Jackwood Laboratory

Daral Jackwood

Food Animal Health Research Program

Edgington Hall – OARDC
Wooster, OH 44691
Phone: 330-263-3964
Fax: 330-263-3777
Email: jackwood.2@osu.edu

Profile Page

Areas of Expertise

Animal Health Veterinary Microbiology
Veterinary Epidemiology Veterinary Infectious Diseases
Infectious Disease Epidemiology Veterinary Virology
Veterinary Diagnostics Veterinary Vaccine Production
Veterinary Preventive Medicine

Research Interests

The food animal industry produces high quality proteins that are part of a healthy diet. Diseases that affect these animals threaten the safety and quantity of this protein source. In particular, the loss of poultry meat and eggs can lead to poor nutrition and starvation since they are an important food source in many developing countries.

To address this problem, we are studying infectious bursal disease (IBD), an economically important immunosuppressive disease of chickens. IBD is caused by infectious bursal disease virus (IBDV), a bisegmented double-stranded RNA avian Birnavirus.

Research in our lab focuses on three main areas:

Disease Control

IBDV is mutating through antigenic drift, enabling it to avoid the immunity produced by current vaccines. In addition, reassortment of strains of IBDV can create viruses with unknown disease potential. We are using genetic engineering to produce IBDV proteins that self-assemble into empty shells known as virus-like particles (VLPs) that trigger an immune response but are completely non-infectious because they do not contain any viral genomic material. They therefore make ideal vaccines. Additionally, VLPs are unique because the proteins can be expressed from several antigenic strains of IBDV and incorporated into a universal vaccine that will protect against multiple strains of the virus. This genetically engineered vaccine is flexible, allowing new antigens to be easily introduced to keep pace with the antigenic changes that result from virus mutations.


To identify new strains of IBDV, we determine the nucleotide and predicted amino acid sequence of the surface viral protein VP2 (hvVP2). Phylogenic analysis using these sequences has provided valuable information into the ancestry of these viruses. In collaboration with scientists from the University of California, Davis, we identified the first North American occurrence of very virulent IBDV (vvIBDV) in California in 2008. This strain causes high morbidity and mortality in chickens. Less than a year later, we identified genome reassorted IBDV in California. Genome segment A of these reassortants was typical of vvIBDV but genome segment B was most closely related to serotype 2 IBDV. Since that time we have identified several genome reassorted viruses that represent combinations of genome segments from vvIBDV, classic virulent (cvIBDV), and serotype 2 IBDV. We have also shown that backyard chicken flocks appear to be contributing to the reservoir of new IBDV strains that impact commercial poultry operations. We are continuing to monitor commercial chicken and turkey flocks for new strains of IBDV using molecular diagnostic assays and nucleotide sequence analysis.


We are also examining the pathogenicity of genome reassorted IBDV from chickens and turkeys. Our studies have shown that genome reassorted viruses appear to be less pathogenic than vvIBDV in chickens. However, these viruses can still cause morbidity and mortality in SPF chickens and they are able to break through maternal immunity produced using commercial classic and variant vaccines. This suggests that current breeder vaccination programs may not adequately protect against these reassorted IBDV strains.



Infectious bursal disease

Infectious bursal disease (IBD) is caused by infectious bursal disease virus (IBDV) an avian Birnavirus first described in the USA near the town of Gumboro Delaware and thus the disease is also known as Gumboro disease. There are 3 recognized pathogenic types of IBDV; classic virulent (cvIBDV), sub-clinical (scIBDV), and very virulent (vvIBDV).

All three pathogenic types of IBDV cause immune suppression which leads to secondary infections and a failure to produce an immune response to vaccines. The cvIBDV typically cause a high morbidity and low mortality disease while the scIBDV cause very little morbidity and no mortality. The vvIBDV cause an acute disease in chickens characterized by high morbidity and high mortality.

These viruses have been controlled using breeder flock vaccination to produce maternal immunity in the chicks. When the breeder vaccines adequately match the antigenicity of the cvIBDV and scIBDV field challenge, this control program is very effective. Antigenic drift by the virus however, has circumvented the efficacy of some vaccination programs. When maternal immunity wanes in the chicks, some producers find that live-attenuated vaccines are needed to extend the protection against IBD in a flock. Day-of-age vaccination with recombinant herpes virus-IBDV vaccines is also an effective control measure because these vaccines are not affected by maternal immunity to IBDV. Control of vvIBDV has been accomplished using both maternal immunity and live-attenuated vaccination of young chicks. Because the vvIBDV are very aggressive and fast replicating viruses, vaccine programs that use intermediate and intermediate-plus viruses have been more successful than those that use more attenuated live vaccines.

The immune suppression resulting from an IBDV infection is the underlying cause of many respiratory and enteric diseases in chickens. IBD is an economic problem throughout much of the world. The type of disease and virus strains varies from continent to continent. Molecular epidemiology has demonstrated that genetic diversity is high among wild-type viruses. Laboratory studies have also shown that antigenic drift can confound control programs and that pathogenicity among IBDV varies with the strain of virus, host immunity and genetic makeup of the host.

We are committed to improving the health of poultry through research on the prevention, control and diagnosis of IBDV.

History and Characteristics

Infectious bursal disease (IBD) has been observed in chickens since 1957. Young birds that survive the disease can be permanently immune suppressed. Therefore they are more susceptible to other disease causing agents and do not respond adequately to vaccinations which are an essential part of poultry management programs. When older birds are infected with infectious bursal disease virus (IBDV), a transient immune suppression is observed during the disease but because their secondary lymphoid organs have already been seeded with lymphocytes, convalescent birds usually recover most of their humoral and cellular immune functions.

The bursa of Fabricius (BF) is the primary target organ of IBDV. The virus replicates in immature B-lymphocytes and causes a depletion of these cells in the BF. Studies have shown that cellular immunity is also compromised during an IBDV infection. The immune suppression that results from an IBDV infection has a major economic impact on the broiler and layer chicken industries. Often the immune suppression goes unnoticed because the disease is sub-clinical in nature. Thus, the true economic impact of IBDV as the underlying cause of opportunistic respiratory and enteric diseases and vaccination failures is difficult to estimate.

Molecular Characteristics
Infectious bursal disease virus (IBDV) is an avian Birnavirus. The viruses are nonenveloped icosahedrons and approximately 58-60 nm in diameter. The genome consists of two double-stranded RNA segments. The larger segment encodes a polyprotein that is post-translationally cleaved in pVP2, VP3 and VP4. The pVP2 protein is further processed into mature VP2 and with VP3 are the major structural proteins of the icosahedron. The large genome segment also contains an overlapping reading frame that encodes VP5, a non-structural protein that is not required for replication but is thought to enhance virulence. The small genome segment encodes the viral RNA-directed RNA polymerase known as VP1.

Antigenic Characteristics
There are two major serotypes of IBDV found in poultry. Serotype 1 viruses cause disease in chickens and are antigenically distinct from serotype 2 viruses that do not cause disease in any poultry species. Serotype 2 viruses were originally found in domestic turkeys. They infect both turkeys and chickens but a disease has yet to be associated with these viruses.

Among the serotype 1 viruses are several antigenic subtypes. Although there are many shades of gray associated with antigenicity among serotype 1 viruses, it is generally recognized that Classic antigenic strains are distinct from Variant antigenic strains. Serologic and molecular studies have demonstrated that antigenic drift accounts for much of the variation and that key amino acids in the VP2 hypervariable sequence region are responsible.


Clinical IBD
In the clinical disease, morbidity can be seen in nearly 100% of the flock and mortality can range from 0% to over 50% with some very virulent IBDV (vvIBDV) strains. Immune suppression is presumably transient in the clinical disease.

Subclinical IBD
The subclinical disease occurs when IBDV breaks through maternal immunity. The degree of immune suppression varies depending on the virulence of the virus strain and when the infection occurs. Immune suppression is greater the closer the infection occurs to hatch and because the birds are a young age, the immune suppression caused can be permanent. The IBDV strains that cause subclinical disease in the face of robust maternal immunity are usually antigenic mutant forms of the virus. These viruses have been called variants because they vary antigenically from known vaccine strains.

Gross lesions can be seen for the most part on the bursa of Fabricius. The bursa may be swollen, or show signs of hemorrhage. In some cases, however, no lesions are observed and the bursa shrinks in size.

Control of IBD
Infectious bursal disease virus is endemic throughout the world and is very stable in the environment. The virus is resistant to most disinfectants and thus control is only practical through the use of vaccination. Since it is important to protect chicks during the first weeks of life, breeder flocks are vaccinated so maternal immunity is passed to their progeny. The maternal immunity protects chickens from infection during the critical first two weeks of life when IBDV is capable of causing a permanent immune suppression.

Maternal immunity does not protect against the clinical form of IBD. Vaccination against the clinical form of the disease is practiced but its success can vary because timing the administration of the vaccine with the waning maternal immunity is difficult. In addition, antigenic variability among wild-type IBDV strains makes it important to select the most antigenically appropriate vaccine.

Worldwide distribution of IBDV
The actual distribution of variant IBDV strains around the world is difficult to ascertain because of the subclinical nature of the disease. These strains may go unreported because an appropriate diagnostic test was not available or the subclinical disease went unnoticed because the acute clinical form of the disease caused by vvIBDV was considered to be an economically more immediate problem. It is clear that antigenic variants of IBDV are widespread in the United States. These viruses have also been identified in Australia, Canada, Central America, South America, South Africa and more recently some European countries.

The vvIBDV strains can cause an acute clinical disease characterized by devastating mortality. The Office of International des Epizooties (OIE) estimates that IBD is present in more than 95% of the Member Countries. The acute clinical form of IBD caused by vvIBDV isolates has been observed in over 80% of these countries. It has been reported in Europe, Asia, Africa, South America, Central America and in 2009 vvIBDV was diagnosed in California, USA. We are not aware of any vvIBDV reports in Australia or New Zealand.

Diagnosis and Prevention

Diagnosis of IBD
Infectious bursal disease virus (IBDV) causes immune suppression of the immune system in young chickens. Although an immune suppression occurs, antibodies are produced as a result of an IBDV infection. These antibodies will neutralize the virus and aid in the recovery of birds from the disease.

Diagnosis of antibodies to IBDV is accomplished using assays such as the enzyme-linked immunosorbent assay (ELISA) and the agar-gel precipitin assay. Detection of the virus is still accomplished using immunofluorescence and antigen capture ELISA, but more often molecular assays that detect the viral genome are being used. The only diagnostic assay that will conclusively differentiate the viral serotypes and antigenic subtypes is virus-neutralization in vivo or in vitro.

Prevention of IBD
Protection of chickens from IBD through the use of vaccines is complicated by the presence of two serotypes and several antigenic subtypes of the virus. Vaccination with a given antigenic subtype of IBDV serotype 1 will not always protect chicks from the disease when the challenge virus is a different antigenic subtype. Recombinant herpes virus-IBDV vaccines are excellent for immunizing young birds because they are not affected by maternal immunity to IBD. Their ability to immunize chickens against a broader range of IBDV antigenic subtypes may be improved over conventional vaccines because of the cellular immunity they induce.

It is important to identify the IBDV serotype because only serotype 1 viruses have been found to cause disease in poultry. In general, serotype 1 viruses have been place into two large antigenic groups: classic and variant. The antigenic variability among serotype 1 IBDV strains has been recognized for decades. It is determined by amino acids that constitute VP2. Specifically, amino acids in the P domain of VP2 are critical for the binding of neutralizing monoclonal antibodies. Neutralizing antibody escape mutant viruses had substitution mutations in the PBC, PDE and PHI domains. Amino acid substitution mutations in the PBC and PDE domains also contributed to antigenic drift among IBDV strains.

At present, a standardized vaccination protocol against IBDV is not ideal for all situations because of variability in the efficacy of current vaccines, variability in maternally transferred immunity, as well as variability in farm operational parameters. Control efforts are also complicated by the fact that frequent genetic mutations, reassorting of genome segments and recombination can potentially increase virulence and alter antigenicity which may render vaccines and vaccine protocols ineffective. Eradication of the virus on infected farms is not practical since the virus is highly contagious and very resistant to chemical and heat inactivation. In typical cases, whenever IBDV becomes established geographically, they spread rapidly and efforts at eradication have so far been unsuccessful. Control has only been possible through the use of efficacious vaccines.

A direct measure of problems related to IBDV induced immune suppression is difficult. Thus, the poultry industry has a false sense that the longstanding vaccines prepared from classic and variant viruses are adequate. The increased use and success of autogenous IBD vaccines and recent publications on the molecular basis for antigenic drift indicate current vaccines are not keeping pace with the evolution of IBDV. The spread of vvIBDV and genome reassorted vvIBDV throughout the world and now the USA suggests the vaccines used for this acute strain of the virus are also not working.

Laboratory Personnel

Selected Publications

  1. Michel LO, Jackwood DJ. 2017. Classification of infectious bursal disease virus into genogroups. Arch. Virol. Aug 19. doi: 10.1007/s00705-017-3500-4.
  2. Nwagbo IO, Shittu I, Nwosuh CI, Ezeifeka GO, Odibo FJ, Michel LO, Jackwood DJ. 2016.Molecular characterization of field infectious bursal disease virus isolates from Nigeria. Vet World. 9:1420-1428.
  3. Gelb J Jr, Jackwood DJ, Brannick EM, and Ladman BS. 2016. Efficacy of Recombinant HVT-IBD Vaccines Administered to Broiler Chicks from a Single Breeder Flock at 30 and 60 Weeks of Age. Avian Dis. 2016 Sep;60(3):603-12.
  4. Binjawadagi B, Lakshmanappa YS, Longchao Z, Dhakal S, Hiremath J, Ouyang K, Shyu D, Arcos J, Pengcheng S, Gilbertie A, Zuckermann F, Torrelles J, Jackwood D, Fang Y, Renukaradhya GJ. 2016. Development of a porcine reproductive and respiratory syndrome virus-like-particle-based vaccine and evaluation of its immunogenicity in pigs. Arch Virol. Jun;161(6):1579-89.
  5. Amin OG, Jackwood DJ. 2014. Identification and molecular analysis of infectious bursal disease in broiler farms in the Kurdistan Regional Government of Iraq.
    Trop Anim Health Prod. Oct;46(7):1297-301.
  6. Pitesky M, Cataline K, Crossley B, Poulos M, Ramos G, Willoughby D, Woolcock P, Cutler G, Bland M, Tran J, Jackwood D, Allen L, Breitmeyer R, Jones A, Forsythe K, Sentíes-Cué CG, and Charlton B. 2013. Historical, spatial, temporal, and time-space epidemiology of very virulent infectious bursal disease in California: a retrospective study 2008-2011. Avian Dis. Mar;57(1):76-82.
  7. Jackwood DJ, and Stoute ST. 2013. Molecular evidence for a geographically restricted population of infectious bursal disease viruses. Avian Dis. 2013 Mar;57(1):57-64.
  8. Jackwood DJ. 2013. Multivalent virus-like-particle vaccine protects against classic and variant infectious bursal disease viruses. Avian Dis. Mar;57(1):41-50.
  9. Stoute ST, Jackwood DJ, Sommer-Wagner SE, Crossley BM, Woolcock PR, and Charlton BR. 2013. Pathogenicity associated with coinfection with very virulent infectious bursal disease and Infectious bursal disease virus strains endemic in the United States. J Vet Diagn Invest. May;25(3):352-8.