Harry B Greenberg

Administrative Appointments

• Senior Associate Dean for Research, Stanford University School of Medicine (2002 - present)

Honors and Awards

• member, ASCI (1980)
• Member, AAP (1992)
• Fellow, AAAS (2003)
• Senior Editor, J Virology (2003-)

Professional Education

Postdoctoral Advisees

Marie Wolf

Graduate & Fellowship Program Affiliations

• Cancer Biology
• Medicine
• Microbiology and Immunology
• Infectious Diseases

Web Site Links

• Stanford Center for Clinical & Translation Education Research

Industry Relationships

Stanford is committed to ethical and transparent interactions with our industry partners. It is our policy to disclose payments of $5,000 or more, equity valued at $5,000 or more in a publicly traded company, or any equity in a privately held company, to physicians and scientists employed by Stanford University from companies or other commercial entities with which they interact as part of their professional activities. View Full Information

Current Research Interests

Dr. Greenberg's current interests are in pathogenic viruses that infect the GI tract, liver and respiratory tract. His primary focus is on molecular mechanisms of pathogenesis, viral determinants of protective immunity, the molecular basis of host range, virulence and tissue tropism, vaccine development, viral immunology, and epidemiology with specific emphasis on the role of enteric viruses in less developed countries. Some of the ongoing studies in the lab deal with the following questions:
(i)What rotavirus gene(s) code for host range restriction, virulence and immunity? These studies involve the use of genetic analysis and studies of humoral and cellular immunity.

(ii)What proteins and what regions of the rotavirus proteins code for neutralizing epitopes, cell fusion activity, viral receptors, protective immunity? These studies involve sequence analysis, site-specific mutagenesis, and expression of viral genes.

(iii)What host cell genes are regulated by rotavirus replication in vitro and in vivo. These studies focus on microarray analysis and cell biology.

(iv)What are the immune effector mechanisms that mediate protection from and resolution of rotavirus infection? These studies involve animal models, cell transfer studies, FACS analysis and transgenic mice.

(v)What are the mechanisms by which class I restricted CD8 T cells modulate HCV infection. These studies involve analysis of peripheral and liver infiltrating human T cells using intracellular cytokine and tetramer techniques.

(vi)What is the basis of interferon effects on HCV? This analysis focuses on in vitro and in vivo microarray studies.

(Vii)What are the determinants of immunity to influenza following live and inactivated virus vaccination?

Clinical Trials

• Blood Sample Study of viral and Immune Responses to Treatment in People with HIV or Hepatitis C Infections Recruiting

Publications

• Variation in antagonism of the interferon response to rotavirus NSP1 results in differential infectivity in mouse embryonic fibroblasts. Feng N, Sen A, Nguyen H, Vo P, Hoshino Y, Deal EM, Greenberg HB. J Virol. 2009; 83 (14): 6987-94
• Rotaviruses: from pathogenesis to vaccination. Greenberg HB, Estes MK. Gastroenterology. 2009; 136 (6): 1939-51
• Differential Transcriptional Responses to Interferon-alpha and Interferon-gamma in Primary Human Hepatocytes. He XS, Nanda S, Ji X, Calderon-Rodriguez GM, Greenberg HB, Liang TJ. J Interferon Cytokine Res. 2009
• VP5* rearranges when rotavirus uncoats. Yoder JD, Trask SD, Vo TP, Binka M, Feng N, Harrison SC, Greenberg HB, Dormitzer PR. J Virol. 2009; 83 (21): 11372-7
• IRF3 inhibition by rotavirus NSP1 is host cell and virus strain dependent but independent of NSP1 proteasomal degradation. Sen A, Feng N, Ettayebi K, Hardy ME, Greenberg HB. J Virol. 2009; 83 (20): 10322-35