Ling Jin, DVM, PhD
Assistant Professor
DVM 1986 Nanjing Agricultural U; College of Vet Med
PhD 1999 U of Illinois Urbana-Champaign; Dept Vet Pathobiology
Professional Affiliations
American Society for Virology
American Association for the Advancement of Science
Phi Zeta-honorary Society of Veterinary Medicine
Gamma Sigma Delta-honorary Society of Agriculture, Illinois
1994: International Student Fellowship at University of Illinois
1994: University Research Grand Award
1995 & 1997: The American Society for Virology Travel Award
1997: University Illinois Graduate College Conference Travel Grant
2001: NIH F32 EY13907-01 Individual Research Service Award
2005: Animal Health and Disease/USDA
2005: Alpaca Research Foundation
2007: CMV Internal Research Grant
Viral Pathogenesis and Diagnosis
Host and virus interaction in central nervous system
Mechanism of herpes virus latency-reactivation cycles
Anti-viral drug development
My laboratory is interested in viral pathogenesis and new emerging viral diseases. One of our main research interests is to understand the mechanism of human herpes simplex type 1 (HSV-1) latency reactivation. HSV-1 infection is very common in humans. Following an initial infection, it becomes latent for life in the host trigeminal ganglion. Many environmental factors, such as UV light, heat, stress, bacterial infection, and immunosuppressant, can lead to HSV-1 reactivation from latency. Frequent HSV-1 reactivation in the eye can lead to corneal blindness in humans. There is no drug that can prevent or stop HSV-1 latent infection. Currently, the mechanism of HSV-1 reactivation is not well understood. We are interested in identifying the common host factors important for HSV-1 reactivation.
In an effort to shorten HSV-1 infection and recurrence, we are investigating the application of phosphorodiamidate morpholino oligomers (PMO) as an antiviral drug for HSV-1, HSV-2, and BVDV. We designed PMOs to block gene expression essential for HSV replication.
In addition, we are characterizing new emerging viral diseases. Currently, we are studying a new alphaherpes viral infection in the domestic rabbit, a deer pox virus infection in wild animals, and coronaviruses in alpacas.
Jin L, Cebra CK, Baker R, Mattson DE, Cohen S and Rohrmann GF. 2007. Analysis of a Genome Sequence of an Alpaca Coronavirus. Virology. 365:198-203.
Jin L, Perng GC, Carpenter D, Mott KR, Osorio N, Naito J, Brick DJ, Jones C, Wechsler SL. 2006. Reactivation Phenotype in Rabbits of a Herpes Simplex Virus Type 1 (HSV-1) Mutant Containing an Unrelated Anti-Apoptosis Gene in Place of LAT. J Neurovirol. 2007;13(1):78-84.
Chen D, Cohen J, Naito J, Mott KR, Osorio N, Jin L, Fraser NW, Jones C, Wechsler SL, and Perng GC. 2006. A mutant deleted for most of the herpes simplex virus type 1 (HSV-1) UOL gene does not affect the spontaneous reactivation phenotype in rabbits. J Neurovirol. 2006 Feb;12(1):5-16.
Naito J, Mott KR, Osorio N, Jin L, Perng GC. 2005. Herpes simplex virus type 1 immediate-early protein ICP0 diffuses out of infected rabbit corneas. J Gen Virol. 86(Pt 11):2979-88.
Jin L, GC Perng, KR Mott, N Osorio, J Naito, D Brick, D Carpenter, C Jones, and SL Wechsler. 2005. A herpes simplex virus type 1 mutant expressing a baculovirus inhibitor of apoptosis gene (cpIAP) in place of LAT (Latency Associated Transcript) has a wild type reactivation phenotype in the mouse. J Virol. 2005 Oct;79(19):12286-95.
Peng W, Jin L, Henderson G, Perng GC, Brick DJ, AB Nesburn, SL Wechsler, and Jones C. 2004. Mapping herpes simplex virus type 1 latency associated transcript sequences that protect from apoptosis mediated by a plasmid expressing caspase-8. J Neurovirol. 2004 Aug;10(4):260-5.
L Jin, GC Perng, KR Mott, N Osorio, J Naito, D Brick, D Carpenter, C Jones, and SL Wechsler. 2004. Replacement of LAT by the well characterized anti-apoptosis gene, cpIAP, results in a high wild type HSV-1 reactivation phenotype. Manuscript
Peng W, L Jin. Henderson G. GC Perng, Brick DJ, AB Nesburn, SL Wechsler, and C Jones. 2004. Mapping herpes simplex virus type 1 latency associated transcript sequences that protect from apoptosis mediated by a plasmid expressing caspase-8. J. NeuroVirol. In press.
L Jin, GC Perng, AB Nesburn, C Jones, and SL Wechsler. 2004. Methods for detecting the HSV-1 LAT anti-apoptosis activity in infected tissue cultures cells. J. Virological Methods. 118:9-13.
L Jin, Weiping Peng, GC Perng, AB Nesburn, C Jones, and SL Wechsler. 2003. Identification of herpes simplex virus type 1 (HSV-1) latency associated transcript (LAT) sequences that both inhibit apoptosis and enhance the spontaneous reactivation phenotype. J. Virol. 77(11): 6556-61.
Henderson G, Peng W, Jin L, Perng GC, Nesburn AB, Wechsler SL, Jones C. 2002. Regulation of caspase 8- and caspase 9-induced apoptosis by the herpes simplex virus type 1 latency-associated transcript. J Neurovirol 8 Suppl 2:103-11
Perng GC, Maguen B, Jin L, Mott KR, L Benmonhamed, Yukht A, Osorio N, Nesburn AB, Inman M, Henderson G, Jones C, Wechsler SL.2002. A novel HSV-1 transcript (AL-RNA) antisense to the 5' end of LAT produces a protein in infected rabbit. J Virol. 76 (16): 8003-8010.
Perng GC, Maguen B, Jin L, Mott KR, Osorio N, Slanina SM, Yukht A, Ghiasi H, Nesburn AB, Inman M, Henderson G, Jones C, Wechsler SL.2002. A gene capable of blocking apoptosis can substitute for the herpes simplex virus type 1 latency-associated transcript gene and restore wild-type reactivation levels. J Virol. 76(3): 1224-1235.
Perng GC, Esmaili D, Slanina SM, Yukht A, Ghiasi H, Osorio N, Mott KR, Maguen B, Jin L, Nesburn AB, Wechsler SL. 2001. Three herpes simplex virus type 1 latency-associated transcript mutants with distinct andasymmetric effects on virulence in mice compared with rabbits.J. Virol. 75(19): 9018-28.
L. Jin, William M. Schnitzlein, and G. Scherba. 2000. Investigation of pseudorabies virus LAT gene promoter activity in vitro and in vivo. J. Virol. 74-14:6333-6338
L. Jin, and G. Scherba. 1999. Expression of pseudorabies virus latency associated transcript gene during productive infection of cultured cells. J. Virol. 73-12:9781-9788.
L. Jin. 1999. Pseudorabies Virus latency associated transcript gene: Expression and Regulation, and role in the establishment of latency in swine. Jin, UMI, Ann Arbor.
G. Scherba, J. F. Wiemers, A.M. Siegel, L. Jin, C.C. Austin, L. Bowman, B. Redeford, N.A. Johnston, and Ronal Weigel. 1999. Application of a quantitative algorithm to restriction endonuclease analysis of Aujeszky's disease (psudorabies) virus from a geographically localized outbreak. J. Vet. Diagn. Invest. 11:423-431.
R.M. Weigel, G. Scherba, J. Wiemers, A. M. Siegel, C.C. Austin, L. Jin, L. Bowman and N.A. Johnston. 1997. Application of quantitative methods and molecular biological techniques to investigation of the spread of Aujeszky's disease virus. Epideiogie et Sante Animal 31-31: 12.17.1-12.17.2.
L. Jin, W.M. Schnitzlein and G. Scherba. 1995. Establishment of latency in the natural host animal by Aujeszky's disease (pseudorabies) virus lacking the putative LAT gene promoter. In: Advances in Swine in Biomedical Research, Vol. 1, M.E. Tumbleson and L.B. Shock (eds), Plenum Publishing, NY. pp395-408.