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Forum: Would HSV Anti-virals Possibly Be Effective for the Flu

27 October 2006

fredness – at 11:31

As I read about herbs that have been shown to have anti-viral properties I notice several interfere with replication of other lipid coated viruses. It just made me wonder if this were true with prescription medications. It might be better than nothing.

Tom DVM – at 11:44

fredness. I agree completely. If the status quo continues…for 99.9 % of the population, there will be no pharmaceuticals at all.

Under these conditions, a re-evaluation of naturopathic remedies would be beneficial. Unfortunately, if the pandemic starts in the fall or winter, there will be few plants avaliable from which to extract naturopathic medications.

I would appreciate a list of readily avaliable native North American plants that might help.

Reconscout – at 12:08

Tom,I read a post of yours on a thread about vetinary medications in which you remarked that you had worked out treatment procedures for animals with similar infections.You said that some of these might apply to humans.Do you recall which thread these procedures were discussed on as I would like to read it. Thank you.

Tom DVM – at 12:19

Reconscout. I don’t remember which thread it was. If you check the news threads for the past couple of days, I think JV mentioned that it was on a ‘pet mediations’ thread.

If I remember, the discussion may have been held on seperate threads…but here is an overview.

I have treated viral pneumonias and the cytokine storm in cattle for many years. It was very depressing at the start because a number of animals would die and a number of animals would end up with serious permanent lung damage. The comment about crepitous gas under the skin in humans with H1N1 in 1918, was a common occurrence with these animals.

I tried many things to counter these effects. I did come up with a treatment protocol that cut mortality in more than half and pretty much removed the lung damage after the fact.

The basis of the treatment was two fold. 1) the use of prednisolone plus antifever drugs in combination to limit the cytokine storm and as importantly limit the intial lung destruction from the virus…

…and 2) the use of spectinomycin which was an off-label use of a drug liscensed for use with Turkeys in North America and liscensed for cattle in France…

…The results indicated to me that this particular antibiotic had a direct effect on viruses which doesn’t make sense for a compound that should only have an effect on bacteria…either way it worked…

Note: I am treating all of you as my colleagues. I have no way to know what effect this antibiotic could have on humans…for all I know it could be directly toxic (there are antibiotics that work perfectly in animals and are poisions to humans and visa versa)…

…I am providing this for interest and discussion only. DO NOT ATTEMPT TO ACCESS THE DRUG FOR HUMAN USAGE UNLESS AS A RESULT OF THE DIRECT INTERVENTION OF A PHYSICIAN.

Thanks for the question.

beehiver – at 23:43

Being curious about the spectinomycin…found that it has been used in humans mainly to treat gonorrhea. But, it is not absorbed well when ingested, this drug needs to be injected. This page said, “Toxicokinetic studies suggested poor absorption after oral dosing in rats, dogs, pigs and cattle, with most of the orally administered dose found in the faeces. Absorption was also poor in humans following oral administration.”

The Wikipedia entry for spectinomycin describes it’s mode of action as: “It binds to the 30S ribosomal subunit in invading bacteria and interrupts protein synthesis.” Another reference got more detailed about it, but I could not immediately get some clue whether the protein synthesis inhibition might apply to other situations.

Anyway, because the drug needs to be injected, it probably wouldn’t be a good candidate for home care, even if it did have some mode of anti-viral activity.

beehiver – at 23:54

However! Fredness your first post at 11:31 jarred my memory about something. There is a breakdown product of coconut oil (monolaurin) which has activity against bacteria and viruses with (respectively) lipid membrane or viral envelope. It’s important to know the coconut oil must go through the human digestive process to produce the active monolaurin component.

A bit from this summary gives more info…I have not had time to chase down specific studies or journal references, but there are references given on the webpage. Author: Mary Enig, PhD.

“The lauric acid in coconut oil is used by the body to make the same disease-fighting fatty acid derivative monolaurin that babies make from the lauric acid they get from their mothers= milk. The monoglyceride monolaurin is the substance that keeps infants from getting viral or bacterial or protozoal infections. Until just recently, this important benefit has been largely overlooked by the medical and nutrition community.

Recognition of the antimicrobial activity of the monoglyceride of lauric acid (monolaurin) has been reported since 1966. The seminal work can be credited to Jon Kabara. This early research was directed at the virucidal effects because of possible problems related to food preservation. Some of the early work by Hierholzer and Kabara (1982) that showed virucidal effects of monolaurin on enveloped RNA and DNA viruses was done in conjunction with the Center for Disease Control of the US Public Health Service with selected prototypes or recognized representative strains of enveloped human viruses. The envelope of these viruses is a lipid membrane.

Kabara (1978) and others have reported that certain fatty acids (e.g., medium-chain saturates) and their derivatives (e.g., monoglycerides) can have adverse effects on various microorganisms: those microorganisms that are inactivated include bacteria, yeast, fungi, and enveloped viruses.

The medium-chain saturated fatty acids and their derivatives act by disrupting the lipid membranes of the organisms (Isaacs and Thormar 1991) (Isaacs et al 1992). In particular, enveloped viruses are inactivated in both human and bovine milk by added fatty acids (FAs) and monoglycerides (MGs) (Isaacs et al 1991) as well as by endogenous FAs and MGs (Isaacs et al 1986, 1990, 1991, 1992; Thormar et al 1987).

All three monoesters of lauric acid are shown to be active antimicrobials, i.e., alpha-, alpha’-, and beta-MG. Additionally, it is reported that the antimicrobial effects of the FAs and MGs are additive and total concentration is critical for inactivating viruses (Isaacs and Thormar 1990).

The properties that determine the anti-infective action of lipids are related to their structure; e.g., monoglycerides, free fatty acids. The monoglycerides are active, diglycerides and triglycerides are inactive. Of the saturated fatty acids, lauric acid has greater antiviral activity than either caprylic acid (C-10) or myristic acid (C-14).

The action attributed to monolaurin is that of solubilizing the lipids and phospholipids in the envelope of the virus causing the disintegration of the virus envelope. In effect, it is reported that the fatty acids and monoglycerides produce their killing/inactivating effect by lysing the (lipid bilayer) plasma membrane. However, there is evidence from recent studies that one antimicrobial effect is related to its interference with signal transduction (Projan et al 1994).”

28 October 2006

fredness – at 02:20

Some of the supplements I plan to stock for influenza treatment include andrographis, black elderberry, chamomile german (aromatherapy for anti-inflammatory), cranberry, eucalyptus globulus and radiata (aromatherapy), forsythia, green tea, lonicera, naouli (melaleuca quinquenervia, aromatherapy ), pomogranate, propolis, ravensara (aromatherapy) reservatrol (knotweed tincture), tea tree (aromatherapy). I have found documentation supporting their use in more than one place. The references I will cite for this post relate to those which also show efficacy against herpes, as listed on PubMed.

Antiviral properties of ent-labdene diterpenes of Andrographis paniculata nees, inhibitors of herpes simplex virus type 1. Phytother Res. 2005 Dec;19(12):1069–70. Andrographolide, neoandrographolide and 14-deoxy-11,12-didehydroandrographolide, ent-labdene diterpenes isolated from Andrographis paniculata showed viricidal activity against herpes simplex virus 1 (HSV-1). None of these compounds exhibited significant cytotoxicity at viricidal concentrations. Copyright 2005 John Wiley & Sons, Ltd. PMID: 16372376

Antiviral activity of Australian tea tree oil and eucalyptus oil against herpes simplex virus in cell culture. Pharmazie. 2001 Apr;56(4):343–7. The antiviral effect of Australian tea tree oil (TTO) and eucalyptus oil (EUO) against herpes simplex virus was examined…In order to determine the mode of antiviral action of both essential oils, either cells were pretreated before viral infection or viruses were incubated with TTO or EUO before infection, during adsorption or after penetration into the host cells. Plaque formation was clearly reduced, when herpes simplex virus was pretreated with the essential oils prior to adsorption. These results indicate that TTO and EUO affect the virus before or during adsorption, but not after penetration into the host cell. Thus TTO and EUO are capable to exert a direct antiviral effect on HSV. Although the active antiherpes components of Australian tea tree and eucalyptus oil are not yet known, their possible application as antiviral agents in recurrent herpes infection is promising. PMID: 16372376

Antiviral properties of prodelphinidin B-2 3′-O-gallate from green tea leaf. Antivir Chem Chemother. 2002 Jul;13(4):223–9. Prodelphinidin B-2 3-O-gallate, a proanthocyanidin gallate isolated from green tea leaf, was investigated for its anti-herpes simplex virus type 2 properties in vitro…Result of time-of-addition studies suggested that prodelphinidin B-2 3′-O-gallate affected the late stage of HSV-2 infection. In addition, it was also shown to inhibit the virus from attaching and penetrating into the cell. Thus, prodelphinidin B-2 3′-O-gallate was concluded to possess antiviral activity with mechanism of inhibiting viral attachment and penetration, and disturbing the late stage of viral infection. PMID: 12495210 Pomegranate… Antiviral activity of tannin from the pericarp of Punica granatum L. against genital Herpes virus in vitro][Article in Chinese. Zhongguo Zhong Yao Za Zhi. 1995 Sep;20(9):556–8, 576, inside backcover. Based on cell culture techniques this study has demonstrated that tannin from the pericarp of Punica granatum is an effective component against genital herpes virus (HSV-2). The tannin not only inhibits HSV-2 replication, but also shows stronger effects of killing virus and blocking its absorption to cells. PMID: 8679095

Anti-herpes simplex virus effect of an aqueous extract of propolis Isr Med Assoc J. 2002 Nov;4(11 Suppl):923–7. …In vivo: as little as 5% propolis prevented the appearance and development of symptoms of local and i.p. HSV-1 infection in rats and of corneal HSV-1 infection in rabbits. There were no cytotoxic effects at a concentration of 10% in vitro or 20% in vivo. CONCLUSIONS: The potent antiviral activity of propolis against HSV-1 infection in vitro and In vivo is probably due to prevention of virus absorption into the host cells and/or inhibition of an internal step(s) during the viral replication cycle.

9 PubMed hits on Propolis and herpes.

15 PubMed hits on Quercetin and herpes.

Resveratrol suppresses nuclear factor-kappaB in herpes simplex virus infected cells. Antiviral Res. 2006 Jul 14; Resveratrol inhibits herpes simplex virus (HSV) replication by an unknown mechanism. Previously it was suggested that this inhibition may be mediated through a cellular factor essential for HSV replication [Docherty, J.J., Fu, M.M., Stiffler, B.S., Limperos, R.J., Pokabla, C.M., DeLucia, A.L., 1999. Resveratrol inhibition of herpes simplex virus replication. Antivir. Res. 43, 145–155]. After examining numerous cellular factors, we report that resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme [Patel, A., Hanson, J., McLean, T.I., Olgiate, J., Hilton, M., Miller, W.E., Bachenheimer, S.L., 1998. Herpes simplex type 1 induction of persistent NF-kappa B nuclear translocation increases the efficiency of virus replication. Virology 247, 212–222; Gregory, D., Hargett, D., Holmes, D., Money, E., Bachenheimer, S.L., 2004. Efficient replication by herpes simplex virus type 1 involves activation of the IkappaB kinase-IkappaB-RelA/p65 pathway. J. Virol. 78, 13582–13590]. Electromobility shift assays determined that resveratrol, in a dose dependent and reversible manner, suppressed activation of NF-kappaB in Vero cells infected with HSV-1, HSV-2 and acyclovir resistant HSV-1. Furthermore, resveratrol did not protect IkappaBalpha, a cytoplasmic NF-kappaB inhibitor, from degradation in HSV-1 infected cells. Immunohistochemical studies demonstrated that RelA/p65, a component of the dimeric NF-kappaB complex, translocated to the nucleus of HSV-1 infected cells in the presence of resveratrol. Finally, direct effects on viral transcription and DNA synthesis were evaluated. Real-time RT-PCR analysis showed that resveratrol treatment of infected cells resulted in reductions of mRNA for ICP0, ICP4, ICP8 and HSV-1 DNA polymerase by 2.1-, 3.3-, 3.8- and 3.1-fold, respectively. Plus, mRNA for glycoprotein C, an HSV late gene, was completely absent in the presence of resveratrol. Lastly, quantitative PCR showed that resveratrol significantly blocked HSV DNA synthesis. Cumulatively, these data indicate that resveratrol (i) suppresses HSV induced activation of NF-kappaB within the nucleus and (ii) impairs expression of essential immediate-early, early and late HSV genes and synthesis of viral DNA. PMID: 16876885

Resveratrol inhibition of herpes simplex virus replication.Docherty JJ, Fu MM, Stiffler BS, Limperos RJ, Pokabla CM, DeLucia AL. Antiviral Res. 1999 Oct;43(3):145–55. 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. PMID: 10551373

There are 3 other listings for resveratrol working against herpes.

Tea tree oil: the science behind the antimicrobial hype. Lancet. 2001 Oct 13;358(9289):1245. No abstract available. PMID: 11675072

Melaleuca alternifolia (tea tree) oil gel (6%) for the treatment of recurrent herpes labialis. J Antimicrob Chemother. 2001 Sep;48(3):450–1. No abstract available. PMID: 11533019

Tom DVM – at 10:58

Beehiver Fredness. Thanks.

31 October 2006

crfullmoon – at 19:58

bump

Bump - Bronco Bill – at 21:26
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