Table 1.
Agents available to treat HCV: mechanisms, activity and major adverse events.
| Name of the antiviral agent | Potential mechanism | Candidates | Spectrum | Major side-effects | Comments |
|---|---|---|---|---|---|
| Interferon | Directly and indirectly suppress HCV replication. | Interferon-α2a, Interferon-α2b, Peginterferon-α2a, Peginterferon-α2b | HCV GT-1 to GT-6 | Constitutional, hematologic (neutropenia, anemia) neuropsychiatric, nausea, rash, and cough | GT-2 and GT-3 are more sensitive than GT-1 |
| Ribavirin | Unclear although multiple mechanisms have been proposed that include inducing host immunity, reducing HCV mutagenicity. | Ribavirin | GT-1 to GT-6 | Anemia, teratogenicity | |
| HCV Protease Inhibitors | HCV NS3/NS4A serine protease inhibitor. Blocks processing of HCV polyprotein and production of new infectious virions. | Boceprevir, Telaprevir, Simeprevir, Asunaprevir+, Faldaprevir+, ABT-450+ | GT-1b > GT-1a | Anemia, dysgeusia, rash | Low barrier to resistance and not to be used as monotherapy |
| HCV NS5A Inhibitors | HCV NS5A inhibitor. Prevents formation of HCV replication complex which is vital for viral RNA replication, and virion assembly. | Daclatasvir+ | All HCV genotypes | Rash | Low barrier to resistance |
| Ledipasvir | |||||
| ABT 267+ | |||||
| HCV NS5B Polymerase Inhibitors | RNA dependent RNA polymerase inhibitor. Competitively binds to the catalytic site of HCV NS5B RNA polymerase and block HCV replication | Sofosbuvir, | All HCV genotypes | Fatigue | High barrier to resistance |
| Headache | Low barrier to develop resistance | ||||
| RNA-dependent RNA polymerase inhibitors. Nonnucleoside analogs. Block HCV replication by binding to an allosteric site of HCV RNA polymerase. | ABT-333+ | GT 1b > 1a | Rash | ||
| Deleobuvir+ | Nausea | ||||
| Vomiting |
+
Agents not yet approved by the FDA at the time of review.
FDA, US Food and Drug Administration; GT, genotype; HCV, hepatitis C virus HCV; RNA, ribonucleic acid.