Enshrined In The Biophysical Mechanism Of Oncogenic Transcription And Replication Of The Virus The Herpes Virus

May 2015, the journal of Virology Journal of Virology "highlights article" research group of the Institute of Biophysics, Chinese Academy of Sciences Deng Hongyu was published entitled Murine Gammaherpesvirus 68 ORF48 Is an RTA-Responsive Gene Product and Functions in both Viral Lytic Replication and Latency during In Vivo Infection research papers reported herpes virus MHV-68 cracking "molecular switch" protein RTA (Replication and Transcription Activator) ORF48 activate the virus early gene transcription regulation mechanism of protein ORF48 and MHV-68 virus in vivo and in vitro replication of important roles.

EBV (EB virus Epstein-Ba Erer virus), KSHV (Kaposi's Sarcoma-associated Herpes virus) are human herpesvirus subfamily members, and directly related to the development and progression of various human tumors. Mouse herpesvirus -68 (MHV-68) high sequence homology with EBV and KSHV, efficient replication in laboratory common cells, and are capable of infecting laboratory mice is a good model to study EBV and KSHV. From scratch in virus infection or reactivation of the conversion process from latency to the cracking issue, herpes virus encodes a key "molecular switch" protein RTA which can promote early gene transcription and expression in the lower reaches, activate the virus replication. Deng Hongyu research group of early identification of the RTA at MHV-68 the first binding site on the genome (RRE:RTA response element) and found that the early virus-mediated transcriptional activation of the gene ORF18.

In this study, Deng Hongyu group directly on the RTA in the viral genome and identified with the second CIS-element ORF48pRRE in viral genome to RRE mutations led to the RTA and the loss of ORF48 promoter binding capacity, and cannot activate the transcription initiation ORF48. By constructing the ORF48 expression of the mutant virus, the study found loss of ORF48 causes the virus cells in vitro and cracking replication in the lungs of mice and then activated in mouse spleen was reduced significantly. Further amplification of the tumors caused by herpes viruses transcription and replication mechanism of the virus.

Deng Hongyu group PhD Qi Jing, Han Chuanhui and Dan Yang to be the joint first author of the paper, Deng Hongyu for the corresponding author. The research was supported by the National Natural Science Foundation and the Department of science and technology "973" project funding.