AIDS

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Introduction

The Acquired Immune Deficiency Syndrome is caused by the Human Immunodeficiency Virus. HIV/AIDS attacks cells of the immune system making the body more susceptible to infections and tumors. As a result, patients often suffer from nausea, loss of appetite, intractable pain and other secondary symptoms often associated with cancer (cachexia/wasting syndrome). These symptoms can be suppressed quite effectively by cannabis/cannabinoids. In addition, THC and other compounds found in cannabis can actually interfere with virus production and viral spread. Thus cannabinoids have excellent therapeutic potential for the treatment of AIDS and related symptoms but more research is required.

Alternative Names

Human Immunodeficiency Virus / HIV
Acquired Immune Deficiency Syndrome

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Phytocannabinoids

THC

Receptors

CB2

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Prescription Advice

Preclinical evidence suggests THC can be therapeutic in AIDS. Clinical data suggests that smoked cannabis (read THC) is therapeutic.

Given the nature of the disease, oral or sublingual application as well as smoking/inhalation may be beneficial.

In case of smoking/inhalation, inhale until the symptoms subside or until side-effects become intolerable.

For oral/sublingual application, please follow generic prescription advice.

Please note that, while based on preclinical and/or clinical research, this prescription advice is solely intended as a guideline to help physicians determine the right prescription. We intend to continuously update our prescription advice based on patient and/or expert feedback. If you have information that this prescription advice is inaccurate, incomplete or outdated please contact us here.

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Literature Discussion

In rhesus macaques, THC (0.32 mg/kg, twice daily, intramuscular) was found to significantly decrease viral load development and decrease mortality from Simian Immunodeficiency Virus (the monkey equivalent of Human Immunodeficiency Virus)(Molina et al., 2011).

This protective effect is at least partially due to a THC-driven change in microRNA expression towards an anti-inflammatory profile (Chandra et al., 2014).

Chronic (1 year) treatment with THC showed persistent therapeutic value (reduced viral load, reduced expression of pro-inflammatory MCP-1, reduced mortality).

Negative side effects of THC use (loss of memory, attention and motor function) were only transient (Winsauer et al., 2011).

Thus it seems that the negative side effects of THC are transient while the therapeutic effects remain in the treatment of Immunodeficiency Viruses.

Infected cells secrete trans-activating factors (Tat), which consequently attract macrophages and macrophage-like cells.

THC blocks this migration in a dose-dependent way via CB2 receptors (Raborn and Cabral, 2010).

Denbinobin is a non-cannabinoid compound found in Cannabis.

Denbinobin prevents binding of transcription factor NFκB to DNA and as such can interfere with diseases like AIDS and cancer.

For instance, denbinobin can inhibit HIV-1 replication and consequently prevent viral spread.

Literature:

Chandra, L.C., Kumar, V., Torben, W., Stouwe, C.V., Winsauer, P., Amedee, A., Molina, P.E., and Mohan, M. (2014). Chronic administration of Δ9-tetrahydrocannabinol induces intestinal anti-inflammatory microRNA expression during acute SIV infection of rhesus macaques.

J. Virol. Molina, P.E., Winsauer, P., Zhang, P., Walker, E., Birke, L., Amedee, A., Stouwe, C.V., Troxclair, D., McGoey, R., Varner, K., et al. (2011). cannabinoid administration attenuates the progression of simian immunodeficiency virus. AIDS Res. Hum. Retroviruses 27, 585–592.

Raborn, E.S., and Cabral, G.A. (2010). cannabinoid inhibition of macrophage migration to the trans-activating (Tat) protein of HIV-1 is linked to the CB(2) cannabinoid receptor. J. Pharmacol. Exp. Ther. 333, 319–327.

Sánchez-Duffhues, G., Calzado, M.A., de Vinuesa, A.G., Caballero, F.J., Ech-Chahad, A., Appendino, G., Krohn, K., Fiebich, B.L., and Muñoz, E. (2008). Denbinobin, a naturally occurring 1,4-phenanthrenequinone, inhibits HIV-1 replication through an NF-kappaB-dependent pathway. Biochem. Pharmacol. 76, 1240–1250.

Winsauer, P.J., Molina, P.E., Amedee, A.M., Filipeanu, C.M., McGoey, R.R., Troxclair, D.A., Walker, E.M., Birke, L.L., Stouwe, C.V., Howard, J.M., et al. (2011). Tolerance to chronic delta-9-tetrahydrocannabinol (Δ9-THC) in rhesus macaques infected with simian immunodeficiency virus. Exp. Clin. Psychopharmacol. 19, 154–172.

Clinical Trials

In one randomized cross-over trial, smoked cannabis was found to significantly reduce neuropathic pain associated with AIDS (Ellis et al., 2009).

Subjects in this study were resistant/refractory to at least two other classes of analgesic.

Of the 28 patients that completed both cannabis and placebo treatment, 46% found cannabis to relief pain by at least 30% compared to 18% for placebo.

Also the amount of pain reduction was significantly greater for cannabis than placebo.

In another study among seroconverted patients, high-intensity cannabis use was associated with significantly lower viral loads (Milloy et al., 2014).

In one case report, dronabinol (synthetic THC) was successfully used to treat, otherwise intractable, failure to thrive secondary to intestinal dysmotility, supporting its use to treat symptoms of AIDS or cancer (Taylor and Schwaitzberg, 2015).

Literature:

Ellis, R.J., Toperoff, W., Vaida, F., van den Brande, G., Gonzales, J., Gouaux, B., Bentley, H., and Atkinson, J.H. (2009). Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial. Neuropsychopharmacol. Off. Publ. Am. Coll. Neuropsychopharmacol. 34, 672–680.

Milloy, M.-J., Marshall, B., Kerr, T., Richardson, L., Hogg, R., Guillemi, S., Montaner, J.S.G., and Wood, E. (2014). High-intensity cannabis use associated with lower plasma human immunodeficiency virus-1 RNA viral load among recently infected people who use injection drugs.

Drug Alcohol Rev. Taylor, G.H., and Schwaitzberg, S.D. (2015). The successful use of dronabinol for failure to thrive secondary to intestinal dysmotility. Int. J. Surg. Case Rep. 11, 121–123.