A Study to Investigate the Safety, Pharmacokinetics, and Efficacy of Combination Treatment of AL-335, Odalasvir, and Simeprevir in Japanese Participants With Chronic Hepatitis C Genotype 1 or 2 Virus Infection, With or Without Compensated Cirrhosis Who Are Direct Acting Antiviral Treatment-naive
A Study to Investigate the Safety, Pharmacokinetics, and Efficacy of Combination Treatment of AL-335, Odalasvir, and Simeprevir in Japanese Participants With Chronic Hepatitis C Genotype 1 or 2 Virus Infection, With or Without Compensated Cirrhosis Who Are Direct Acting Antiviral Treatment-naive
The main purpose of this study is to evaluate the safety and tolerability of a combination
 treatment of AL-335, odalasvir (ODV), and simeprevir (SMV) for 8 weeks in Japanese
 participants with genotype 1 or 2 chronic hepatitis C virus (HCV) infection without cirrhosis
 and for 12 weeks in direct-acting antiviral (DAA)-naive Japanese participants with genotype 1
 or 2 chronic HCV infection with compensated cirrhosis.
Inclusion Criteria:

 -  Chronic hepatitis C virus (HCV) infection

 -  All participants must have HCV genotype 1 or 2 infection, determined at screening

 -  HCV ribonucleic acid (RNA) plasma levels greater than or equal to (>=)10,000
 international units per Milliliter (IU/mL), determined at screening

 -  Direct-acting antiviral (DAA)-naive participants, defined as not having received
 treatment with any approved or investigational DAA drug for chronic HCV infection;
 prior HCV therapy consisting of interferon (IFN, pegylated or nonpegylated) with or
 without ribavirin (RBV) is allowed

 -  Participants without cirrhosis or with compensated cirrhosis

 Exclusion Criteria:

 -  Infection with HCV genotype - 3, 4, 5, or 6

 -  Co-infection with human immunodeficiency virus (HIV 1 or HIV 2 antibody positive) or
 hepatitis B virus (HBV) (hepatitis B surface antigen [HBsAg] positive)

 -  Prior treatment with any investigational or approved HCV DAA, either in combination
 with PegIFN or IFN free

 -  Any evidence of liver disease of non-HCV etiology. This includes, but is not limited
 to, acute hepatitis A infection (immunoglobulin M), drug or alcohol related liver
 disease, autoimmune hepatitis, hemochromatosis, Wilson's disease, alpha 1 antitrypsin
 deficiency, primary biliary cirrhosis, or any other non-HCV liver disease that is
 considered clinically significant by the investigator

 -  Evidence of hepatic decompensation as assessed with Child-Pugh Class B or C or any of
 the following: history or current clinical evidence of ascites, bleeding varices, or
 hepatic encephalopathy