The Evolution of Hepatitis C Virus (HCV)

I was running my eyes up and down on the 2016 projects and I acknowledged that someone has already done research on Tuberculosis. So, I am doing Hepatitis C Virus instead and I will be discussing many important and interesting topics relating to this field including the current disease state, treatment, and the future advancements. I will begin by explaining the history of the virus and the effort of the science community up till today’s date. Within the context, I will connect the dots between different themes while adding awareness to your wisdom about the virus.

The discovery of this new virus came in 1975 which gave the scientists a reason to move forward in the field. Feinstone et al. found out that most transfusion hepatitis cases didn’t have serological markers for hepatitis A and B 1. The virus caused chronic liver disease and was becoming a great threat in the eyes of the public. So, few years later a study by Houghton was carried on in his laboratory at Chiron Corporation which placed this virus in the Flaviviridae family and termed it the HCV2. The virus is a single-stranded, positive-sense RNA about 9.5 kilobases (kb) in length2. Although, Houghton was able to identify and describe the virus, he lacked viral culture system. Wakita et al. brought forward the field by discovering a new system to allow the culturing of the virus for easier study of the viral life cycle and to be able to develop antiviral drugs. In the study, they transfected in vitro, a full-length of the JFH1 RNA into Huh7 cells which resulted in secretion of viral particles that are infectious for human cultured cells and a chimpanzee4.

Hepatitis C is able to evolve since it has a single strand RNA and that is frightening. It has multiple genotypes 1-6 and some of them are more treatable than others. The divergent genotypes in the virus are caused by the mutations. When the host immune system tries to respond to the virus, the virus genetically transforms into different groups called quasispecies5. In this article, “Hepatitis C virus: virology and life cycle” by Kim and Chang, clarified the HCV virology and life cycle6. Upon entry, the human scavenger receptor class B type I (SRB1) binding assist in lipid transfer and CD81 comes after which aids in endocytosis7, 8.

The many field advancements came due to the previous work of Wakita et al., the founder of the cell culture and replication systems. The inside out structure of the virus was finally understood. The virus has a nucleocapsid viral core protein and the E1/E2 are envelops of glycoproteins surrounding the core. The virus also contains viral autoprotease, are nonstructural proteins that are able to block the type 1 interferons (IFN) induction pathway9. Many clinical trials of different types of medicinal dozes came in last few years. I will include different clinical results with varies treatments used against the virus. A new study came in 2016 by Harwood et al., stating that galectin-9 has been found elevated in the liver and serum of HCV patients. Galectin-9 induces apoptosis of hepatitis C virus-specific T cells, and increases inhibitory regulatory T cells10.

I came across few articles that highlighted the importance of routine serologic testing. The disease was becoming a burden. In 1992, the annual cost for chronic hepatitis C was more than $600 million3. Currently, many people are living and suffering from Hepatitis C. HCV is a major cause for chronic hepatitis that can lead to the development of liver cirrhosis and hepatocellular carcinoma if left untreated5. I will add a discussion on the importance of exercising and healthy supplements for patients currently living or treated with HCV. Also, on the importance of protecting your own identity from people with HCV.

The story does not end by stopping the virus through treatment with heavy-duty medications for long periods of time, about 24-48 weeks. The medications have different side effects and some patients were harmed followed by death. Our duty is to treat the HCV patients before any further damages (fibrosis/ hepatocellular carcinoma) with treatments that are cost-effective and less toxic therapeutics. There is also a need to construct a prevention plan for people who might be new victims of the HCV.

 

References:

  1. Feinstone, S. M., Kapikian, A. Z., Purcell, R. H., Alter, H. J. & Holland, P. V. Transfusion-Associated Hepatitis Not Due to Viral Hepatitis Type A or B. New England Journal of Medicine 292, 767–770 (1975).
  2. Houghton, M. Discovery of the hepatitis C virus. Liver International 29, 82–88 (2009).
  3. Alter M. Epidemiology and disease burden of hepatitis B and C. Antiviral Therapy. 1996;1:9–14
  4. Wakita, T. et al. Production of infectious hepatitis C virus in tissue culture from a cloned viral genome. Nat Med 11, 791–796 (2005).
  5. Bukh, J., Miller, R. H. & Purcell, R. H. Genetic Heterogeneity of Hepatitis C Virus: Quasispecies and Genotypes. Seminars in Liver Disease 15, 41–63 (1995).
  6. Kim, C. W. & Chang, K.-M. Hepatitis C virus: virology and life cycle. Clin Mol Hepatol 19, 17–25 (2013).
  7. Pileri, P. et al. Binding of Hepatitis C Virus to CD81. Science 282, 938–941 (1998).
  8. Scarselli, E. et al. The human scavenger receptor class B type I is a novel candidate receptor for the hepatitis C virus. The EMBO Journal 21, 5017–5025 (2002).
  9. García-Sastre, A. & Biron, C. A. Type 1 Interferons and the Virus-Host Relationship: A Lesson in Détente. Science 312, 879–882 (2006).
  10. Harwood, N. M. K., Golden-Mason, L., Cheng, L., Rosen, H. R. & Mengshol, J. A. HCV-infected cells and differentiation increase monocyte immunoregulatory galectin-9 production. J Leukoc Biol 99, 495–503 (2016).

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