The Hepatitis C Virus
Although its means of transmission is fairly well documented, the hepatitis C virus itself largely remains a mystery. Hepatitis C is extremely small, even for a virus - it is only about 50 nanometers in diameter. A nanometer is one billionth of a meter - if you placed 200,000 hepatitis C viruses end to end, they would be only a single centimeter long. (They are so small that they have no color - they are in fact smaller than the wavelength of visible light.) However, what is known about hepatitis C underscores the type of threat that it poses.
Hepatitis C is an RNA virus - which means that it mutates frequently. Once an infection has begun, hepatitis C creates different genetic variations of itself within the body of the host. The mutated forms are frequently different enough from their ancestors that the immune system cannot recognize them. Thus, even if the immune system begins to succeed against one variation, the mutant strains quickly take over and become new, predominant strains. As a result, the development of antibodies against HCV does not produce an immunity against the disease like it does with most other viruses. More than 80% of the individuals infected with HCV will progress to a chronic form of the disease.
As a result of this, hepatitis C is usually not self-limited as a disease. In more than 85% of all cases, whether they progress to chronic liver disease or not, the infected individual carries the virus for life. This means that they also remain
contagious for a lifetime, able to transmit the virus to others. And because of the long progression of the illness, even patients who will eventually die as a result of hepatitis C carry the virus for decades before it takes their lives. Most epidemics are self-limiting - they spread rapidly, but over a short period of time the affected population either dies or develops an immunity to the disease, and it stops spreading. Not so with hepatitis C. Much like HIV and AIDS, it lasts a lifetime, and kills slowly - giving the virus plenty of time to spread.
There are six basic genotypes of HCV, with 15 recorded subtypes, which vary in prevalence in different regions of the world. Each of these major genotypes can differ
significantly in their biological effects - in terms of replication, mutation rates, type and severity of liver damage, and detection and treatment options. However, these differences are not yet clearly understood.
The 21 current variations in genotype, complicated by the constant mutation of the virus within infected individuals, represents a major challenge for the development of treatments and vaccines against HCV - and even for reliable detection of the virus. There is no guarantee that a treatment, test, or vaccine against one strain will be effective against all of them. Moreover, individuals cured of one strain will be prone to reinfection by any of the other strains.