Mya Symons
Mya Symons
- Messages
- 1,029
- Location
- Washington
I have been trying a variety of supplements and herbs to see how they work for CFS and Fibromyalgia. Recently, it has been supplements for Herpes Viruses. I have wanted to get off the Valtrex for a long time because it can interfere with Cell Mitochondria development (this is how it also stops HSV). I have had some success with some herbs and have not had to use the Valtrex for months now and I wanted to share that with you. I also have had no swollen lymph nodes which I believe has to do with Epstein Barr.
First, I have been using Curcumin, which slows herpes viruses down.
Next, Resveratrol, which interferes with HSV1 and HSV2 replication.
Third, Moringa Oliefera leaf and seed extract which interferes with Epstien Barr replication (this one is also a superfood that provides many vitamins, minerals, amino acids, etc. that are good for the body.)
Fourth, the Pall protocol. I don't have evidence that it helps with Herpes Viruses, but it makes me feel so much better, I believe it does.
Finally, Chaparral Extract. This I only use when I feel swollen lymph nodes coming on because it can be toxic to the liver so it has to be used sparingly. I think there is an article on Phoenix Rising somewhere about this one.
Here are some journal articles on the herbs I mentioned:
Pharmacology
© Georg Thieme Verlag Stuttgart · New York
Niaziminin, a Thiocarbamate from the Leaves of Moringa oleifera, Holds a Strict Structural Requirement for Inhibition of Tumor-Promoter-Induced Epstein-Barr Virus Activation
Akira Murakami1 , Yumi Kitazono2 , Suratwadee Jiwajinda3 , Koichi Koshimizu1 , Hajime Ohigashi2
PDF Download Buy Article Permissions and Reprints
Abstract
Three known thiocarbamate (TC)- and isothiocyanate (ITC)-related compounds have been isolated from the leaves of Moringa oleifera, a traditional herb in southeast Asia, as inhibitors of tumor promoter teleocidin B-4-induced Epstein-Barr virus (EBV) activation in Raji cells. Interestingly, only niaziminin among 10 TCs including 8 synthetic ones showed considerable inhibition against EBV activation. The structure-activity relationships indicated that the presence of an acetoxy group at the 4′-position of niaziminin is important and indispensable for inhibition. On the other hand, among the ITC-related compounds, naturally occurring 4-[(4′-O-acetyl-α-L-rhamnosyloxy)benzyl]ITC and commercially available allyl- and benzyl-ITC significantly inhibited activation, suggesting that the isothiocyano group is a critical structural factor for activity.
Key words
Anti-tumor promoter - niaziminin - Epstein-Barr virus - thiocarbamate - isothiocyanate - Moringa oleifera - Moringaceae
Curcumin inhibits herpes simplex virus immediate-early gene expression by a mechanism independent of p300/CBP histone acetyltransferase activity
Abstract
Curcumin, a phenolic compound from the curry spice turmeric, exhibits a wide range of activities in eukaryotic cells, including antiviral effects that are at present incompletely characterized. Curcumin is known to inhibit the histone acetyltransferase activity of the transcriptional coactivator proteins p300 and CBP, which are recruited to the immediate early (IE) gene promoters of herpes simplex virus type 1 (HSV-1) by the viral transactivator protein VP16. We tested the hypothesis that curcumin, by inhibiting these coactivators, would block viral infection and gene expression. In cell culture assays, curcumin significantly decreased HSV-1 infectivity and IE gene expression. Entry of viral DNA to the host cell nucleus and binding of VP16 to IE gene promoters was not affected by curcumin, but recruitment of RNA polymerase II to those promoters was significantly diminished. However, these effects were observed using lower curcumin
oncentrations than those required to substantially inhibit global H3 acetylation. No changes were observed in histone H3 occupancy or acetylation at viral IE gene promoters. Furthermore, p300 and CBP recruitment to IE gene promoters was not affected by the presence of curcumin. Finally, disruption of p300 expression using a short hairpin RNA did not affect viral IE gene expression. These results suggest that curcumin affects VP16-mediated recruitment of RNA polymerase II to IE gene promoters by a mechanism independent of p300/CBP histone acetyltransferase activity.
Resveratrol inhibition of herpes simplex virus replication
Resveratrol, a phytoalexin, was found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner. The observed reduction in virus yield was not caused by the direct inactivation of HSV by resveratrol nor inhibition of virus attachment to the cell. The chemical did, however, target an early event in the virus replication cycle since it was most effective when added within 1 h of cell infection, less effective if addition was delayed until 6 h post-infection and not effective if added 9 h post-infection. Resveratrol was also found to delay the cell cycle at S–G2–M interphase, inhibit reactivation of virus from latently-infected neurons and reduce the amount of ICP-4, a major immediate early viral regulatory protein, that is produced when compared to controls. These results suggest that a critical early event in the viral replication cycle, that has a compensatory cellular counterpart, is being adversely affected.
First, I have been using Curcumin, which slows herpes viruses down.
Next, Resveratrol, which interferes with HSV1 and HSV2 replication.
Third, Moringa Oliefera leaf and seed extract which interferes with Epstien Barr replication (this one is also a superfood that provides many vitamins, minerals, amino acids, etc. that are good for the body.)
Fourth, the Pall protocol. I don't have evidence that it helps with Herpes Viruses, but it makes me feel so much better, I believe it does.
Finally, Chaparral Extract. This I only use when I feel swollen lymph nodes coming on because it can be toxic to the liver so it has to be used sparingly. I think there is an article on Phoenix Rising somewhere about this one.
Here are some journal articles on the herbs I mentioned:
Pharmacology
© Georg Thieme Verlag Stuttgart · New York
Niaziminin, a Thiocarbamate from the Leaves of Moringa oleifera, Holds a Strict Structural Requirement for Inhibition of Tumor-Promoter-Induced Epstein-Barr Virus Activation
Akira Murakami1 , Yumi Kitazono2 , Suratwadee Jiwajinda3 , Koichi Koshimizu1 , Hajime Ohigashi2
PDF Download Buy Article Permissions and Reprints
Abstract
Three known thiocarbamate (TC)- and isothiocyanate (ITC)-related compounds have been isolated from the leaves of Moringa oleifera, a traditional herb in southeast Asia, as inhibitors of tumor promoter teleocidin B-4-induced Epstein-Barr virus (EBV) activation in Raji cells. Interestingly, only niaziminin among 10 TCs including 8 synthetic ones showed considerable inhibition against EBV activation. The structure-activity relationships indicated that the presence of an acetoxy group at the 4′-position of niaziminin is important and indispensable for inhibition. On the other hand, among the ITC-related compounds, naturally occurring 4-[(4′-O-acetyl-α-L-rhamnosyloxy)benzyl]ITC and commercially available allyl- and benzyl-ITC significantly inhibited activation, suggesting that the isothiocyano group is a critical structural factor for activity.
Key words
Anti-tumor promoter - niaziminin - Epstein-Barr virus - thiocarbamate - isothiocyanate - Moringa oleifera - Moringaceae
Curcumin inhibits herpes simplex virus immediate-early gene expression by a mechanism independent of p300/CBP histone acetyltransferase activity
- a Graduate Program in Cell and Molecular Biology, Michigan State University, East Lansing, MI 48824, USA
- b Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA
- c Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, USA
- d Van Andel Research Institute, Grand Rapids, MI 49503, USA
Abstract
Curcumin, a phenolic compound from the curry spice turmeric, exhibits a wide range of activities in eukaryotic cells, including antiviral effects that are at present incompletely characterized. Curcumin is known to inhibit the histone acetyltransferase activity of the transcriptional coactivator proteins p300 and CBP, which are recruited to the immediate early (IE) gene promoters of herpes simplex virus type 1 (HSV-1) by the viral transactivator protein VP16. We tested the hypothesis that curcumin, by inhibiting these coactivators, would block viral infection and gene expression. In cell culture assays, curcumin significantly decreased HSV-1 infectivity and IE gene expression. Entry of viral DNA to the host cell nucleus and binding of VP16 to IE gene promoters was not affected by curcumin, but recruitment of RNA polymerase II to those promoters was significantly diminished. However, these effects were observed using lower curcumin
oncentrations than those required to substantially inhibit global H3 acetylation. No changes were observed in histone H3 occupancy or acetylation at viral IE gene promoters. Furthermore, p300 and CBP recruitment to IE gene promoters was not affected by the presence of curcumin. Finally, disruption of p300 expression using a short hairpin RNA did not affect viral IE gene expression. These results suggest that curcumin affects VP16-mediated recruitment of RNA polymerase II to IE gene promoters by a mechanism independent of p300/CBP histone acetyltransferase activity.
Resveratrol inhibition of herpes simplex virus replication
- John J Docherty
,
, - Ming Ming H Fu,
- Brian S Stiffler,
- Richard J Limperos,
- Christopher M Pokabla,
- Angelo L DeLucia
- Department of Microbiology and Immunology, Northeastern Ohio Universities College of Medicine, P.O. Box 95, Rte. 44, Rootstown, OH 44272, USA
Resveratrol, a phytoalexin, was found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner. The observed reduction in virus yield was not caused by the direct inactivation of HSV by resveratrol nor inhibition of virus attachment to the cell. The chemical did, however, target an early event in the virus replication cycle since it was most effective when added within 1 h of cell infection, less effective if addition was delayed until 6 h post-infection and not effective if added 9 h post-infection. Resveratrol was also found to delay the cell cycle at S–G2–M interphase, inhibit reactivation of virus from latently-infected neurons and reduce the amount of ICP-4, a major immediate early viral regulatory protein, that is produced when compared to controls. These results suggest that a critical early event in the viral replication cycle, that has a compensatory cellular counterpart, is being adversely affected.