The HCV-RNA (Hepatitis-C RNA) diagnosed
patients are recommended interferon free Direct-Acting Antiviral (DAAs) therapy.
Although the treated patients are reported viral resistance to DAAs, the genotype
3a infection is challenge to NS5A inhibitors leading to cirrhosis. Therefore,
the patients with chronic Hepatitis-C treated with DAAs, nucleotide analogue
inhibitors or NS5B protein have high risk of resistance. Breakthrough or
relapse is not common with these drugs when used as monotherapy.NS3-4A protease
inhibitors and non-nucleoside inhibitors have low susceptibility to resistance.
Sofosbuvir-resistant variants have been discovered that disappear after
treatment withdrawal. Patients who experience relapse after an INF-free
treatment have large fraction of drug resistant viruses. .
The quantification of Hepatitis-C RNA has
been made possible by means of commercial and standardized assays in mid 90’s.
These assays were used in retrospective and prospective cohort studies and also
used in clinical trials. Currently, the most diagnostic and research laboratories
used Real Time PCR (RT-PCR) based assays. In theory these methods give better
analytical sensitivity, improved sensitivity, broader dynamic ranges of
quantification, precision and reproducibility. [2,3] RT-PCR methods can detect
and quantify minute amounts of circulating HCV RNA i.e, 12 IU/ml. This
technique is used to assess the response to antiviral therapy. 
Genotype 3 infections can cause rapid development
to cirrhosis and increased rates of hepatocellular carcinomas than other
genotypes. Patients with genotype 3 infection have lower sustained virologic
response rates than other genotypes treated with DAAs. Antiviral treatment for
hepatitis C is changing rapidly.  Current therapy is based on direct acting
antiviral agents due to their efficacy, improved safety and sustained virologic
response. Though some patients show resistance to therapy.
1. Kohli A., & Shaffer A. Treatment of hepatitis C: a
systemic review. Journal of the American
Medical Association, 2014; 13;312(6). 631-40.
2. McEwan P., & Webster S. Estimating the
cost-effectiveness of daclatasvir + sofosbuvir versus sofosbuvir + ribavirin
for patients with genotype 3 hepatitis C virus. Japan Society of Hepatology,
2017; 46(5), 423-33.
R, Young J, Saeed S, Cooper C, Cox J, Martel-Laferriere V, Hull M, Walmsley S,
Tyndall M, Wong A, Klein MB; Canadian Co-Infection Cohort Study. Variation in
hepatitis C virus treatment uptake between Canadian centres in the era of
direct-acting antivirals. Int J Drug Policy. 2018 Dec 26;65:41-49. doi: 10.1016/j.drugpo.2018.08.012.
4. Patoli BB, Patoli AA, Balani NK, Korejo AA. Molecular
surveillance of HCV mono-infection and HCV-HBV co-infection in symptomatic
population at Hyderabad, Pakistan. Afr Health Sci. 2018 Sep;18(3):531-538. doi:
10.4314/ahs.v18i3.9. PubMed PMID: 30602984; PubMed Central PMCID: PMC6307001.
Skladany L, Janceková D, Svac J. Hepatitis C
virus antibodies in outpatients with chronic kidney disease. Clin Exp Hepatol.
2018 Dec;4(4):267-270. doi: 10.5114/ceh.2018.80129