Introduction

HCV statistics

HCV is the most common chronic blood borne infection in the United States. It has significant medical, social, and economic impact. The current U.S. medical costs associated with HCV approach $6.5 billion per year and it is expected to peak at $9.1 billion in 2024.

HCV is involved in about 40% of all chronic liver disease and hepatocellular cancer in America.  About 85 percent of untreated persons infected with HCV ultimately will develop chronic infection, and most untreated patients will progress to some form of chronic liver disease. Liver failure resulting from HCV induced chronic liver disease is the primary indication for liver transplant in the USA today. Hepatitis C causes an estimated 15,000 deaths annually in the United States.

The CDC estimates the prevalence of HCV in non-institutionalized Americans to be about 3.2 million. More than 75% of infected adults are baby boomers, born between 1945 and 1965. CDC estimates that during the 1980s, an average of 230,000 new infections occurred each year. Most of these infections were as a result of blood transfusion. Others boomers may have become infected from injecting drugs but many do not know how or when they were infected.

After 1992, the incidence of new HCV infections decreased by more than 80% as a result of: 1) blood bank screening for high risk donors, 2) HCV testing of blood products, 3) procedures to inactivate viruses in blood products and 4) implementation of Universal Precautions. The CDC estimates that the incidence of new cases in 2010 was 17,000.

Many of the infected are unaware of their disease. Acute HCV infections are often asymptomatic and it may take 10-20 years to develop the symptoms of chronic liver disease. Throughout this period, patients are infectious and able to transmit the disease through


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The virus

Hepatitis C is a ribonucleic acid (RNA) virus in the Flaviviridae family. RNA based viruses, like HCV, store their genetic code within ribonucleic acid, rather than DNA. HCV's RNA is protected within a lipid coat that allows it to fuse to the host cell's outer membrane and merge with it. The virus's lipid coat essentially becomes part of the host cell membrane, depositing the virus RNA inside. Once inside, the virus takes over the host cell and begins to create viral components. The newly created viral components attach to the inside of the host membrane. When the components attach, they deform the membrane causing it to bulge out, creating a bud. The bud pinches off from the host and a new virus is released. This process continues over and over again until the cell is exhausted and dies. Once outside the host cell, the new virus contacts a new host and begins replication, each time creating many, many new viruses.

RNA viruses, like HCV, HIV and Influenza A, are notorious for their ability to mutate and confound vaccines and treatments. HCV's RNA amino acids differs from DNA by only one base. It is composed of adenine, guanine, cytosine and uracil, rather than thymine. It is also a single strand rather than a double. Being a single strand means that it's elements don't have to match up with a complimentary base on an opposing strand, as does DNA. One base can often be substituted for another without inactivating the virus. A substitution usually results in a protein of a slightly different shape. It is the change in shape that confounds vaccines and drugs by moving the position of binding sites.

Researchers have found that half of the virus's mutations are in sites that our immune system attacks. As the virus mutates, it changes the location of the binding site that our immune system can recognize. It can then change back to the “ancestral” set of amino acids. That is, when the virus is under attack, it changes, and then when it's safe, it changes back. Thus, if the virus moves from one host to another, it may lose the mutations that it needed to escape the immune system of the first host, if they aren't needed in the second host. Researchers have found that the mutations are not random, as had been earlier assumed, and the viruses in different people infected by the same ancestral virus have similar genetic elements and mutations. This new information could make it easier to target a vaccine in the future.


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HCV gets inside of the host cell and replicates, creating thousands of copies of itself.
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Genotype

Hepatitis C contains a range of viruses that are similar enough to be classified as HCV, but different enough to be classified as subgroups. There are main types of Hepatitis C that are called genotypes, and there are subtypes of those. Some viral differences are not significant enough to form another sub-type, and these are known as quasi-species. It is believed that within an HCV sub-type, there may be several million quasi-species. All this variation affects response to treatment and progression of the disease. Some researchers classify all HCV into 6 genotypes and others into 11. HCV is classified according to the genotype (1 to 11) as well as the subtype (1a, for example):

Genotype/Subtype
Geographic distribution
1a
North & South America, Australia (most common in US)
1b
Europe & Asia
2a
Japan & China
2b
US and Northern Europe
2c
Western & Southern Europe
3a
Australia & South Asia
4a
Egypt
4c
Central Africa
5a
South Africa
6a
Hong Kong, Macau, & Vietnam
7a, 7b
Thailand
8a, 8b, 9a
Vietnam
10a & 11a
Indonesia


The distribution of genotypes in the United States involves primarily the genotypes 1, 2, and 3:

Genotype
Percentage of total HCV cases in US
1a
36%
1b
38%
1a & 1b
1%
2a
6%
2b
9%
1 & 2
2%
3
6%
4
1%

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The most common HCV in the USA is genotype 2.
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