‫مقتطفات‬
ILT
= Gallid herpesvirus 1
=Latency ,persistent infection , intranuclear IB
=ILT vaccine induces protection against challenge in 1 wk. Humoral
immunity is not the major immune response against ILTV in chickens
=Egg production in laying flocks will usually decrease 10 to 50 %, but
will return to normal after 3 to 4 weeks.
=local CMI responses in the trachea produced protection from ILTV
challenge in bursectomized chickens. Mucosal antibodies were not
essential for resistance to challenge[65].
=ILT vaccine viruses can create latent infected carrier chickens. These
latent carriers are a source for spread of virus to non-vaccinated flocks.
Therefore, it is recommended that ILT vaccines be used only in endemic
areas
=Investigations of ILTV isolates collected from around the world were
analyzed by PCR-RFLP. They revealed that some current field virulent
isolates were closely related to vaccine strains. This implies that field
isolates originated from vaccine strains after back passage in chickens
=These recombinant ILTV vaccines did not cause latent infections and
virulent reversion they reduced the clinical signs, but not virus replication
after challenge
=Live vaccines improve bird performance and ameliorate clinical signs of the disease
but fail to reduce shedding of the challenge virus increasing the likelihood of
outbreaks.
=ILT continues as an economical important poultry disease. House
management and biosecurity measures should be performed for disease
control. For eradication ILT, the modified-live vaccines need to be
replaced by improved recombinant vaccines for the prevention of latent
infection and virulent reversion..
=genomes in darkling beetles detection of viral
=In most countries the outbreak related‐strains were either viruses closely
related to the chicken embryo origin (CEO) vaccines “Vaccinal LT”
(CEO‐like virus), “vaccinal LT” cocirculating with field viruses, or field
virus by itself (31, 90).
Newcastle disease
= Protection against NDV is through the use of vaccines generated with
low virulent NDV strains. Immunity is derived from neutralizing
antibodies formed against the viral hemagglutinin and fusion
glycoproteins, which are responsible for attachment and spread of the
virus. However, new techniques and technologies have also allowed for
more in depth analysis of the innate and cell-mediated immunity of
poultry to NDV. Gene profiling experiments have led to the discovery of
novel host genes modulated immediately after infection.
=NDV is known to infect over 236 species of birds (Kaleta and Baldauf,
1988) and besides poultry species virulent NDV (vNDV) strains are
commonly found in pigeons and double crested cormorants (Diel et al.,
2012b; Kim et al., 2008; Pchelkina et al., 2013) and occasionally in some
other wild bird species (Kaleta and Kummerfeld, 2012). Typically, the
concern is that pigeons will transmit their vNDV strains of genotype VIb
to poultry (Abolnik et al., 2004; Alexander and Parsons, 1986), however,
poultry are able to transmit their vNDV strains to pigeons, as well
(Merino et al., 2009). The incubation period and clinical disease observed
with a NDV infection depends on multiple factors.
= Because layers receive multiple NDV vaccinations during their
production cycle, and thus have persistent immunity, they may not show
signs of infection except a drop in egg production
=the V protein, which has anti-interferon properties
=Even though all strains of NDV are contained in one serotype, there are
phylogenetic differences found when comparing genome relatedness.
Strains are divided into two classes, class I and class II, with class II
further divided into 16 genotypes (Diel et al., 2012a). Class I viruses are
typically isolated from wild birds and all reported strains are of low
virulence except for one strain, chicken/ Ireland/1990 (Alexander et al.,
1992). Class II, genotype I NDV are all of low virulence except for the
vNDV that caused the ND outbreak in 1998 in Australia (Gould et al.,
2001). Class II, genotype II viruses contain NDV of low virulence, some
of which (B1, LaSota, VG/GA) are used as NDV vaccines, and vNDV
that are not commonly isolated (Miller et al., 2010). NDV strains of class
II, genotypes III–IX, and XI–XVI are all virulent (Courtney et al., 2012;
Diel et al., 2012a).
=The early reactions of the innate immune system use germ-line encoded
receptors, known as pattern recognition receptors (PRR’s), which
recognize evolutionarily conserved molecular markers of infectious
microbes, known as PAMP’s (pathogen associated molecular patterns).
Recognition of PAMPs by PRRs, either alone or in heterodimerization
with other PRRs, (toll-like receptors (TLR); nucleotide-binding
oligomerization domain proteins (NOD); RNA helicases, such as retinoic
acid-inducible gene 1 (RIG-I) or MDA5; C-type lectins), induces
intracellular signals responsible for the activation of genes that encode for
pro-inflammatory cytokines, anti-apoptotic factors, and antimicrobial
peptides. The virus is first recognized by host sentinel proteins, including
TLR and NOD proteins, producing rapid signaling and transcription
factor activation that lead to production of soluble factors, including
interferon and cytokines, designed to limit and contain viral replication.
=At best, NDV vaccines induce an immune response that reduces or
completely prevents clinical disease and mortality from ND, decreases
the amount of vNDV shed into the environment, and increases the
amount of virus needed to infect the vaccinated animal (Marangon and
Busani, 2006; Miller et al., 2009).
=Until recently the dogma is that inactivated vaccines will not induce a
mucosal immune response, but a recent study demonstrated that both live
and inactivated NDV vaccines induced antibodies other than IgA, not
only in serum, but also in tracheal and intestinal washes
= In the United States the intracloacal inoculation pathogenicity test is
used to distinguish viscerotropic velogenic NDV from neurotropic
velogenic viruses [1,6].
= Additionally, virulent NDV can be differentiated by its ability to
replicate in most avian and mammalian cell types without the addition of
trypsin
=]. These live-virus vaccines induce high levels of IgA, IgY and IgM
antibodies in sera of newly hatched chicks [64]. They also induce local
antibody response such as IgA production in the Harderian gland [65]
along with lacrimal IgM following intraocular inoculation with NDV
[66].
History of ND
= Do
you know when and where was the first
outbreak of Newcastle disease?
The first recognized outbreak of Newcastle disease, disease caused
by the Paramyxovirus Type 1, was in Java (Indonesia) in 1926 and
in Newcastle-upon-Tyne in 1927 (Doyle, 1927).
However similar disease outbreaks were reported in Central
Europe before this date. Fowl plague was identified clinically during
the period of 1833 or earlier (Manninger, 1949) and the viral cause of
this disease was established in 1900 (Jacotot, 1950).
Fowl Plague virus is classified as Avian Influenza (Easterday and
Tumova, 1972), however the lesions of classical fowl plague in
chickens were very similar to the acute form of Newcastle disease.
Source: United States Department of Agriculture (USDA)
Newcastle disease: From an unknown disease
to a pandemic situation
The name “Newcastle disease” was given by Doyle as a temporary
measure in order to avoid descriptive names that could confused with
other diseases (Doyle, 1935).
The pattern of outbreaks that are due to virulent NDV throughout
the world suggest that several outbreaks have occurred in
poultry since 1926.
The first reported pandemic situation started in 1926 and took 20
years to become pandemic.
The second started in 1960 and took just 4 years to reach most
countries (Hanson, 1972), the difference in time being because of the
changes in transportation (air transportation).
There was probably another pandemic situation in the late 1970’s
(Alexander et al., 1997; Lomniczi et al., 1998; Herczeg et
al., 2001) and in the 1980’s in racing pigeons.
= ). It has been reported that intense innate immune response was induced by virulent
NDV infection in chickens, including producing a mass of inflammatory factors and
interferon stimulates genes (ISGs) (Hu et al., 2015; Jia et al., 2018). However, this
strong host antiviral response did not clear the virus and eventually caused highly
mortality in chickens. The virus completely depends on the host cells to complete its
life cycle. In this process, the virus may exploit or interrupt some of the host antiviral
mechanisms or host genes to escape the host immune system. The mechanism by
which viruses disrupt and exploit host genes in host cells may be the key to
understand the virus-host interactions. SOCS3 belongs to suppressor of cytokine
signaling (SOCS) proteins, which were shown to exert negative feedback regulation
function on the JAK/STAT signaling pathway (Baker et al., 2009; Qin et al., 2016). A
variety of viruses escape the host immune system by inducing the SOCS protein
expression. Some previous studies reported that influenza A virus upregulated SOCS1
and SOCS3 expression and inhibited STAT 1-3 signaling by NS1 protein to promote
virus replication (Jia et al., 2010). Additionally, phosphorylation of STAT1 was
promoted in SOCS3 knockdown cells, and the expression of interferon-stimulated
genes (ISGs) was also increased (Pauli et al., 2008). However, the potential molecular
mechanism by which NDV activates SOCS3 expression is unclear.