Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 5th World Congress on Hepatitis & Liver Diseases London, UK.

Day 2 :

Keynote Forum

Ann D Kwong

Trek Therapeutics, USA

Keynote: Why Highly Effective Drugs Are Not Enough: An Affordable Solution to Eradicating HCV

Time : 09:30-10:15

OMICS International Hepatitis 2017 International Conference Keynote Speaker Ann D Kwong photo

Ann Kwong is an internationally recognized industry leader in antiviral drug discovery and development and a co-founder of HCV DRAG (HCV Drug Development Advisory Group), a consortium of industry, clinical trial, community, and regulatory leaders working to optimize HCV drug development.  Ann is the co-founder, President and CEO of Trek Therapeutics which is committed to developing affordable and accessible drugs to treat infectious diseases. Trek is conducting Ph2 clinical trials to develop a potentially best-in-class and affordable regimen to cure HCV.  Prior to Trek, Ann founded the infectious disease group at Vertex Pharmaceuticals and played a leading role in the discovery, development, and commercialization of VX-787, a PB2 flu inhibitor currently in Ph2, and telaprevir (INCIVEK), a HCV inhibitor with >$2B in sales (Kwong, et al. (2011). Discovery and development of telaprevir: an NS3-4A protease inhibitor for treating genotype 1 chronic hepatitis C virus. Nat Biotech 29:1-11.


Global eradication of HCV is possible because it is the only chronic virus infection that can be cured with a drug. The last decade has been a period of incredible advancements where the “Holy Grail” of an all-oral, highly tolerable therapy with a >95% SVR12 (sustained viral response or cure) rate for chronic HCV infections was achieved. However, high prices in many middle- and high-income countries have resulted in severely restricted access, straining private and public healthcare resources (even in high-income countries such as those in Western Europe, and the US). 

This situation has presented a significant impediment to the development of i) “test-and-treat” programs with inexpensive, decentralized, and rapid HCV RNA diagnostic assays; ii) affordable and accessible HCV drugs for all patients; and iii) a medical infrastructure that is able to treat all patients effectively and efficiently. Current HCV treatment is focused on treating a pool of rapidly diminishing, already-diagnosed patients. 3.4 million people in the EU have chronic HCV infections; this includes injection drug users, prisoners, and migrants. Depending on the country, ~50-90% of patients have not been diagnosed, and <10% of HCV patients are treated each year (Romania and Poland treat £ 2% of up to 1 million HCV patients).  Lack of timely diagnosis and cure increases the risk of liver cirrhosis, liver failure, liver cancer, and premature death. Within high-income countries, pockets of high unmet medical need also exist. Germany treated 20,100 patients in 2015 at a cost of €1.3 billion, yet they have 129,000 immigrants alone with HCV. In the United States, 1 in 3 HCV-infected people pass through the US Corrections Systems each year and the vast majority remains untreated.

Trek Therapeutics, PBC (Trek) is an infectious disease pharmaceutical public benefit corporation (PBC) based in Cambridge, MA, USA whose mission is to make affordable and accessible drugs to treat infectious diseases AND be profitable. Trek has an integrated management team with deep experience in discovery, clinical & CMC development, pricing and medical affairs, and has helped launch 8 antiviral drugs, including 5 HCV drugs. Trek is developing drugs to address the remaining barrier to hepatitis C virus (HCV) care by providing ACCESS to curative treatment.  The goal is to develop an HCV regimen at a $10,000 price point that is as good or better than the standard of care  (~$40,000 to $95,000/treatment). Trek will drive revenue with a volume-based, value-driven, “test-and-treat” strategy.

 Trek has in-licensed a pipeline of four HCV drugs, most of which are second- and third-generation drugs with Phase 2 and 3 clinical data. They include TD-6450 (third-generation NS5A inhibitor from Theravance), MIV-802 (second-generation nucleoside inhibitor from Medivir), faldaprevir (FDV, second-generation NS3 protease inhibitor from Boehringer Ingelheim), and VX-222 (first-generation non-nucleoside inhibitor from Vertex).

Trek’s clinical program is risk-reduced with favorable Ph2a clinical data: Patients receiving FDV + TD-6450 + ribavirin for 12 weeks had no SAEs or discontinuations, and achieved SVR12 (viral cure) in 16/16 patients with HCV genotype (GT) 4, and in 14/15 patients with HCV GT1b. Trek is developing 3 HCV regimens:  TRK-1 to treat HCV GT1&4 and launch in 2021 in the EU; TRK-1SD (short duration) will also target GT1&4 in the US, EU, and Mexico and launch in 2022; TRK-2/3 will target GT2&3 in high prevalence countries, and launch in 2023.

It is not enough to have highly effective and safe HCV treatment regimens.  Industry, academia, patients and their families, non-government organizations (NGOs), ministries of health, regulators, and the investment community need to collaborate to apply the same ingenuity, energy, and funding used to develop highly effective HCV drugs, to eradicate HCV. Trek will partner with providers, insurers, patients, and government health authorities to promote testing and other care necessary to identify and cure patients, and to help the World Health Organization (WHO) reach their goal of eliminating HCV by 2030.

  1. Tong, X and AD Kwong (2014). Barrier to resistance: lessons from two direct-acting HCV inhibitors: MK-5172 and sofosbuvir. Clin Infect Dis. 59:1675-7. doi: 10.1093/cid/ciu700
  2. Hutchison, C, Kwong, A, Ray, S, Struble, K, Swan, T and V Miller (2014). Accelerating drug development through collaboration: the Hepatitis C Drug Development Advisory Group. Clinical Pharmacology & Therapeutics 96:162-5. doi: 10.1038/clpt.2014.113
  3. Kwong, AD (2014). The HCV revolution did not happen overnight. ACS Med Chem Lett. 5:214-220 doi:10.1021/ml500070q.
  4. Zalesak, M, Francis, K, Gedeon, A, Gillis, J, Hvidsten, K, Kidder, P, Li, H, Martyn, D, Orne, L, Smith, A, and A Kwong (2013). Current and future disease progression of the chronic HCV population in the United States. PLoS One.

Keynote Forum

Ming Luo

Georgia State University, USA

Keynote: A Virus-like Particle of HBV preS Elicits Robust Immune Responses
OMICS International Hepatitis 2017 International Conference Keynote Speaker Ming Luo photo

Dr. Ming Luo works on structures of viruses by employing X-ray crystallography and cryo-EM image reconstruction. His primary studies focus on RNA viruses and HBV. He discovered that the nucleocapsid of negative strand RNA viruses sequestered the genomic RNA by polymerization of a capsid protein. During viral RNA synthesis, the nucleocapsid is used as the template in coordination with the viral polymerase. With his knowledge of virus structure, he has been involved in design of novel antiviral drugs and vaccines. His work resulted in a FDA-approve flu drug. For this study, he combines the proteins from influenza virus and HBV to generate a preS VLP that is highly immunogenic. Further development of preS VLP prophylactic and therapeutic vaccines is in progress.


The preS antigen of hepatitis B virus (HBV) corresponds to the N-terminal polypeptide in the large (L) antigen in addition to the small (S) antigen. The virus like particle of the S antigen is widely used as a vaccine to protect the population from HBV infection. The presence of the S antigen and its antibodies in patient blood has been used as markers to monitor hepatitis B. However, there is very limited knowledge about the preS antigen. Previous studies of preS employed recombinant preS proteins or polypeptides from preS. These molecules do not have the proper folded structure, nor proper post-translational modifications. We generated a virus-like particle (preS VLP) that is formed by a chimeric protein between preS and hemagglutinin (HA), and the matrix protein M1 of influenza virus. preS VLP was produced from 293T cells. The HBV preS antigen is displayed on the surface of preS VLP. Asn112 and Ser98 of preS in VLP were found to be glycosylated and O-glycosylation of Ser98 has not been reported previously. Biochemical characterization confirmed that preS in VLP was properly folded. The preS VLP shows a significantly higher immunogenicity than recombinant preS, eliciting robust anti-preS neutralizing antibodies. In addition, preS VLP is also capable of stimulating strong preS-specific T cell responses in Balb/c mice and HBV transgenic mice. Furthermore, preS VLP immunization provided protection against HBV challenge in mice. The data clearly suggest that this novel preS VLP could recapitulate the immunological properties of the L antigen in HBV particles, and can be potentially developed into prophylactic and therapeutic vaccines.