Poster Presentation 12th Australian Peptide Conference 2017

A novel bifunctional chimera targeting both HIV-1 Env and host cell co-receptor (#200)

Lirui Song 1 , Andrew Patrick Holmes 2 , Adel A. Rashad 2 , Zhi-Long Wang 1 , Kriti Acharya 2 , Shiyu Zhang 2 , Ebony Gary 2 , Michele Kutzler 2 , Xin Xie 1 , Irwin Chaiken* 2 , Ya-Qiu Long* 1 3
  1. Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai
  2. Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia
  3. School of Pharmaceutic Sciences, SooChow University, Suzhou

It has been about 30 years since the human immunodeficiency virus (HIV) were identified as the pathogenic agent for the acquired immunodeficiency syndrome (AIDS).[1] Though significant progress has been achieved in the antiretroviral therapy, there is still an urgent need for new agent to reduce the global occurrence and spread of AIDS.

As the initiating step of the HIV-1 cell infection, the entry process served as an attractive therapeutic target for HIV-1 intervention. During the HIV-1 entry process, endogenous chemokine receptors CCR5 or CXCR4 binds to viral envelope (Env) glycoprotein gp120, finally leading to the fusion of viral envelope with cell membrane. We hypothesis that antagonists of HIV-1 Env gp120[2] and host cell co-receptor proteins[3] can be covalently joined into bifunctional synergistic combinations that will improve antiviral activity and ultimately decrease susceptibility to function-compromising viral resistance. Hence, a covalently combined conjugate of CCR5 small molecule antagonist LJC240[4] and gp120 peptide antagonist UM15[5] was designed and synthesized. The resulting bifunctional chimera LJC240-L4-UM15 exhibited a sub-nanomolar potency in inhibiting virus cell infection that was substantially greater than that of a non-covalent mixture of the components by almost two order of magnitude. The functional analysis indicated LJC240-L4-UM15 preserved the specific targeting properties of the chimera components, including the UM15 function of irreversible inactivation of HIV-1 Env trimer by gp120 shedding. Furthermore, the chimera was specific for CCR5-expressing cells, had minimal if any general cellular toxicity and exhibited no detectable unwanted infection enhancement of CD4-negative cells. The results demonstrate that covalent conjugates of coordinately acting inhibitors targeting virus Env and host cell co-receptor can be composed to synergistically enhance the potential use of these types of inhibitors for irreversible virus inactivation upon HIV-1/host cell encounter, paving a new way for long-term anti-HIV treatment.

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