Infectious Bursal

Disease Virus
IBD Virus
⚫ belongs to the family Birnaviridae of the genus
Avibirnavirus

⚫ Two serotypes exist for IBD virus;

⚫ Serotype 1 – pathogenic strain affecting chickens
⚫ Vaccine strains under the serotype 1 is further classified into 6
subtypes
⚫ Serotype 2 – nonpathogenic strain

⚫ Serotypes 1 and 2 do not confer cross protection.

Negative contrast electron micrograph of IBD virus
IBD Virus serotypes
Standard Variant Very Serotype 2
serotype 1 serotype 1 Virulent
serotype 1

Mortality ++ - +++ -
Immunosuppresion ++ +++ +++ -
Index: - none ++ moderate +++ high

Note:

Variant serotype 1 – found in US

Very virulent serotype 1 – found in Asia, Europe and Africa
IBDV vaccine strain subtypes
Virus Synonym Subtype
SAL Bursine A
UV Univax BD B
D78 Clonevac D 78 C
BVM Bursa/Vac-M D
BLN IBD-Blen (2512) E
MD Variant MD F
E Variant E F
F Variant A F
STC Standard Challenge Untyped/
OH Serotype 2 OH Distinct
Morphology
⚫ nonenveloped
⚫ 60 nm in diameter
⚫ hexagonal in outline
⚫ with a single shell having icosahedral
symmetry
⚫ relatively heat stable
⚫ resistant to exposure at pH3 and to ether
and chloroform
Morphogenesis
⚫ External surface of the virion is composed
of trimeric sub-units formed by VP2.

⚫ Inner capsid is composed of trimeric

subunits formed by VP3.
Nucleic acid
⚫ consists of two molecules of linear,
double-stranded RNA designated as Segment A
and B

⚫ 6 kb overall size
⚫ Segment A is 3.2 kbp in size and contains two open
reading frames
⚫ Segment B is 2.8 kbp in size and encodes VP1 (viral RNA
polymerase)
Schematic representation of the segmented dsRNA
linear genome of IBD virus
Genome segment Protein Function

unknown
(said to play a role in the
small VP5 pathogenesis of the virus in
ORF (1) the host)
a) major antigenic site
VP2 b) responsible for virus
tropism
Segment A a) inner capsid structure
VP3 protein
large b) implicated in either
ORF (2) packaging or stabilizing
the RNA genome within
the interior of the capsid
a) viral protease involved
VP4 in the processing of the
precursor polyprotein
a) dsRNA dependent RNA
Segment B VP1 polymerase (RdRp)
b) encapsidation of viral
particle
Replication
⚫ occurs in the cytoplasm
⚫ single replication cycle takes about 68 hours

⚫ Attachment
⚫ IBDV ligand: VP2
⚫ Cell receptor: N-glycosylated protein associated with
the subtle differentiation stage of Surface
IgM-bearing B-lymphocytes

⚫ Entry
⚫ receptor mediated endocytosis
⚫ Transcription
⚫ Upon entry, VP1 (RdRp) becomes activated and produces 2
genome length mRNA from each of the 2 dsRNA genome
segments.

⚫ There is no specific early or late proteins.

⚫ mRNA from Segment A is translated into a polyprotein that

contains pre-VP2, VP4 and VP3.

⚫ VP4 protease co-translationally cleaves the polyprotein into

three polypeptides (pre-VP2, VP3, VP4)

⚫ Pre-VP2 is latter processed by slow maturation cleavage to

produce VP2
Translation of Segment A
 ⚫ mRNA from Segment B is translated into VP1 that could
be found both as free and genome-linked (VPg)

⚫ Virus particles assemble and accumulate into the

cytoplasm

⚫ Encapsidation of VP1 is mediated by its interaction with

inner capsid (VP3)

⚫ Egress
⚫ cell lysis ???
Epidemiology
Epidemiology

Taken from OIE-WAHID

Economic importance
⚫ causes severe mortality in chickens of 3
weeks of age and older

⚫ causes immunosuppresion that leads to

vaccination failure and infection of
oppurtunistic pathogens
Infectious Bursal
Disease
Infectious bursal disease
⚫ an acute, highly contagious viral infection of young
chickens

⚫ in 1962 it was first recognized and referred to as

“avian nephrosis” by Albert S. Cosgrave

⚫ first outbreak occured in Gumboro, Delaware thus it

is now called “Gumboro disease”

⚫ Winterfield and Hitchner (1962) successfully

isolated the virus and it was referred to as “infectious
bursal agent”
Pathogenesis
oral infection

virus replicates in gut- associated lymphoid

tissues (GALT) and macrophages

enters the portal circulation (primary viremia)

Within 11 hours of infection, viral antigen

is detectable in the bursal lymphoid cells

large amounts of virus released from the bursa (secondary viremia)

localization in other tissues

Clinical Forms
⚫ Clinical IBD
⚫ high mortality
⚫ temporary immunosuppresion
⚫ birds above 3 weeks of age

⚫ Sub-clinical IBD
⚫ no mortality due to IBD
⚫ permanent immunosuppresion (viral bursectomy)
⚫ birds below 3 weeks of age
Clinical IBD
⚫ onset of the disease is sudden after an incubation of 2-3
days.

⚫ Clinical signs
⚫ ruffled feathers
⚫ severe prostration
⚫ incoordination
⚫ watery diarrhea
⚫ soiled vent feathers
⚫ vent picking
⚫ inflammation of the cloaca
⚫ dehydration and nephrosis with swollen kidneys were observed in
classical IBD as described by Cosgrove in 1962
⚫ Lesions
⚫ varying degrees of hemorrhages on pectoral or
thigh muscles

⚫ peak virus titers in the bursa can be detected

between 3 to 5 days after IBDV infection

⚫ classical changes in the bursa includes;

⚫ 3rd day of infection – bursa increase in size and weight
due accumulation of fluid (edema) and blood (hyperemia)
⚫ 4th day of infection – bursa doubles in weight and size,
then decrease
⚫ 5th day of infection – bursa returns to its normal size
and continues to decrease
⚫ 8th day of infection – bursa is about 1/3 of its original
size and shows necrotic foci with cheezy mass on the
lumen
Hemorrhages of the pectoral and thigh muscles
Hemorrhages of the pectoral and thigh muscles
Swelling of the Bursa of Fabricius
Edematous bursa of Fabricius with gelatinous coat
Hemorrhagic Bursa of Fabricius
Mortality pattern
⚫ In broilers
⚫ mortality between 3-6 weeks
⚫ 2-5% mortality rarely goes beyond 10%
⚫ peak on 2nd – 3rd day
⚫ no mortality on the 5th day

⚫ In layers
⚫ Mortality between 7-12 weeks of age
⚫ 30-70% mortality
⚫ mortality runs from 7-14 days
⚫ two peaks: 3rd and 4th day; 7th and 8th day
⚫ unvaccinated flock 90% mortality
⚫ caged layer has high mortality
Subclinical infection
⚫ the most important form of the disease because of
economic losses

⚫ severe, long-lasting immunosuppression due to;

⚫ destruction of immature lymphocytes in the bursa of
Fabricius, thymus and spleen
⚫ bursal atrophy occurs as early as 3-4 days with vvIBD
and 8 days in classical IBD
⚫ infection persists for approximately 12 weeks
Vaccination
Types of IBD Vaccines
⚫ Live vaccines
⚫ Mild vaccines (Leukert’s strain)
⚫ Standard intermediate (79-B, Bursin-S-2, Gaivellelae
strain, Georgea strain)
⚫ Intermediate plus (MB strain, B-2K)
⚫ Hot (invasive, pathogenic) vaccine (228-E)

⚫ Killed vaccines
Vaccination Schedule
⚫ For commercial broilers
⚫ day 13 of an intermediate plus strain in drinking water

⚫ For commercial layers

⚫ day 14 and 28 of an standard intermediate strain in
drinking water and on day 21 with an intermediate plus
in drinking water

⚫ For breeder hens

⚫ traditionally at prelay stage and midlay stage with an
inactivated vaccine
Immunity
⚫ Passive immunity
⚫ antibody transmitted through the yolk of the egg
⚫ protects chicks against early infection
⚫ half-life of maternal antibody is between 3-5 days thus,
if the antibody titer of the progeny is known, the time
when chicks will be susceptible can be said.

⚫ Active immunity
⚫ natural infection
⚫ vaccination with either killed or live vaccine
⚫ Active immunity
⚫ Lucio and Hitchner demonstrated that;
⚫ antibody titers falling below 1:100 makes chicks 100%
susceptible to IBDV
⚫ titers 1:100 to 1:600 gave 40% protection against
challenge.

⚫ Skeeles et. al. Reported that the antibody titer must

fall 1:64 before chickens can be vaccinated with
attenuated IBDV.
Thank you!
The four colored structures (A, B, 1 and 2) on each VP2
molecule represent clusters of amino acids. These clusters
form the 3 peaks of each attachment site (red surfaces of the
IBD virus in Figure 1).
Schematic representation of IBD viral proteins