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Hepatitis C virus is a positive single stranded RNA virus that quietly attacks the liver producing no symptoms until it is too late. It is transferred by blood and though not every aspect of the virus is known researchers have been working to provide better treatments and possibly a vaccine one day. The following describes what is known about HCV, its structure, function, where it attacks, possible treatments, the progression of the disease if left untreated, and prevention of transmission.
2. Structure and classification
Hepatitis C virus (HCV) belongs to the Flaviviridae family and genus Hepacivirus and it is a positive single stranded icosahedral enveloped virus (Shors 494). The icosahedral shape of the nucleocapsid allows for a more stable virus particle (Shors 74). The envelope is a lipid bilayer where envelope proteins are anchored (Chevaliez, ncbi.gov) Its Baltimore classification is class IV (Shor 76). The hepatitis C virus genome includes an IRES and a long open reading frame (ORF), which encodes for a large polyprotein precursor that is cleaved by host and viral proteases (http://www.who.int/csr/disease/hepatitis/whocdscsrlyo2003/en/index2.html).
The major core protein cleaved from the polyprotein precursor is the N-terminal product. (Klein, jvi.org). Other structural proteins are the envelope proteins, E1 and E2 (Shor 496). Hepatitis C virus NS5b gene is the portion that encodes for its RNA-dependent RNA-polymerase, which is crucial for its replication (Shors 495-496). Another important nonstructural protein is NS3, which codes for protease, helicase, and NTPase (Shor 496). Receptors for entry have been identified but their mechanisms of entry still remain not fully understood. For example, the interaction between receptor CD-81 and co-receptors SR-B1 and claudin-1 on host cells and viral structural proteins E-1 and E-2 (Zhang, jvi.org; Shors 495).
3. Life Cycle
HCV binds to receptors and is endocytosed. After entry and loss of the envelope, the nucleocapsid is transported to the cytoplasm where it looses it nucleocapsid and translation of viral RNA begins (Chevaliez, ncbi.gov). Since HCV is a positive single stranded RNA virus, its RNA can be used directly as a polycistronic mRNA to produce a single polyprotein precursor (Shors 59). The host ribosomes are used for cap-independent translation of the viral RNA because the HCV 5' UTR (untranslated region) is not capped (Shors 495; Chevaliez, ncbi.gov). The translated "polyprotein precursor is cleaved into structural and nonstructural proteins by cellular and viral proteases" (Shor 495). After cleavage occurs the NS5b protein, which encodes for RNA- dependent RNA polymerase, is free to begin replication (Shors 59, 495). HCV is transcribed from positive single stranded RNA to an intermediate negative single stranded RNA. The negative intermediate is then used as a template to make more positive single stranded RNA (Shors 59). Assembly occurs in the, "cytoplasmic vesicles formed by budding through intracellular membranes" and mature virions are then released by exocytosis (Chevaliez, ncbi.gov). HCV is contracted via blood-to-blood contact. It travels to the liver and infects the hepatocytes where it can spread and replicate. (Shor 488).
Once the liver is infected with HCV it can become actively inflamed and ALT levels can increase, this is known as chronic hepatitis (Shor 486). If there are detectable virus particles in the blood and ALT levels are really high then a liver biopsy is performed to analyze the level of tissue damage and stage of disease (Shor 486). If chronic liver damage goes unnoticed for a period of time cirrhosis and possibly hepatocellular carcinoma can occur (Shor 486). Research is ongoing in the effort to find what causes the liver damage, whether it is the virus itself or the hosts' immune system. Researchers have found that the damage to liver may be due to the body's, "autoimmune reaction directed against hepatocyte membrane antigens that is initiated by viral infection" (Shor 497). With the release of inflammatory cytokines comes tissue damage as well and it is, "the inflammatory response that activates the process of liver fibrosis" (Shor 497). The liver fibrosis is what leads to cirrhosis and scarring which impairs liver cell function and circulation (Shor 486). Symptoms of HCV go unnoticed for years until a blood screen or symptoms occur (Tan, ncbi.gov). When symptoms do occur they include jaundice, fatigue, abdominal pain and/or flu like symptoms (Shor 482). Viral clearance of HCV is linked to cytotoxic T cells and not through antibodies (Cerny, jci, ncbi.gov). Though there are promising effects from treatment but the mechanism of viral clearance isn't fully understood (Shors 497).
There is no vaccine for HCV and if left untreated HCV can progress to liver disease in 85% of patients (Shor 499). Progression of liver disease will lead to liver cancer and/or liver failure and at that point the only treatment available is a donor liver. Treatment includes pegylated interferon Î±-2a or pegylated interferon Î±-2b, with or without ribavirin (Shor 499). With treatment, especially the combination of pegylated interferon Î±-2b and ribavirin, patients can increase their likelihood of curing the disease (Shor 500). The main problem with the treatment is the side effects. The combination of drugs is chemotherapy and it destroys infected cells as well as white blood cells. Close monitoring of the patient is required during treatment. Prevention of HCV comes from abstaining from intravenous drugs, needlesticks (hospital/medical care), and though rare, unprotected sex.
6. Public Health Impact
Intravenous drug users are found to be the most at-risk or high-risk group for HCV. Since the 1980's the number of infected people has decreased but it has recently reached a plateau (cdc.gov/mmwr/PDF). The most common age group is 25-39 years and the highest incident reports are found in the American Indian and Alaska Native. Though in some cases there were high levels of incidence in non-Hispanic blacks (cdc.gov/mmwr/PDF). Donated blood is screened for HCV as well which contributed to a decline in incidents from transfusions. Hepatitis C can be found anywhere in the world and within a range of demographics due to its asymptomatic nature. The only rare cases were the really young children. Precautionary steps have been taken to inform people about transmission and prevention of transmission (cdc.gov/mmwr/PDF).
Even though not everything about HCV is known, it is apparent that measures are being taken to address this silent killer. Ongoing research for HCV viral proteins involved in attachment and replication and mutations of the RNA viral genome prove hopeful for a new treatment and possibly a vaccine. Understanding how the virus affects liver cells and the autoimmune responses produced will also open the door as to how to treat the virus and disease. Prevention and education seem to be the best candidate for slowing the progression of the virus in any demographic.