gut health

Oral virome

Avoiding viral infections in microbiome transplantations

“These viruses all have latent stages that allow them to escape immune detection and reactivate after exposure to various stimuli. Furthermore, their tropism for CNS and immune system cells explains their possible deleterious function in neuroinflammation.”[1] This image came from a review on Epstein Bar Virus and multiple sclerosis. [1]

The immunological mechanism involved in EBV can cause MS.

  1. EBV infects naive B cells, so these cells proliferate in the germinal centers. Then the receptor of B cells or BCR and proteins of EBV are latent in the self-reactive memory cells.
  2. B: blood circulation:. Memory cells infected with EBV leave the lymph node and enter the bloodstream.
  3. C: Brain: Memory cells that are EBV-infected will enter the brain cells (neurons) and stay there.
  4. In neurons, autoreactive T-cells that have already entered the brain cause damage to neurons in two ways.
  5. Infected memory cells signal B7 stimulus to CD28 receptors on the surface of active autoreactive T-cells.
  6. These co-stimulus signals activate T-cells by producing interferon-gamma, interferon-beta, and IL-2.
  7. Autoreactive T-cells detect apoptotic myelin fragments by microglia (brain macrophages) through MCH, eventually causing further apoptosis of the myelin sheath around neurons.
  8. Autoantibodies produced by B cells infected with EBV sit on the myelin sheath, releasing myelin and oligodendrocyte fragments.
  9. Released myelin fragments by MHC memory cells that are EBV-infected are given to the autoreactive T-cells, and this degradation process by the T-cells continues

If not EBV, could other human viruses enter through the tonsils?

Herpes Simplex Virus and two periodontal pathogens [2]

“Alpha-herpesviridae include HSV 1 & 2 and VZV. After primary infection of epithelial cells, latent infection in peripheral trigeminal ganglia.218 Beta-herpesviridae include CMV & HHV 6 & 7. Tropism is broad, although CMV is preferentially found in monocytes/macrophages, endothelial cells.219 The lymphotropic gamma-herpesviridae include EBV & HHV8 Kaposi that establish latent infections in lymphoid cells.” [2]

The Chen review came out of the Herman Ostrow School of Dentistry, University of Southern
California, Los Angeles. [2] This 40+ page document compared virulence factor of two periodontitis producing bacteria: Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis.

  • A actinomycetemcomitans serotype b predominates in severe periodontitis and serotype c is associated with a healthy periodontium in the USA and Finland Then the freview starts into the
  • The genetic locus of A. serotype b JP2 clone of A actinomycetemcomitans expresses leukotoxin A whose gene is in a single operon of 4 genes, namely, ltxC, ltxA, ltxB, and ltx D.
  • The other 3 genes encode proteins involved in the transportation (ltxB and ltxD) and post-translational modification (ltxC) of the toxin

The PDF file of this review was key word searched for “ferment”. Only a reference was found “Fermentable-sugar-level-dependent regulation of leukotoxin synthesis in a variably toxic strain of Actinobacillus” Reading of just the abstract on PubMed revealed that leukotoxin A is induced when the medium is fructose limited via the second messenger cAMP. So fructose is good? what about pectin? Nothing we can easily obtain in North America, but there is there was something on orange peel extract. [3]

“Prevotella intermedia and Porphyromonas gingivalis were resistant to aqueous extracts while Aggregatibacter actinomycetemcomitans was inhibited at very high cncentrations. Hot ethanolic extracts showed significantly higher zone of inhibition than cold ethanolic extract. Minimum inhibitory concentration of hot and cold ethanolic extracts of Citrus sinensis peel ranged between 12-15 mg/ml against all three periodontal pathogens.”

Pseudomonas aeruginosa intestinal carriage rates are significantly higher in immunosuppressed individuals and hospitalized patients who therefore have increased risk of infections and antibiotic-associated diarrhea. To combat intestinal dysbiosis and decolonize P. aeruginosa from gastrointestinal tract, we investigated the anti-adherence and gut microbiota modulation properties of marine prebiotic fucoidans.

Methods: Proteomic analysis of culture supernatant was performed by LC-MS/MS. Using lectin-based enzyme-linked immunosorbent assay, hemagglutinin domain interaction and inhibition with biomolecules were studied. We investigated the role of nutritional grade fucoidans in a mouse model and used 16S ribosomal RNA sequencing to examine fecal microbiota composition.

Analysis of culture supernatant proteins indicated the secretion of two-partner secretion (TPS) family proteins, including TpsA1/CdiA2 and TpsA2/CdiA1. Lectin like activity at the N-terminal of TpsA due to a conserved hemagglutinin domain (Pfam identifier [ID] PF05860) mediates binding to mucins that carry multiple fucosylated glycans. Fucose-rich sulfated polysaccharides (fucoidans) and sulfated dextrans were found to be potent inhibitors of the recombinant N-terminal hemagglutinin domain of TpsA (TpsA-NT-HAD) binding to mucins.


  1. Sedighi S, Gholizadeh O, Yasamineh S, Akbarzadeh S, Amini P, Favakehi P, Afkhami H, Firouzi-Amandi A, Pahlevan D, Eslami M, Yousefi B, Poortahmasebi V, Dadashpour M. Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis. Curr Microbiol. 2022 Dec 2;80(1):15.PMC free article
  2. Chen C, Feng P, Slots J. Herpesvirus-bacteria synergistic interaction in periodontitis. Periodontol 2000. 2020 Feb;82(1):42-64. PMC free article
  3. Hussain KA, Tarakji B, Kandy BP, John J, Mathews J, Ramphul V, Divakar DD. Antimicrobial effects of citrus sinensis peel extracts against periodontopathic bacteria: an in vitro study. Rocz Panstw Zakl Hig. 2015;66(2):173-8. free article
  4. Janapatla RP, Dudek A, Chen CL, Chuang CH, Chien KY, Feng Y, Yeh YM, Wang YH, Chang HJ, Lee YC, Chiu CH. Marine prebiotics mediate decolonization of Pseudomonas aeruginosa from gut by inhibiting secreted virulence factor interactions with mucins and enriching Bacteroides population. J Biomed Sci. 2023 Feb 2;30(1):9. PMC free article

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