Hua Zhu

Hua Zhu

University of Medicine and Dentistry of New Jersey, USA

Title: Varicella zoster virus tissue tropism and development of a neuroattenuated vaccine


Hua Zhu is an Associate Professor of Department of Microbiology and Molecular Genetics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Adjunct Professor, Xiamen University, China. He has received a PhD in Philosophy from the Columbia University, New York in 1993. He received John S Newberry Prize for the most promising student of the year from Department of Biological Sciences, Columbia University. He has completed his postdoctoral training in herpesviruses in Princeton University, New Jersey from 1993-98. He received Gall Award and New Jersey Cancer Research Award for Scientific Excellence 19961008. He was named as American Cancer Society Research Scholar. He is serving as an editorial board member of reputed journals and reviewer of 6 journals. He has published 40 research articles, reviews and book chapters.


"Varicella zoster virus (VZV) infection causes chickenpox. After the primary infection, VZV remains latent in sensory ganglia, and reactivates upon weakening of the immune system, resulting shingles. The factors involved in neuronal invasion and establishment of latency are still elusive. In our previous work, we employed a VZV bacterial artificial chromosome system in order to characterize a comprehensive library of VZV open reading frame (ORF) deletion mutants. We reported 18 ORFs to be fully dispensable in melanoma cells. We postulated that the latter category is comprised of elements responsible for specific tissue tropism and, when removed, would yield a live neuroattenuated vaccine. By screening the 18 dispensable gene mutants in differentiated neurons, we found that ORF7 is a neurotropic factor adding to our previous report that ORF7 is also a skin tropic factor. ORF7 is a virion component localized to the Golgi compartment in infected cells, whose deletion causes loss of polykaryon formation in vitro and severely impairs viral spread in human nervous tissue ex vivo. Furthermore, we demonstrated that ORF7 is required for VZV replication in xenografts of human skin and dorsal root ganglia in a humanized mouse model. Now show that the ORF7 deletion virus is able to infect dendritic cells, which in turn can infect T cells. Since VZV lacking ORF7 cannot cause either primary chickenpox or the secondary herpes zoster diseases, these discoveries facilitate the development of a neuroattenuated vaccine against chickenpox and shingles, and a possible vector for delivery of other antigens."

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