferation. Such immune features in severe/critically ill COVID-19 patients with highly elevated systemic IL-10 have led us to speculate that IL-10 might play a pathological role in COVID-19 disease progression. However, this hypothesis remains to be rigorously tested.
In this scenario, how might elevated IL-10 contribute to COVID-19 mortality – if at all? The immunopathological pathway leading to patient death following SARS-CoV-2 infection can be divided into three stages: initiation, amplification, and consummation. We propose that early induction of IL-10 upon SARS-CoV-2 infection during the initiation phase in the lung might indeed represent a negative feedback mechanism that serves as a countermeasure to inflammation caused by other proinflammatory mediators. However, as endogenous IL-10 production increases, we speculate that it might function as an immune activating/proinflammatory agent that stimulates the production of other mediators of the cytokine storm. As reported for human endotoxemia, IL-10 might also amplify the viral sepsis-related hyperinflammation observed in some severe/critically ill COVID-19 patients. Because IL-10 directly expands cytotoxic effector CD8+ T cells in human studies, hyperactivation of adaptive immunity in COVID-19 patients might contribute to exacerbating disease severity. Although this possibility remains conjectural, we posit that the combined effects of IL-10 in promoting systemic inflammatory cytokine production and stimulating T cell activation and proliferation in COVID-19 patients might contribute to a lethal immunopathological process.
Currently, clinical trials are underway to test the therapeutic efficacy of blocking agents, either alone or in combination with more than ten inflammatory mediators reported as highly elevated in COVID-19 patients presenting a cytokine storm. Preliminary results from using blocking/neutralizing antibodies against IL-6/IL-6R, GM-CSF, and IL-1 suggest that further improvement is necessary to lower mortality in COVID-19 patients. By attempting to block its pathological proinflammatory function, we suggest that IL-10 might constitute a potential target to reduce COVID-19 mortality. As such, the timing of blocking IL-10 activity in severe/critically ill COVID-19 patients might be crucial. We propose that using a neutralizing antibody to block IL-10 to limit its potential immune-activating effects in the initiation phase of COVID-19 may be worth testing. Furthermore, we argue that combinatorial targeting of multiple proinflammatory mediators including IL-10, chemokines, IL-6, and IL-1 might be necessary to substantially reduce mortality in severe/critically ill COVID-19 patients. Evidently, the potential roles of systemically elevated IL-10 in COVID-19 pathogenesis and putative treatments warrant robust experimental validation, but certainly merit further attention."
IL-10 / IL-6 : Covid Severity
The ratio of IL-6/lymphocytes was positively correlated with the risk of mortality, while IL-10/lymphocytes ratio could predict respiratory failure in ICU. IL-6/IL-10 profiling revealed that deceased patients have different magnitudes of both IL-6 and IL-10 cytokine release. Notably, excessive levels of IL-6 concomitant with high levels of IL-10 were more common in diseased COVID-19 patients. Taking into account the IL-6/IL-10 profiling may help clinicians to identify the right time of anti-inflammation treatment and select patients who will respond to anti-cytokine therapies and maintain an adequate inflammatory response for SARS-CoV-2 clearance."
Mini-review The paradoxical role of IL-10 in immunity and cancer Mark H. Mannino a , Ziwen Zhu. Cancer Letters (2015) By Mark H. Mannino, et al., The paradoxical role of IL-10 in immunity and cancer, Cancer Letters (2015), doi: 10.1016/j.canlet.2015.07.009 Contents lists available at ScienceDirect Cancer Letters.
The role of IL-10 in regulating immunity to persistent viral infections
Cytokine Profiles Associated With Acute COVID-19 and Long COVID-19 Syndrome
Deciphering the balance of IL-6/IL-10 cytokines in severe to critical COVID-19 patients International Journal of Infectious Diseases. Volume 96, July 2020, Pages 260-265.
Genetic variation in IL-10 influences the progression of hepatitis B infection. By Magda Rybicka a, Anna Woziwodz. Int J Infect Disease. 2020 Jul:96:260-265.
Association between interleukin-10 gene polymorphisms (rs1800871, rs1800872, and rs1800896) and severity of infection in different SARS-CoV-2 variants. By Sattar Jabbar Abbood Abbood,1 Enayat Anvari. Hum Genomics. 2023; 17: 19. Published online 2023 Mar 7. doi: 10.1186/s40246-023-00468-6. PMCID: PMC9990970. PMID: 36882862
A database of human genes and a gene network involved in response to tick-borne encephalitis virus infection. Elena V. Ignatieva,1,3,4 Alexander V. Igoshin, BMC Evol Biol. 2017; 17(Suppl 2): 259. Published online 2017 Dec 28.https://doi.org/10.1186/s12862-017-1107-8. PMCID: PMC5751789. PMID: 29297316
Martinez-Ocan˜a J, Olivo-Diaz A, Salazar-Dominguez T, et al. Plasma cytokine levels and cytokine gene polymorphisms in Mexican patients during the influenza pandemic A(H1N1)pdm09. J Clin Virol 2013;58:108–113.
Norepinephrine preferentially modulates memory CD8 T cell function inducing inflammatory cytokine production and reducing proliferation in response to activation
Expanding the Current Knowledge About the Role of Interleukin-10 to Major Concerning Bacteria. By Hernán F. Peñaloza1 Loreani P. Noguera. Front. Microbiol., 18 September 2018
Association of polymorphisms in the IL-10 promoter region with Crohn's disease
Interleukin 10 gene promoter polymorphisms (rs1800896, rs1800871 and rs1800872) and haplotypes are associated with the activity of systemic lupus erythematosus and IL10 levels in an Iranian population. Saeed Mohammadi 1, Marie Saghaeian Jazi. Int J Immunogenet. 2019 Feb;46(1):20-30. doi: 10.1111/iji.12407. Epub 2018 Nov 15. PMID: 30430731. DOI: 10.1111/iji.12407