Schizophrenia And Marijuana Use May Be Linked By The Same Set Of Genes

“A new study published in Molecular Psychiatry suggests that people who are genetically predisposed to developing schizophrenia may also have the propensity for cannabis use, influenced by the same set of genes. The study is a collaboration between King’s College London and the Queensland Institute of Medical Research in Australia, partly funded by the UK Medical Research Council (MRC).

“We know that cannabis increases the risk of schizophrenia. Our study certainly does not rule this out, but it suggests that there is likely to be an association in the other direction as well – that a pre-disposition to schizophrenia also increases your likelihood of cannabis use,” Power said. “Our study highlights the complex interactions between genes and environments when we talk about cannabis as a risk factor for schizophrenia. Certain environmental risks, such as cannabis use, may be more likely given an individual’s innate behaviour and personality, itself influenced by their genetic make-up.””

http://www.medicaldaily.com/schizophrenia-and-marijuana-use-may-be-linked-same-set-genes-289574

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Genetic predisposition to schizophrenia associated with increased use of cannabis.

“Although considerable evidence implicates cannabis use as a component cause of schizophrenia, it remains unclear whether this is entirely due to cannabis directly raising risk of psychosis, or whether the same genes that increases psychosis risk may also increase risk of cannabis use.

Although directly predicting only a small amount of the variance in cannabis use, these findings suggest that part of the association between schizophrenia and cannabis is due to a shared genetic aetiology. This form of gene-environment correlation is an important consideration when calculating the impact of environmental risk factors, including cannabis use.”

http://www.ncbi.nlm.nih.gov/pubmed/24957864

http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201451a.html

http://www.thctotalhealthcare.com/category/schizophrenia/

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Marijuana Ingredient Kills Herpes Virus, Study Says

“Marijuana’s active ingredient killed herpes viruses in test-tube experiments…

University of South Florida microbiologist Gerald Lancz said his study may help scientists discover new anti-herpes medicines.

http://articles.orlandosentinel.com/1990-05-15/news/9005150630_1_herpes-virus-people-with-herpes-anti-herpes

 

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THC in marijuana may block the spread of forms of cancer causing herpes viruses

Medical News

“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.”

http://www.news-medical.net/news/2004/09/22/4990.aspx

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‘Achilles’ Heel’ of the Herpes Virus Possibly Found in Marijuana

“It’s one of the most common viruses in America, and one that causes the most guilt and shame. It can get inside almost any kind of human cell, reproduce in vast numbers, and linger for years in the body, causing everything from recurrent genital blisters to sores around the mouth. Its complications can kill, and it may increase susceptibility to many nerve and brain disorders.

But until now, scientists haven’t fully understood how the herpes simplex virus (HSV) manages to do all of this. And that has stood in the way of developing more targeted, effective treatments against it to help those infected.

New research from the University of Michigan Medical School may help change that.

An estimated 45 million Americans have genital herpes and millions more have the more visible oral variety. Once someone is infected, they’re infected for a lifetime. New medicines for herpes infection are badly needed; currently, antiviral drugs can quell symptoms of an outbreak, but not eliminate the virus. And, there’s increasing evidence that HSV may damage the nerve cells in which it hides between outbreaks, possibly contributing to neurological disease.

In a presentation Sunday at the International Congress of Virology and in two new papers in the Journal of Virology, U-M researchers are reporting the discovery of a receptor that appears to function as one “lock” that HSV opens to allow it to enter human cells. They’ve also found the gene that controls the production of that receptor, deciphered some aspects of the receptor’s structure, and developed a pig-cell system that could be used to test new anti-herpes drugs.

The findings may help explain why the oral and genital herpes virus has such a successful track record: The receptor, dubbed B5, is made by most cells for another purpose not yet understood. HSV appears to have evolved a way to latch onto it, and fool the cell into letting the virus in. And since most cells express the gene for the B5 receptor, this may be a reason HSV can get into most kinds of cells.

“This may be one central part of the Achilles’ heel in interactions of herpes virus with a cell to start infection. We can use the receptor molecule to try to understand the process and perhaps combat infection at this vulnerable site,” says A. Oveta Fuller, Ph.D. the leader of the U-M team, senior author on the two papers and an associate professor in the U-M Medical School’s Microbiology and Immunology Department. “While we’re still a few years away from being able to use this new knowledge to find effective drug candidates, this is a very exciting confluence of discoveries.”

The U-M holds a patent on the system and methods that the team used to make the discoveries.

Coincidentally, the U-M team’s findings about the B5 receptor are being published at about the same time as an Italian team’s reports about a possible ‘key’ on the herpes simplex virus surface that may match the ‘lock’ found by the U-M team. The Italian team has identified a region of a viral surface protein that matches the U-M team’s predictions of what the virus likely would use to bind and engage the B5 receptor.

“It appears that B5 is a new class of viral receptor. Unlike other viruses so far, HSV seems to have evolved to take advantage of a broadly present cellular protein that has properties like that of known cellular fusion machinery,” says Fuller. “No other virus has been shown to use a cellular fusion protein for entry into cells.”

She explains that the search for the mechanisms by which HSV enters cells has been hindered by the fact that the virus is very good at entering so many kinds of cells. The many possibilities for virus binding to cells make deciphering the entry process a difficult problem to solve.

The gene that encodes B5 had in fact been sequenced, but not characterized, as part of the Human Genome Project. Discovering its role and studying the HSV entry mechanism was tricky and near impossible until Fuller’s team discovered a type of pig kidney cell that isn’t vulnerable to infection by human herpes virus. They searched the genome library to find genes essential to HSV infection, isolated the B5-coding sequence, and figured out how to get pig cells to express the human B5 protein to allow the pig cells to be infected with human herpes virus.

For these studies, Fuller credits the persistence of research team members in working with the genomic library and culture of human and pig cells, especially U-M doctorate graduate Aleida Perez and postdoctoral fellows Qingxue Li and Pilar Perez-Romero. Perez-Romero is first author of one of the two new papers, and a co-author on the other.

The two new papers show that the B5 receptor has important features that could explain why it is important to HSV’s ability to fuse with the fluid membrane that encloses every human cell. The researchers were able to show that by placing only the DNA sequence that encodes B5 into HSV-resistant pig cells, they could make the pig cells susceptible to HSV. They were also able to block viral infection of both human cells and susceptible pig cells by adding to cell cultures a synthetic peptide made to mimic the structure of a smaller region of the B5 receptor. This peptide looks like a functional region of B5 and apparently interferes with virus engaging of the cell receptor.

The papers detail how the team isolated and characterized the gene that encodes B5, called hfl-B5, and used the DNA sequence to find out more about the protein structure of the B5 receptor. In the presentation at the International Congress for Virology, Fuller will describe recent findings that further confirm B5’s importance in HSV infection.

The virology team reports that the B5 molecule appears to form a shape called a coiled coil. This intricately wound structure, they believe, may be similar to the structure of some fusion proteins of viruses and also to cellular proteins called SNAREs. Typically, SNARE proteins help cells to manage the fusion of membranes of vesicles inside the cell with other specific vesicles. Vesicles are tiny membrane-encased packets that encapsulate neurotransmitters, enzymes or other important substances and allow them to be transported within and between cells.

The researchers were able to show that B5 sits in the cell membrane with one end of the protein exposed outside of the cell ready to link up with viruses — or to serve the receptor’s “real” function, which still remains to be discovered. They also showed that HSV does not enter into pig cells that have an altered human B5 protein that is changed by mutations that affect a functional region important to forming a coiled coil.

“If B5 is a SNARE-like cell fusion receptor”, Fuller says, “it may turn out to be useful for more than HSV drug treatment. It could act as a way to link vesicles containing drugs with cells, and deliver them inside”. She is currently collaborating with U-M nanotechnology researchers on this concept.

The findings suggest that B5 or its viral ligand could be a target for antiviral treatment, much like cell receptors for the entry of human immunodeficiency virus (HIV) into cells have become targets for new AIDS drugs.”

http://www.hightimes.com/read/achilles-heel-herpes-virus-possibly-found-marijuana

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Common weed helps treat herpes, study finds

herpes

“Tansy, a flowering plant that has long been used as a folk remedy to treat fevers, rheumatism, and other conditions, may now have another known health benefit. According to a recent study published in the journal Phytotherapy Research, antiviral compounds naturally present in tansy show effectiveness in treating the herpes virus.”

http://www.naturalnews.com/031510_weed_herpes.html

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The effect of delta-9-tetrahydrocannabinol on herpes simplex virus replication.

“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.”

http://www.ncbi.nlm.nih.gov/pubmed/6255077

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Inhibition of cell-associated herpes simplex virus type 2 glycoproteins by delta 9-tetrahydrocannabinol.

“This study was conducted to define the effect of micromolar concentrations of delta 9-tetrahydrocannabinol (delta 9-THC) on the biosynthesis and expression of herpes simplex virus type 2 (HSV2)-specified glycoproteins. Dose-related reductions in all species of virus glycoproteins were recorded by one-dimensional SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and autoradiography of [14C]glucosamine-labeled infected Vero cells treated with 10(-7) to 10(-5) M delta 9-THC. A drug dose-related depletion of the mature HSV2 major envelope glycoprotein complex (119-kDa average molecular weight), accompanied by accumulation of immature unglycosylated species, was demonstrated by two-dimensional SDS-PAGE in concert with Western immunoblotting or autoradiography. Light and electron microscopy immunoperoxidase staining revealed that delta 9-THC effected depletion of 119-kDa determinants from the infected cell surface. This depletion occurred concomitantly with accumulation of 119-kDa components at the perinucleus. However, the expression of 119-kDa glycoproteins on the virion envelope was not affected. These results indicate that delta 9-THC inhibits the synthesis, maturation, and cellular transport of HSV2-specified glycoproteins. Decreased expression of virus glycoproteins on the infected cell surface may affect host immune responsiveness to HSV2.”

http://www.ncbi.nlm.nih.gov/pubmed/3033681

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Suppressive effect of delta-9-tetrahydrocannabinol on herpes simplex virus infectivity in vitro.

“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.”

http://www.ncbi.nlm.nih.gov/pubmed/1848937

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Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro

Figure 2

“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.

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.

 We believe that studies on cannabinoids and herpesviruses are important to continue because there are obvious potential benefits. Better understanding may lead to the development of specific non-psychoactive drugs that may inhibit reactivation of oncogenic herpesviruses.”
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