Yanjin Zhang

RESEARCH FOCUS

• Molecular virology of porcine reproductive and respiratory syndrome virus (PRRSV), hepatitis E virus (HEV), Zika virus and others.
• Viral pathogenesis and virus-cell interactions
• Mechanisms of viral interference of host innate immunity - Interferon induction and downstream signaling
• Development of effective vaccines and novel antiviral therapeutics

Viruses are infectious agents that replicate inside the cells, like obligate intracellular parasites. To invade the host, viruses must overcome antiviral defense and induce a conducive environment for their own replication and spread. To prevent and control invading pathogens, the host has developed various strategies, including innate and adaptive immunity. The virus-cell interactions are complex, and the context of the interactions may determine the consequence of the viral infection. Dr. Zhang’s research interests are on molecular virology, virus-cell interactions, viral pathogenesis, and vaccine development. His current projects are on positive-sense RNA viruses, including hepatitis E virus (HEV), porcine reproductive and respiratory syndrome virus (PRRSV), and Zika virus (ZIKV). HEV is the causative agent of endemic and epidemic acute human hepatitis in many parts of the world. It is a zoonotic infectious agent that has been identified in swine, rat, rabbit, chicken, and deer. We have discovered that HEV ORF1 product blocks interferon induction and that HEV ORF3 product increases RIG-I level and activates RIG-I signaling. PRRSV has been causing heavy economic losses to the swine industry worldwide since it was first reported in 1987. An improved vaccine is needed to prevent and control the disease. ZIKV is a mosquito-borne flavivirus, which has drawn public attention due to its association with severe microcephaly in newborns and Guillain-Barre syndrome (GBS) in adults. Dr. Zhang’s lab is conducting research on elucidating mechanisms of viral replication in the host cells, viral interference with the innate immunity, especially interferon production and interferon-activated JAK-STAT signaling, and other aspects of virus-cell interactions. His lab has discovered that PRRSV inhibits the signaling of STAT1, STAT2, and STAT3. His lab also studies karyopherins, which are a group of proteins mediating the nucleocytoplasmic trafficking of numerous proteins including those transcription factors involved in host defense. He is also interested in vaccine development against PRRSV, and his team discovers a novel PRRSV strain that is able to induce interferon production. This strain elicits earlier onset and higher virus-neutralizing antibodies. Further research on the strain is undertaken to develop an improved vaccine against PRRSV infection.