Bernard Roizman, Sc.D.

Bernard Roizman received his Sc.D (1956) from Johns Hopkins University in Baltimore and remained on the faculty at Johns Hopkins until he came to The University of Chicago in 1965 as an Associate Professor of Microbiology. He is the Joseph Regenstein Distinguished Service Professor of Virology in the Departments of Microbiology and Molecular Genetics & Cell Biology.

He was elected Member of the National Academy of Sciences, 1979; Fellow, American Academy of Arts and Sciences, 1991; Fellow, American Academy of Microbiology, 1992; Institute of Medicine, 2001; Fellow, American Association for the Advancement of Science, 2004, Honorary Member, Hungarian Academy of Sciences, 1995, Foreign member, Chinese Academy of Engineering (Medicine), 2000. He is the recipient of honorary degrees from Governors State University, 1984; University of Ferrara, Italy 1991; University of Paris, France, 1997, Univ. of Valladolid, Spain, 2001; Professor (honoris causa) Shandong Academy of Medical Sciences, China, 1985; Peking Union Medical College, China, 2002, Shandong Univ, 2003; Qingdao Univ. 2003. He is the recipient of the first annual ICN International Prize in Virology, 1988; J. Allyn Taylor International Prize in Medicine, 1997; Bristol-Myers Squibb Award for Distinguished Achievement in Infectious Disease Research, 1998. NIH Outstanding Investigator Award 1988-2001; NIH-NCI Merit award, 2003; ASM-Abbot Lifetime Achievment Award, 2008.

Dr. Bernard Roizman currently participates in the teaching of Virology in the Division of Biological Sciences. His primary research interests is the function of herpes simplex virus genes with particular emphasis on the mechanisms by which the virus takes over the host cell and on development of therapeutic viruses for treatment of human cancer.


Bernard Roizman, Sc.D.

Joseph Regenstein Distinguished Service Professor Emeritus of Virology

Herpes simplex viruses cause two kinds of infections. On initial infection at the portal of entry into the body, the virus replicates and kills the infected cell (lytic infection). In the course of its replication, the virus infects nerve endings and is transported retrograde to neuronal nuclei of peripheral ganglia where it remains latent (silent) and does not harm the neuron. In some individuals the virus periodically reactivates, and is transported anterograde to a site near the portal of entry where it can cause recurrent lesions.

The focus of the research conducted in this laboratory is on the mechanism by which herpes simplex virus with less than 100 genes takes over a human cell with more than 20,000 genes in both lytic and latent infection.

Current studies on lytic infection indicate that both the virus and the cell have evolved a large number of functions designed to thwart each other’s efforts. The cell attempts to silence viral DNA and preclude the expression of its genes. The virus has evolved a large number of functional domains in its proteins that are designed to silence the cell and prevent it from shutting down the virus. In the course of these studies we have identified both the mechanisms by which the cell attempts to shut down the virus and virus-encoded functions that instead silence the cell and block the activation cellular innate immune responses.

The exciting results of the studies on latent infection are two fold: in peripheral neurons the virus allows itself to be silenced by host repressors. At the same time it has evolved the machinery that enables it to reactivate when the neuron harboring the latent virus is stressed by external stimuli such as fever, UV light or emotional/hormonal stress.

The laboratory has trained approximately 50 graduate students and approximately the same number of post-doctoral fellows. The majority of the trainees are in Universities engaged in research and teaching.

  • She M, Jiang H, Chen X, Chen X, Liu X, Zhang X, Roizman B, Zhou GG. GADD45? Activated Early in the Course of Herpes Simplex Virus 1 Infection Suppresses the Activation of a Network of Innate Immunity Genes. J Virol. 2019 Apr 01; 93(7). PMID: 30700604. View in PubMed.
  • Liu Y, Liu Y, Wu J, Roizman B, Zhou GG. Innate responses to gene knockouts impact overlapping gene networks and vary with respect to resistance to viral infection. Proc Natl Acad Sci U S A. 2018 04 03; 115(14):E3230-E3237. PMID: 29559532. View in PubMed.
  • Wang L, Chen X, Zhou X, Roizman B, Zhou GG. miRNAs Targeting ICP4 and Delivered to Susceptible Cells in Exosomes Block HSV-1 Replication in a Dose-Dependent Manner. Mol Ther. 2018 04 04; 26(4):1032-1039. PMID: 29526650. View in PubMed.
  • Liu Y, Qu L, Liu Y, Roizman B, Zhou GG. PUM1 is a biphasic negative regulator of innate immunity genes by suppressing LGP2. Proc Natl Acad Sci U S A. 2017 08 15; 114(33):E6902-E6911. PMID: 28760986. View in PubMed.
  • Xu P, Roizman B. The SP100 component of ND10 enhances accumulation of PML and suppresses replication and the assembly of HSV replication compartments. Proc Natl Acad Sci U S A. 2017 05 09; 114(19):E3823-E3829. PMID: 28439026. View in PubMed.

View more of Dr. Roizman's papers on PubMed.