Dr. Yanjin Zhang

Yanjin Zhang, Associate Professor

Virus-Cell. Interactions, Viral Pathogenesis & Vaccine Development


1998 - 2001: Postdoctoral Fellow, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA

1998: Ph.D., Immunobiology, Department of Veterinary Microbiology and Preventive Medicine, Iowa State University, Ames, IA, USA

1989: M.S., Microbiology & Immunology, The National Control Institute of Veterinary Bioproducts and Pharmaceuticals, Beijing, China

1984: DVM, Veterinary Medicine, Shandong Agricultural University, Tai’an, Shandong, China

Professional Experiences

2012 - present: Associate Professor VA-MD Regional College of Veterinary Medicine, University of Maryland, College Park, MD

2007 - present: Faculty Member Molecular & Cellular Biology (MOCB) University of Maryland, College Park, MD

2005 - 2012: Assistant Professor, VA-MD Regional College of Veterinary Medicine, University of Maryland, College Park, MD

2002 - 2005: Assistant Professor, Center for Pediatric Research, Eastern Virginia Medicine School, Norfolk, VA

2001 - 2002:  Instructor, University of Texas, Health Science Center, San Antonio, TX

1989 - 1993: Research Associate, China Institute of Veterinary Drug Control, Beijing, China

1984 - 1986: Research Assistant, China Institute of Veterinary Drug Control, Beijing, China

Research Interests

Viruses, like obligate intracellular parasites, are infectious agents that replicate inside the cells.
To invade the host, viruses must overcome the host’s antiviral defense and induce a conducive
environment for their own replication and spread. The host has developed various strategies to
prevent and control invading pathogens, mainly innate and adaptive immunity. The virus-host
interactions are complex and lead to a myriad array of responses. The context of the interactions
often determines the consequence of the viral infection: recovery or disease. Understanding the
interactions helps elucidate viral pathogenesis and develop novel antiviral strategies and
vaccines. Dr. Zhang’s research interests are molecular virology, virus-cell interactions, viral
pathogenesis, antiviral drug, and vaccine development. His current projects are on positive-sense
RNA viruses, including porcine reproductive and respiratory syndrome virus (PRRSV), Zika
virus (ZIKV), hepatitis E virus (HEV), and the coronavirus SARS-CoV-2. 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. 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, rats, rabbits, chickens, and deer. We have
discovered that the HEV ORF1 product and the capsid protein antagonize host interferon
induction to generate a conducive environment for HEV replication. ZIKV is a mosquito-borne
flavivirus that has drawn public attention due to its association with severe microcephaly in
newborns and Guillain-Barre syndrome (GBS) in adults. SARS-CoV-2 is the causative agent of
COVID-19. Dr. Zhang’s lab is conducting research on elucidating mechanisms of viral
replication in the host cells, viral interference with 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, which play essential roles in host defense. 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 discovered a novel PRRSV strain that can 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.
His lab is also studying SARS-CoV-2 virology and developing antiviral drugs against the virus.
In collaboration with other teams and a biotech company, his lab is exploring novel antiviral
drugs. BSL-3 suite in the department is being used to propagate SARS-CoV-2 and test the
antiviral drugs.


He, J; Yang, .; Chang, P; Yang, S; Wang, Y; Lin, S; Tang, Q; and Zhang, Y. Zika Virus Induces
the Degradation of the Numb Protein that is Required through Embryonic Neurogenesis. Viruses
2023, 15(6), 1258;

Lin S and Zhang YJ. Advances in Hepatitis E Virus Biology and Pathogenesis. Viruses 2021,
13(2), 267;

He J, Yang L, Chang P, Yang S, Lin S, Tang Q, Wang X, and Zhang YJ. Zika virus NS2A
protein induces the degradation of KPNA2 (karyopherin subunit alpha2) via chaperone-mediated
autophagy. Autophagy. 2020 Dec;16(12):2238-2251. doi: 10.1080/15548627.2020.1823122.

Yang L, He J, Wang R, Zhang X, Ma Z, and Zhang YJ: Porcine reproductive and respiratory
syndrome virus inhibits STAT2 signaling via nsp11-mediated downregulation. J Virol 2019 Aug
28. pii: JVI.01352-19. doi: 10.1128/JVI.01352-19.

Lin S, Yang S, He J, Guest JD, Ma Z, Yang L, Pierce BG, Tang Q, Zhang YJ.2. Zika virus NSS
protein antagonizes type I interferon production via blocking TBK1 activation. Virology. 2019
Jan 15;527:180-187. doi: 10.1016/j.virol.2018.11.009. 

Yang L, Wang R, Yang S, Ma Z, Lin S, Nan Y, Li Q, Tang Q, Zhang YJ. Karyopherin Alpha 6 Is
Required for Replication of Porcine Reproductive and Respiratory Syndrome Virus and Zika.
Virus. J Virol. 2018 May 1;92(9). doi: 10.1128/JVI.00072-18.

Yang L, Wang R, Ma Z, Xiao Y, Nan Y, Wang Y, Lin S, Zhang YJ. Porcine Reproductive and.
Respiratory Syndrome Virus Antagonizes JAK/STAT3 Signaling via nsp5, Which Induces
STAT35. Degradation.J Virol. 2017 Feb 1;91(3). doi: 10.1128/JVI.02087-16.

Ma Z, Yu Y, Xiao Y, Opriessnig T, Wang R, Yang L, Nan Y, Samal SK, Halbur PG, Zhang YJ.
Sustaining Interferon Induction by a High.    Passage Atypical Porcine Reproductive and. 
Respiratory Syndrome Virus Strain. Sci Rep. 2016 Nov 2;6:36312. doi: 10.1038/srep36312.

Nan Y, Yu Y, Ma Z, Khattar SK, Fredericksen B, Zhang YJ. Hepatitis E virus inhibits type
I.interferon induction by ORF1 products. J Virol. 2014 Oct;88(20):11924-32.

Wang R, Nan Y, Yu Y, Zhang YJ. Porcine reproductive and respiratory syndrome virus Nsp1β8.
inhibits interferon. activated JAK/STAT signal transduction by inducing karyopherin α18.
degradation.J Virol. 2013 May;87(9):5219-28. doi: 10.1128/JVI.02643-12.

Patel D, Nan Y, Shen M, Ritthipichai K, Zhu X, Zhang YJ. Porcine reproductive and respiratory.
syndrome virus inhibits type I interferon signaling by blocking STAT1/STAT2 nuclear.
translocation.  J Virol. 2010 Nov;84(21):11045-55. doi: 10.1128/JVI.00655-10.

Kannan H, Fan S, Patel D, Bossis I, Zhang YJ. The hepatitis E virus open reading frame 310. 
product interacts with microtubules and interferes with their dynamics. J Virol. 2009
Jul;83(13):6375-82. doi: 10.1128/JVI.02571-08.