Hepatitis C Virus or HCV is a virus that attacks liver cells and causes both acute and chronic inflammation of the liver. About 15-45% of the patients spontaneously clear the virus within half of a year of infection without any medicine. The remaining will develop chronic HCV infection and after 20 years post-infection, the risk of cirrhosis of the liver can be 15-30%.
In general, it is a disease that affects more than 70 million people worldwide. The HCV is a bloodborne virus. The most common ways of infection may happen through sharing of injection equipment by drug users, the transfusion of unscreened blood and blood products and the inadequate sterilization of medical equipment.
Hepatitis C Virus can also be passed from an infected mother to her baby but it is less common. The virus is not spread through breast milk, hugging, kissing or sharing drinks and food.
What treatments for Hepatitis C virus?
Drugs with direct-acting antivirals such as Sofosbuvir, daclatasvir, and sofosbuvir/ledipasvir combination, are recommended by the World Health Organization.
There are 6 genotypes of the Hepatitis C Virus and they react differently to treatment. Currently, antiviral treatments can cure more than 95% of patients with hepatitis C infection, normally in 12 weeks but access to diagnosis and medicine remains limited. In the meantime, ribavirin and pegylated interferon remains a very restricted role in certain situations1. Unfortunately, nausea, anorexia, insomnia, fatigue, headache, depressive symptoms and weight loss are the most common side effects.
Are there any alternative treatments?
In 2008, it was the Department of Medicine at the University of Ottawa that highlighted that the use of oral cannabinoid medication could help HCV patients treated with interferon and ribavirin by allowing individuals to stabilise weight loss, one month after the initiation (median 0.5 kg additional loss). Anorexia and nauseas were managed effectively, which could led to diminished weight loss.
Cannabinoids work by activating two main receptors, cannabinoid receptor CB1 and CB2. CB1 is widely distributed in peripheral and central nervous system (the basal ganglia, cerebellum and hippocampus). This localization contributes to the benefit observed.
In 2006, a study by the Department of Medicine at the University of California has previously demonstrated that the moderate use of cannabis decreased treatment interruption of interferon/ribavirin combination therapy by improvements in symptom management. In addition, cannabis increased sustained virologic response (SVR) in patients with the HCV. Both, marijuana and ribavirin are metabolized by the same family of protein, the cytochrome P450 system. However, these were not assessed.
In 2014, a study by University of Sydney proved that lipid metabolism is closely linked with hepatitis C virus (HCV) replication, and cannabinoid 1 (CB1) receptor mediates lipid dynamic state of equilibrium in the liver. In patients with chronic hepatitis C virus, CB1 receptor are overexpressed. Interestingly, in this preclinical study, CB1 blockade by an antagonist, inhibited HCV replication, viral protein, virus infectivity and the production of new virus particles. Additionally, this effect stimulated genes that promoted lipid oxidation and reduced the expression of pro-lipogenic genes. This may be due by AMPK activation, and It may represent an entirely new class of drug with activity against HCV, but more clinical investigation is required.
In 2017, a new study (4) conducted by Dr Lowe of the Maryland School of Medicine revealed that cannabidiol (CBD) for the treatment of viral hepatitis has significant properties that could be effective against the Hepatitis C Virus. The researchers combined CBD with HCV under laboratory conditions and were able to demonstrate that CBD inhibited HCV reproduction by 86.4%. Sofosbuvir and interferon were used as positive controls (to compare the same effectiveness). CBD activates CB2 receptor and induces apoptosis (a form of programmed cell dead) in splenocytes and thymocytes inhibiting the proliferation of T-cells and macrophages which are responsible for either inducing the release of pro-inflammatory proteins or attacking liver cells.
“CB2 receptor activation is as such known to modulate immune responses to viral infection and suppress inflammation”. In addition, one of the consequences of untreated viral hepatitis is liver fibrosis, which is the formation of scar tissue in reaction to liver injury by the activation of hepatic stellate cells (HSCs). CBD was shown to induce apoptosis in activated HSCs. Based on these results, CBD has potential as a combination therapy with the currently existing antiviral drugs. However, further clinical studies are needed.
Contradictions among the different studies
Despite the positive results demonstrated in previous studies, there are also studies showing negative effects of cannabinoid consumption in the treatment of Hepatitis C.
Indeed, a 2008 study showed that daily cannabis smoking is a risk factor of steatosis severity in patients with chronic hepatitis C. CB1 receptors are widely distributed not only in the peripheral and central nervous system but also in organs that control energy balance such as the liver. Steatosis is a process describing abnormal retention of fat in the liver cells by activation of the CB1 receptors. Furthermore, viral replication into hepatic cells produces some undefined proteins that interact with these fats, worsening the condition. Results suggest that a highly cannabis use disrupt conventional HCV treatment.
In contrast, in 2014, researchers at the University of Ottawa proved that cannabis use did not promote steatosis, inflammation or fibrosis in hepatitis C infection. It is uncertain why results differ, but amount of alcohol consumption and body mass index may have contributed. Results also showed, sustained virologic response rates were not increased in marijuana consumers. This also contradict finding from previous studies. Nevertheless, marijuana again seems to increased appetite and alleviated on-treatment side effects, particularly in patients with ribavirin and interferon based treatment.
In summary, because of these contradictions, researchers are therefore calling for further studies in order to try to determine the effectiveness of cannabinoid consumption for Hepatitis C Virus medication.
 Costiniuk, C. T., Mills, E. & Cooper, C. L. Evaluation of oral cannabinoid-containing medications for the management of interferon and ribavirin-induced anorexia, nausea and weight loss in patients treated for chronic hepatitis C virus. Can. J. Gastroenterol. 22, 376–380 (2008).
 Sylvestre, D. L., Clements, B. J., & Malibu, Y. (2006). Cannabis use improves retention and virological outcomes in patients treated for hepatitis C. European Journal of Gastroenterology & Hepatology, 18(10), 1057–1063.doi:10.1097/01.meg.0000216934.22114
 Shahidi, M., Tay, E. S. E., Read, S. A., Ramezani-Moghadam, M., Chayama, K., George, J., & Douglas, M. W. (2014). Endocannabinoid CB1 antagonists inhibit hepatitis C virus production, providing a novel class of antiviral host-targeting agents. Journal of General Virology, 95(Pt_11), 2468–2479. doi:10.1099/vir.0.067231-0
 Lowe HIC, Toyang NJ, McLaughlin W. Potential of cannabidiol for the treatment of viral hepatitis. Pharmacognosy Res (2017) 9:116–8. doi:10.4103/ 0974-8490.199780
 Hézode, C., Zafrani, E. S., Roudot–Thoraval, F., Costentin, C., Hessami, A., Bouvier–Alias, M., … Mallat, A. (2008). Daily Cannabis Use: A Novel Risk Factor of Steatosis Severity in Patients With Chronic Hepatitis C. Gastroenterology, 134(2), 432–439.doi:10.1053/j.gastro.2007.11.039
 Liu T, Howell GT, Turner L, et al. Marijuana use in hepatitis C infection does not affect liver biopsy histology or treatment outcomes. Can J Gastroenterol Hepatol. 2014;28:381–384.