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HERPES VIRUS & Cannabis studies completed 

Herpes is a common sexually transmitted disease (STD) that any sexually active person can get. Their are 8 different types of this virus that affect human beings.

It appears that the topical use of cannabis oil  may indeed be curative in many dermatologic applications. It makes sense because phytocannabinoids are potent anti-inflammatory compounds.

Video- Will THC Help Treat Herpes?

Most people with the virus don’t have symptoms. It is important to know that even without signs of the disease, it can still spread to sexual partners.

Science & Research

THC inhibits lytic replication of gamma oncogenic herpes viruses in vitro

 
Published online 2004 September 15. doi: 10.1186/1741-7015-2-34.
PMCID: PMC521080
Copyright © 2004 Medveczky et al; licensee BioMed Central Ltd.
Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro
 
Maria M Medveczky, Tracy A Sherwood, Thomas W Klein, Herman Friedman, and Peter G Medveczky
Department of Medical Microbiology and Immunology, MDC Box 10, University of South Florida, and the H. Lee Moffitt Cancer Center, 12901 Bruce B. Downs Blvd, Tampa, FL 33612-4799, USA
Corresponding author.
 
Maria M Medveczky: mmedvecz@hsc.usf.edu; Tracy A Sherwood: tsherwoo@hsc.usf.edu; Thomas W Klein: tklein@hsc.usf.edu; Herman Friedman: hfriedma@hsc.usf.edu; Peter G Medveczky: pmedvecz@hsc.usf.edu
 
Received February 20, 2004; Accepted September 15, 2004.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Abstract
 
Background
 
The major psychoactive cannabinoid compound of marijuana, delta-9 tetrahydrocannabinol (THC), has been shown to modulate immune responses and lymphocyte function. After primary infection the viral DNA genome of gamma herpesviruses persists in lymphoid cell nuclei in a latent episomal circular form. In response to extracellular signals, the latent virus can be activated, which leads to production of infectious virus progeny. Therefore, we evaluated the potential effects of THC on gamma herpesvirus replication.
 
 
Methods
 
Tissue cultures infected with various gamma herpesviruses were cultured in the presence of increasing concentrations of THC and the amount of viral DNA or infectious virus yield was compared to those of control cultures. The effect of THC on Kaposi's Sarcoma Associated Herpesvirus (KSHV) and Epstein-Barr virus (EBV) replication was measured by the Gardella method and replication of herpesvirus saimiri (HVS) of monkeys, murine gamma herpesvirus 68 (MHV 68), and herpes simplex type 1 (HSV-1) was measured by yield reduction assays. Inhibition of the immediate early ORF 50 gene promoter activity was measured by the dual luciferase method.
 
 
Results
 
Micromolar concentrations of THC inhibit KSHV and EBV reactivation in virus infected/immortalized B cells. THC also strongly inhibits lytic replication of MHV 68 and HVS in vitro. Importantly, concentrations of THC that inhibit virus replication of gamma herpesviruses have no effect on cell growth or HSV-1 replication, indicating selectivity. THC was shown to selectively inhibit the immediate early ORF 50 gene promoter of KSHV and MHV 68.
 
 
Conclusions
 
THC specifically targets viral and/or cellular mechanisms required for replication and possibly shared by these gamma herpesviruses, and the endocannabinoid system is possibly involved in regulating gamma herpesvirus latency and lytic replication. The immediate early gene ORF 50 promoter activity was specifically inhibited by THC. These studies may also provide the foundation for the development of antiviral strategies utilizing non-psychoactive derivatives of THC....more
 
 
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Suppressive effect of delta-9-tetrahydrocannabinol on herpes simplex virus infectivity in vitro

Proc Soc Exp Biol Med. 1991 Apr;196(4):401-4.

 

Lancz G, Specter S, Brown HK.

Source

Department of Medical Microbiology and Immunology, University of South Florida, Tampa 33612.

Abstract

Delta-9-Tetrahydrocannabinol (THC) was found to reduce the infectivity of herpes simplex virus and was without effect against adenovirus type 2 or poliovirus.

 

The effective THC concentration resulting in an 80% decrement in virus viability was dependent upon the presence or absence of serum in the incubation mixture, as a 5% serum concentration decreased the drug activity by approximately 50-fold. THC-mediated inactivation of herpes simplex virus was both time and dose dependent and did not result in virion disassembly or clumping.

 

The THC-related effect was not influenced by the pH of the suspending medium, suggesting that the mechanism of inactivation differed from that associated with the thermal inactivation of the virus. Thus, the data suggest that THC preferentially reduces the infectivity of the enveloped herpes simplex virus, and that this activity is modulated by the presence of serum proteins.

 

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The Effect of {Delta}-9-Tetrahydrocannabinol on Herpes Simplex Virus Replication


R. Dean Blevins and Michael P. Dumic

 

Department of Biological Sciences Division of Health Sciences East Tennessee State University, Johnson City, Tenn. 37601, U.S.A.

 

Both herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) failed, in an identical fashion to replicate and produce extensive c.p.e. in human cell monolayer cultures which were exposed (8 h before infection, at infection, or 8 h p.i.) to various concentrations of {Delta}-9-tetrahydrocannabinol. Similar results were obtained with a plaque assay utilizing confluent monkey cells. Possible mechanisms for this antiviral activity are discussed.

 

Received 25 January 1980; accepted 26 February 1980.

 

 

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Adjuvant topical therapy with a cannabinoid receptor agonist in facial postherpetic neuralgia

J Dtsch Dermatol Ges. 2010 Feb;8(2):88-91. Epub 2009 Sep 10.

[Article in English, German]
Phan NQ, Siepmann D, Gralow I, Ständer S.

Source

Competence Center for the Diagnosis and Treatment of Pruritus, Clinic and Polyclinic for Skin Diseases, University Hospital of Münster, Germany. sonja.staender@uni-muenster.de

Abstract

BACKGROUND:

Postherpetic neuralgia is a frequent adverse event in herpes zoster patients and difficult to treat. Conventional analgetic therapy often fails to reduce the burning pain transmitted by unmyelinated nerve fibers. These nerves express cannabinoid receptors which exert a role in modulation of nociceptive symptoms. Therefore, topical therapy with cannabinoid receptor agonist seems likely to suppress local burning pain.

PATIENTS AND METHODS:

In an open-labeled trial, 8 patients with facial postherpetic neuralgia received a cream containing the cannabinoid receptor agonist N-palmitoylethanolamine. The course of symptoms was scored with the visual analog scale.

RESULTS:

5 of 8 patients (62.5 %) experienced a mean pain reduction of 87.8 %. Therapy was tolerated by all patients. No unpleasant sensations or adverse events occurred.

CONCLUSIONS:

Topical cannabinoid receptor agonists are an effective and well-tolerated adjuvant therapy option in postherpetic neuralgia.

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Herpes virus: 8 types

The herpes family of viruses includes 8 different viruses that affect human beings. The viruses are known by numbers as human herpes virus 1 through 8 (HHV1 - HHV8).

Human herpes virus 1

Human herpes virus 1 (HHV1) is also known as herpes simplex virus 1 (HSV1). It is typically the cause of cold sores around the mouth. HHV1 can also lead to infection in the genital area causing genital herpes usually through oral-genital contact, such as during oral sex. HHV1 infections are contagious and are usually spread from skin-to-skin contact with an infected person through small breaks in the skin or mucous membrane. The HHV1 virus is more likely to be spread through things like sharing eating utensils, razors, and towels from a person who has an active lesion.

Human herpes virus 2

Human herpes virus 2 (HHV2) is also called herpes simplex virus 2 (HSV2). It typically causes genital herpes, a sexually transmitted infection. However, it can also cause cold sores in the facial area. Like HHV1, the HHV2 infection is contagious and is spread by skin-to-skin contact. The main route of transmission is through sexual contact, as the virus does not survive very long outside the body.

Human herpes virus 3

Human herpes virus 3 (HHV3) is also called varicella-zoster virus. HHV3 causes chickenpox. It can also cause a recurrent virus infection of the skin, which is called herpes zoster or shingles. Shingles occurs when dormant varicella-zoster virus from an initial bout of chickenpox becomes reactivated. Like its close relative, HHV1, herpes zoster likes to infect skin cells and nerve cells. This virus may also recur along nerve fibre pathways, causing multiple sores where nerve fibres end on skin cells. Because an entire group of nerve cells is often affected, shingles is generally much more severe than a recurrence of herpes simplex. The lesions generally appear in a band-like or belt-like pattern occurring on one side of the body and are often accompanied by itching, tingling, or even severe pain. Healing usually occurs in 2 to 4 weeks, and scars may remain. Postherpetic neuralgia is a complication of shingles where the pain associated with the infection can persist for months and even years. Most people who experience shingles once do not experience it again.

Human herpes virus 4

Human herpes virus 4 (HHV4) is also known as the Epstein-Barr virus. It is the major cause of infectious mononucleosis, or "mono" - the "kissing disease." It is a contagious infection and is transmitted through saliva. Coughing, sneezing, or sharing eating utensils with an infected person can pass the virus from one person to another.

Human herpes virus 5

Human herpes virus 5 (HHV5) is the official name of cytomegalovirus (CMV). CMV is also a cause of mononucleosis. In people with healthy immune systems, the virus may not even cause any symptoms. It can be sexually transmitted, can cause problems to newborns, and can cause hepatitis. CMV can be transmitted through sexual contact, breast-feeding, blood transfusions, and organ transplants. CMV infection is one of the most difficult complications of AIDS. It may lead to diarrhea, severe vision problems including blindness, infections of the stomach and intestines, and even death. For a virus that barely causes a problem in most people with healthy immune systems, it can be amazingly nasty in people with damaged immune systems, such as people with AIDS.

Human herpes virus 6

Human herpes virus 6 (HHV6) is a recently observed agent found in the blood cells of a few patients with a variety of diseases. It causes roseola (a viral disease causing high fever and a skin rash in small children) and a variety of other illnesses associated with fever in that age group. This infection accounts for many of the cases of convulsions associated with fever in infancy (febrile seizures).

Human herpes virus 7

Human herpes virus 7 (HHV7) is even more recently observed and is closely related to HHV6. Like other human herpes viruses, HHV6 and HHV7 are so common that most of humankind has been infected at some point, usually early in life. HHV7 can also cause roseola, but it is not clear what other clinical effects that this virus causes.

Human herpes virus 8

Human herpes virus 8 (HHV8) was recently discovered in the tumours called Kaposi's Sarcoma (KS). These tumours are found in people with AIDS and are otherwise very rare. KS forms purplish tumours in the skin and other tissues of some people with AIDS. It is very difficult to treat with medication. HHV8 may also cause other cancers, including certain lymphomas (lymph node cancers) associated with AIDS. The fact that these cancers are caused by a virus may explain why they tend to occur in people with AIDS when their immune systems begin to fail. The discovery also provides new hope that specific treatments for these tumours will be developed that target the virus.

 
Stephen Sacks, MD, FRCPC, with revisions by the MediResource clinical team
 
 
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Cannabis May Help Combat Cancer-causing Herpes Viruses

ScienceDaily (Sep. 24, 2004) — Tampa, FL (Sept. 22, 2004) -- The compound in marijuana that produces a high, delta-9 tetrahydrocannbinol or THC, may block the spread of several forms of cancer causing herpes viruses, University of South Florida College of Medicine scientists report.

The findings, published Sept. 15 in the online journal BMC Medicine, could lead to the creation of antiviral drugs based on nonpsychoactive derivatives of THC.

The gamma herpes viruses include Kaposi's Sarcoma Associated Herpes virus, which is associated with an increased risk of cancer that is particularly prevalent in AIDS sufferers. Another is Epstein-Barr virus, which predisposes infected individuals to cancers such as Burkitt's lymphoma and Hodgkin's disease.

Once a person is infected, these viruses can remain dormant for long periods within white blood cells before they burst out and begin replicating. This reactivation of the virus boosts the number of cells infected thereby increasing the chances that the cells will become cancerous.

The USF team, led by virologist Peter Medveczky, MD, found that this sudden reactivation was prevented if infected cells were grown in the presence of THC. While cells infected with a mouse gamma herpes virus normally died when the virus was reactivated, these same cells survived when cultured in the laboratory along with the cannabinoid compound – further evidence that THC prevents viral reactivation.

Furthermore, the researchers showed that THC acts specifically on gamma herpes viruses. The chemical had no effect on another related virus, herpes simplex-1, which causes cold sores and genital herpes.

Small concentrations of THC were more potent and selective against gamma herpes viruses than the commonly used antiviral drugs acyclovir, gancicyclovir and foscamet, said Dr. Medveczky, a professor in the Department of Medical Microbiology and Immunology.

The USF researchers suggest that THC selectively inhibits the spread of gamma herpes viruses by targeting a gene these viruses all share called ORF50.

Dr. Medveczky emphasized that more studies are needed. "We have not evaluated the effect of THC in an animal model yet so we do not recommend people start using pot to prevent or treat cancers."

In fact, Dr. Meveczky said, THC has also been shown to suppress the immune system so smoking marijuana could "do more harm than good" to patients whose immune systems are often already weakened.

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