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Volume 49, Number 2, April 2016

A trapping ligand antagonist peptide H22-LP inhibition of human cytomegalovirus infection 

Wenjun Shi, Bo Xu, Peng Tian, Xiuying Li, Hanxiao Sun
Wenjun Shi, Bo Xu, Peng Tian, Xiuying Li, Hanxiao Sun


Corresponding author:

Corresponding author. Hanxiao Sun, Institute of Genomic Medicine, College of Pharmacy, Jinan University, 601 Huangpu Street, Tianhe District, Guangzhou 510632, China. 


Background and purpose: 

Human cytomegalovirus (HCMV) can cause acute or chronic diseases, especially in immunocompromised patients. Currently, most drugs licensed for the treatment of the herpes virus are nucleoside analogs that have been developed over the past 25 years. Drug resistance, development of drug related toxicity, and side effects limit their clinical use in patients. In a previous study, we found a trapping ligand H22-LP (the conservative sequence is NAHCALL) from a random phage library according to the broad-spectrum trapping receptor H22, which derived from the residue 14-35 near the N-terminal region of receptor US28 on HCMV. Here, the aim was to evaluate the anti-HCMV activity of H22-LP. 



Antivirus activity of H22-LP on HCMV replication was visualized by fluorescence microscopy. We determined the effects of H22-LP on the expressions of HCMV late protein using q-PCR and Western blot. Comprehensive analysis of the characteristics of H22LP-mediated inhibition of HCMV were quantitatively analyzed by flow cytometry. 



H22-LP showed a 65.4% inhibition of viral infection at a concentration of 10 ng, and 50% inhibition at concentrations of 5 ng. The levels of mRNA and proteins were also found to have decreased by H22-LP in a concentration-dependent manner. The mode of antiviral action is based on a block of viral entry cells during HCMV cell adsorption/entry.



These results demonstrated that H22-LP could inhibit HCMV by direct interaction with the viral particle. 


Key words:

human cytomegalovirus, peptide, viral G-protein-coupled receptors, viral replication