COVID-19, Epigenetic Changes, and Atopic Dermatitis: Potential Links to Genetic Markers Like LMAN2, RPS20P17, and rs9313758

By SWA

A detailed explanation to COVID-19 related epigenetic changes and atopic dermatitis

The COVID-19 pandemic has unveiled complex interactions between viral infections, immune responses, and pre-existing conditions such as atopic dermatitis (AD). Beyond viral pathogenesis, emerging research highlights the interplay of epigenetic changes and genetic factors in influencing disease severity and individual susceptibility. Genes like LMAN2, pseudogenes such as RPS20P17, and single nucleotide polymorphisms (SNPs) like rs9313758 have become focal points for understanding how COVID-19 exacerbates inflammatory diseases, including atopic dermatitis.

LMAN2: A Glycoprotein Regulator in Viral and Immune Pathways

LMAN2 encodes a mannose-binding lectin protein that plays a vital role in the transport and quality control of glycoproteins in the endoplasmic reticulum (ER) and Golgi apparatus. This gene has implications for immune regulation and cellular stress, both of which are critical in COVID-19 infection and atopic dermatitis.

Biological Functions of LMAN2

  • Glycoprotein Processing: LMAN2 ensures proper folding and trafficking of glycoproteins, which are critical for immune system function, including cytokine signaling. Dysregulated glycoprotein transport can lead to ER stress, a key driver of inflammation in conditions like AD and viral infections.
  • Viral Hijacking of Host Systems: Viruses such as SARS-CoV-2 exploit glycoprotein pathways to assemble and secrete viral particles. A compromised LMAN2 system could impair viral clearance, prolonging inflammation and immune activation.

LMAN2 in Atopic Dermatitis and COVID-19

  • In AD, heightened ER stress and glycoprotein misprocessing contribute to increased inflammation and barrier dysfunction. COVID-19 may amplify these effects, as viral infections are known to exacerbate AD symptoms via cytokine storms and immune dysregulation.
  • LMAN2 dysfunction may also fuel systemic inflammation in COVID-19 patients, particularly in individuals with pre-existing inflammatory conditions like AD.

RPS20P17: Pseudogenes and Immune Modulation

While pseudogenes like RPS20P17 are traditionally viewed as "non-functional," growing evidence suggests they play a role in gene regulation and immune responses. RPS20P17 shares homology with the ribosomal protein S20, which is involved in protein synthesis, and may indirectly influence immune activity.

Potential Roles in COVID-19 and AD

  • MicroRNA Decoys: RPS20P17 may act as a decoy for microRNAs that regulate ribosomal or immune-related genes, potentially affecting inflammatory responses during COVID-19 infections or in chronic diseases like AD.
  • Inflammatory Pathways: If RPS20P17 modulates immune gene expression, it could serve as a reservoir for regulatory interactions under conditions of immune activation, such as viral infections or eczema flares.

rs9313758: A Genetic Marker with Context-Specific Effects

The SNP rs9313758, identified in genome-wide association studies (GWAS), has been linked to metabolic traits such as fasting glucose and Type 2 diabetes. It is located near LMAN2 and may influence its expression or regulation, with broader implications for inflammatory and viral diseases.

Tissue-Specific Implications

  • Pancreatic Islets and Liver: rs9313758 has shown tissue-specific effects as an expression Quantitative Trait Locus (eQTL) for LMAN2 in the liver and pancreas. Dysfunction in these tissues could exacerbate metabolic complications in COVID-19 patients, compounding inflammation and oxidative stress.
  • Immune Cells and Skin: In tissues relevant to AD, such as immune cells and skin, rs9313758 may alter LMAN2 expression. This could affect glycoprotein-mediated signaling, potentially worsening the inflammatory profile of AD during viral infections.

Link to Epigenetics

Epigenetic modifications such as DNA methylation and histone modifications could amplify the functional effects of rs9313758. For example:

  • COVID-19 has been shown to induce global changes in DNA methylation patterns, which may intersect with the regulatory effects of rs9313758.
  • These interactions could exacerbate AD by upregulating pro-inflammatory genes or suppressing genes involved in skin barrier repair.

Epigenetic Changes in COVID-19 and Atopic Dermatitis

Epigenetic modifications, which control gene expression without altering DNA sequences, are pivotal in both COVID-19 pathogenesis and AD exacerbations.

  1. DNA Methylation and LMAN2: Viral infections can trigger hypomethylation of genes like LMAN2, leading to overexpression and potential glycoprotein transport dysfunction. In AD patients, this could exacerbate inflammatory cascades and disrupt barrier function.
  2. Histone Modifications and Immune Genes: Histone acetylation patterns associated with RPS20P17 or nearby immune-related genes may shift during viral infections, promoting inflammatory cytokine production.
  3. Non-Coding RNAs and SNP Regulation: SNPs like rs9313758 may interact with non-coding RNAs (e.g., microRNAs) to fine-tune the expression of LMAN2, especially in immune or skin tissues. Dysregulation of these pathways could worsen AD symptoms during COVID-19.

Crossroads of COVID-19, Atopic Dermatitis, and Genetic Markers

The intersection of COVID-19, atopic dermatitis, and genetic/epigenetic factors underscores the importance of personalized medicine. Here's why:

  • Pre-existing Conditions: AD patients may already have heightened ER stress and inflammatory signaling. A genetic variant like rs9313758 could exacerbate this vulnerability during COVID-19.
  • Therapeutic Implications: Drugs targeting glycoprotein processing pathways, ER stress, or epigenetic modifiers could hold promise for patients with overlapping conditions.
  • Biomarker Potential: SNPs like rs9313758 and epigenetic profiles of LMAN2 could serve as biomarkers for predicting COVID-19 severity in AD patients or the likelihood of flare-ups during viral infections.

Conclusion

COVID-19 has shed light on the intricate relationship between genetic factors, epigenetic changes, and pre-existing conditions like atopic dermatitis. Genes like LMAN2, pseudogenes like RPS20P17, and variants like rs9313758 provide valuable insights into the molecular mechanisms linking viral infections to inflammatory diseases. Future research unraveling these connections will pave the way for targeted therapies and precision medicine approaches to mitigate the burden of both COVID-19 and atopic dermatitis.

 © 2000-2025 Sieglinde W. Alexander. All writings by Sieglinde W. Alexander have a fife year copy right. Library of Congress Card Number: LCN 00-192742 ISBN: 0-9703195-0-9

Comments

Post a Comment

Popular posts from this blog

Toxic Skin Condition Post-mRNA COVID-19 Vaccination

By SWA
Image
Identifying Severe Skin Conditions Post-Vaccination Following administration of the BioNTech mRNA vaccine, a small subset of individuals may develop severe and complex reactions. These reactions are often misdiagnosed or misunderstood due to their rarity and diverse presentation. This essay examines a case characterized by severe skin conditions, systemic symptoms, and complications such as hypercalcemia and crystal formation. It highlights the need for accurate diagnosis, holistic management, and increased awareness of these rare but significant vaccine-related adverse events. Initial Symptoms and Misdiagnoses Severe symptoms began shortly after the first dose of the BioNTech vaccine, initially presenting as petechiae, diagnosed by a rheumatologist. However, following the second dose, symptoms rapidly escalated, resulting in intense burning pain and thinning of the skin. The skin on the legs and thighs became paper-thin and could tear with the slightest touch, with the affected area e...
Read more

Dysferlin Protein: Key Roles, Genetic Locations

By SWA
Image
The purpose of this article is to share and discuss the details of a new discovery, which is highlighted within: CRISPR-Cas9: A Breakthrough Tool to Repair the DYSF Gene The dysferlin protein plays an essential role in maintaining the integrity of muscle cell membranes, particularly in tissues that endure significant mechanical stress, such as skeletal and cardiac muscles . Encoded by the DYSF gene , dysferlin is indispensable for repairing damaged cell membranes after injury caused by muscle contraction or external forces. This article explores the main locations where dysferlin is produced, its role in muscle repair, and supportive nutritional and therapeutic strategies for individuals with dysferlin deficiency, such as those affected by dysferlinopathies (e.g., Limb-Girdle Muscular Dystrophy Type 2B or Miyoshi Myopathy). Currently, there is no definitive answer as to why the severity of dysferlin protein expression or depletion varies. Do pathogens play a role in the methylation o...
Read more

Is ME CFS connected to Spinal Muscular Atrophy (SMA) or Post Polio?

By SWA
Image
Today, I understand why Spinal Muscular Atrophy (SMA) received little attention, particularly in the mid-50s. This complex and debilitating genetic illness was poorly understood, and patients' symptoms were often minimized or even dismissed. For more information, please visit the Spinal Muscular Atrophy (SMA) page on MalaCards . Even now, many neurologists lack detailed knowledge of SMA, and comprehensive examinations mentioned in research are rarely pursued. In 2008, while investigating permanent adrenal insufficiency, an MRI ordered by my endocrinologist unexpectedly revealed Chiari Malformation II. However, surgery in 2009 brought no improvement. In 2010, a DNA test showed a genetic marker in the ACTN3 gene: https://www.malacards.org/search/results?q=ACTN3%20gene%20and%20Spinal%20Muscular%20Atrophy%20(SMA) A 2015 MRI revealed ankylosing spondylitis, multiple Tarlov cysts, stenosis at L4 and L5, spinal canal narrowing, and widespread degenerative changes. Surgery on L4 and L5 ...
Read more