Hepatitis C (isolate 1)

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Classification

Lineage

Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Flaviviridae; Hepacivirus; Hepatitis C virus (1)

Description and significance 

The Hepatitis C Virus is comprised of 6 seperaate genotypes. Genotype 1a (isolate 1) being the most prevalent and hard to cure strain (cite pub med). This genotype is estimated to have evolved from its ancestral strain some 400 years ago, this information was deduced using gene sequencing (5).

The Hepatitis C Virus 1a genotype (isolate 1), or HCV, is pathogenic to humans. HCV is a blood-blood transmitted virus. HCV is not a vector borne virus and is only transferred from humans to humans. The primary mode of transmittance in developed countries is injection drug use, it is estimated that 90% of HCV cases in developed countries are attributed to injection drug use (2). Other modes of transmittence include:

-Blood Products/contact; this includes blood transfusions, occupational contact, sexual contact(known to be unlikely during vaginal intercourse. Risk increases during unprotected anal sex).

-Body piercings and tattoos(highly unlikely, unless proper sanitation of needles is not ensured).

-Vertical transmission has been documented but is unlikely (2)

Image: http://upload.wikimedia.org/wikipedia/commons/e/e7/Hepatitis_C_infection_by_source_%28CDC%29_-_en.svg


It is estimated that some 150 million people are infected with HCV worldwide (3). HCV prevalence is higher in developing countries, but is not eradicated in developed countries. In Africa HCV infections have been on the rise, this phenomenon is primarily attributed to the cessation of a widespread effort to eradicate schistosomiasis in sub-Saharan Africa (4). There is no known vaccine for HCV however research is currently underway to develop such a vaccine.

Genome structure 

HCV is a positive single stranded RNA virus whose RNA genome is about 9000 nucleotides long (6)


Cell structure, metabolism & life cycle 

The HCV is a small virus that contains a single stranded positive RNA genome, this genome is encased in a spherical protein coat which is in turn coated by a lipid layer.

The HCV life cycle is not well understood in detail, as the virus can not be cultivated outside of the body as of yet. However the life cycle is postulated to be similar to that of other single-stranded positive RNA viruses. That is the virus replicates by binding to a cell, injecting its genome into the cytoplasm, at which point a negative copy of its genome is synthesized by the cell and more positive RNA is constructed from that negative template which then creates the viral structures from the RNA.


Ecology (including pathogenesis) 


The Hepatitis C Virus 1a genotype (isolate 1), or HCV, is pathogenic to humans. An infection of HCV can result in two types of infections, a chronic or an acute infection. Those who contact HCV and display no symptoms are considered to have a chronic infection, however a chronic infection is not characterized by infection without symptoms as a chronic infection can be an infection displaying symptoms for 3-20 years (cite pub med). Symptoms for a HCV infection include: -Abdominal pain (right upper abdomen) -Abdominal swelling -Bleeding from the esophagus or stomach (due to dilated veins in the esophagus or stomach called varices -Dark urine -Fatigue -Fever -Itching -Jaundice -Loss of appetite -Nausea -Pale or clay-colored stools -Vomiting (2)

Most of these symptoms stem from the nature of the HCV. This 'nature' is that the HCV infects the liver, this infection is manifested as swelling or inflammation of the liver.

The genotype 6 of HCV was recently discovered and treatment for this strain is not yet understood and no treatment has been proven effective as of yet (3).

References 1: http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=11104&lvl=3&lin=f&keep=1&srchmode=1&unlock

2: Ghany MG, Strader DB, Thomas DL, Seeff LB. American Association for the Study of Liver Diseases. Diagnosis, management, and treatment of hepatitis C: an update. Hepatology. 2009;49:1335-1374.

3: O'Leary JG, Davis GL. Hepatitis C. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 9th ed. Philadelphia, Pa: Saunders Elsevier; 2010:chap 79.

4: Frank C, Mohamed MK, Strickland GT, Lavanchy D, Arthur RR, Magder LS, ElKholy T, Abdel-Wahab Y, Aly Ohn ES, Anwar W, Sallam L. The role of parentral antischistosomal therapy in the spread of HCV in Egypt. Lancet. 2000;355:887–91. doi: 10.1016/S0140-6736(99)06527-7

5: http://www.uniprot.org/uniprot/P26664

6: Poynard T, Ratziu V, Benhamou Y, Opolon P, Cacoub P, Bedossa P: Natural history of HCV infection. Best Pract Res Clin Gastroenterol 2000, 14: 211–228.

7: http://upload.wikimedia.org/wikipedia/commons/e/e7/Hepatitis_C_infection_by_source_%28CDC%29_-_en.svg