Drugs

Interferon Alpha is a messenger substance produced by the body that activates immune cells of the virus defence (lymphocytes). However, since the activity of the lymphocytes is normally not sufficient to contain hepatitis C, interferon alpha is added therapeutically to increase the activity to a sufficient level. However, since interferon alpha is excreted by the body quite quickly via the kidneys (half of the substance within 4 hours (plasma half-life 4 h), the active substance is bound to a polyethylene glycol (PEG), which slows its excretion by a factor of 10.

Thus, weekly administration (by syringe) is now possible. Ribavirin is a so-called nucleoside analogue. This means that its chemical structure is so similar to a building block of genetic material (DNA and RNA) – in this case guanosine – that cells want to incorporate it into a hereditary strand instead of the normal building block.

The therapeutic benefit is explained by the fact that it is so foreign to the actual building block that ribavirin blocks the genetic construction tools (polymerases) and thus inhibits the proliferation of viral genetic material. This effect of the multiplication inhibition is called virostatic. The immune system is also affected to a certain extent.

The combination therapy with pegylated interferon alpha and ribavirin is standard today. In some cases, a so-called protease inhibitor is given as a supplement, which is intended to inhibit protein-cleaving enzymes of the virus. Other antiviral drugs, which are intended to erase the viral from the human genome or make it illegible, for example, are currently being developed and promise fewer side effects with increased chances of cure.

Until a few years ago, the standard therapy for hepatitis C was the administration of pegylated alpha-interferon with ribavirin. This combination had to be administered over many months and achieved cure rates of 70-80% depending on genotype. In the meantime, there are new drugs that can effectively stop the virus from multiplying in liver cells.

Among the new drugs are: Protease inhibitors: They stop the breakdown of hepatitis C virus proteins into effective viral proteins. These include Simeprevir, Paritaprevir, Grazoprevir, Glecaprevir and Voxilaprevir. Polymerase, NS5A and cyclophilin inhibitors: They stop the copying and assembly of the viral genome.

These include sofosbuvir, dasabuvir, daclatasvir, ledipasvir, ombitasvir, velpatasvir, elbasvir and pibrentasvir. These drugs are often administered in combinations to combat the hepatitis C virus as effectively as possible.

Protease inhibitors: They stop the breakdown of hepatitis C virus proteins into effective viral proteins.
These include Simeprevir, Paritaprevir, Grazoprevir, Glecaprevir and Voxilaprevir.
Polymerase, NS5A and cyclophilin inhibitors: They stop the copying and assembly of the virus genome. These include sofosbuvir, dasabuvir, daclatasvir, ledipasvir, ombitasvir, velpatasvir, elbasvir and pibrentasvir.

In the past, cure rates of only 70-80% could be achieved even with long therapy durations, but the new drugs are very effective against hepatitis C because over 90% of infected patients can be cured and have no hepatitis C virus in their blood even six months after completion of therapy. The new hepatitis C drugs can also be given for a shorter period of time than the older drugs (usually about three months) and have fewer side effects.

Since 2016, all genotypes can be treated with new drugs. Exact cost details are difficult to find. What is certain is that the new drugs are very expensive and a three-month therapy can easily cost five-figure sums, a six-month therapy six-figures.