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viruses may constantly evade the immune system resulting in 2008). The expression of collectins is also regulated in vivo during
persistent infections. In fighting diseases, the host has adapted to infection with IBV (Kjaerup et al., 2014, Hamzic et al., 2016). In
viruses and chickens especially have evolved and are genetically contrast to collectins, members of the pentraxin family – long
selected for disease resistance. pentraxin PTX3, short pentraxin, and serum amyloid P compo-
The first line of defence at mucosal surfaces is a complex nent – provide sialylated ligands that mimic the structure of the
physiochemical barrier of epithelial cells lined by a mucus layer. cellular receptors used by IAVs, thereby blocking the receptor-
Depending on the tissue, additional mechanisms such as cili- binding site of haemagglutinin of influenza. PTX3 is stored in
ary movement in airways, peristaltic movement in the intestine neutrophils, whereas dendritic cells and macrophages produce
and gastric acidic pH are also present. Mucus provides a semi- PTX3 de novo upon inflammatory stimulation (reviewed by Bot-
permeable barrier that enables the exchange of nutrient and tazi et al., 2010). PTX3 in chickens is highly up-regulated after
gases but prevents pathogens adhering to the epithelium. Many in vivo inoculation of type I IFN (Röll et al., 2017) and infection
different components in mucus are described to have antimicro- with AIV.
bial properties, such lysozyme and defensins, and an increase in
mucus production induced by many viruses including ILTV, AIV, Sensing of viruses
and IBV, allows for improved trapping and clearance of viral par- In contrast to bacteria, viruses do not contain many easily recog-
ticles. Beside their role as a barrier, epithelial cells regulate innate nizable microbe-specific structures since they are made up from
and adaptive responses by recognition of virus through host sen- host-derived products. However, the host has evolved the ability
tinel proteins, rapid signalling and transcription factor activation to recognize virus specific structures or evolutionary conserved
that will in turn lead to the production of antiviral molecules and molecular markers, known as pathogen or microbe associated
recruitment of immune cells (reviewed by Vareille et al., 2011). molecular patters (PAMPs or MAMPs). PAMPs are sensed by
pathogen recognition receptors (PRRs) expressed either on the
Inducible antimicrobial components cell surface or intracellularly. Binding of viral PAMPs to these sen-
Innate inhibitors with antimicrobial properties are already pre- sors recruits downstream signalling molecules and either directly
sent at mucosal surfaces and their composition changes during an or indirectly activates transcription factors, and production of
acute phase response. They belong to families of proteins that are soluble factors such as interferons (IFNs), pro-inflammatory
highly conserved in evolution and some members are also found cytokines and chemokines that lead to an antiviral state of the
in invertebrates, plants and fungi. cell. Cells have the amazing capability to distinguish self-products
A variety of proteins are involved in the early responses and from viral products through the use of cellular sensors that rec-
include acute phase protein, C-reactive protein, serum amyloid A, ognize for example nucleic acids in unusual locations which are
collagenous lectins (e.g. collectins, surfactants and ficolins), pen- associated with viral infections. Several PRRs have been identi-
traxins, alpha macroglobulin families and host defence peptides fied that recognize viral PAMPs in birds (reviewed by Chen et al.,
(e.g. defensins and cathelicidins). Host defence peptides (HDPs) 2013) and they include Toll-like receptors (TLRs), nucleotide-
were originally called antimicrobial peptides because of their abil- binding oligomerization domain (NOD) like receptors (NLRs),
ity to kill bacteria, but further research indicated that they also RIG-I like receptors (RLRs) such as retinoic acid-inducible
play a role against a wide variety of pathogens including viruses gene 1 (RIG-I), Melanoma Differentiation-Associated protein 5
and in immune modulation. (MDA5), Laboratory of Genetics and Physiology 2 (LGP2), and
The antiviral activities of innate inhibitors can be divided into C-type lectins (CLRs). Similar to human TLRs, 10 chicken TLRs
direct and indirect activities. Direct activities include inhibition have been described (reviewed by Keestra et al., 2013), but there
of viral attachment and agglutination, whereas indirect antiviral are noticeable differences including the presence of TLR1La,
properties include complement activation induced cell lysis, TLR1Lb, TLR15 (avian specific), TLR21 (equivalent of mam-
phagocytosis and immunomodulation. Although not studied in malian TLR9), the absence of TLR9 and a pseudogene TLR8.
depth in chickens, some examples are described and the need The role of TLR1 and TLR5 in antiviral responses is not well
for development of novel antiviral control strategies is expected documented and the mechanisms of virus recognition by TLR2
to drive future research in this field. Collectins such as mannose and TLR4 still remains to be elucidated, although recently NDV
binding lectin (MBL) express carbohydrate recognition domains virus-like particles were shown to activate murine dendritic cells
(CRDs) that bind to mannose rich glycans on for example spike (DC) through the TLR4/NF-κB pathway (Qian et al., 2017).
protein of IBV to mediate aggregation and thereby neutraliza- A major antiviral role is exerted by TLRs that recognize nucleic
tion of viral particles (Zhang et al., 2017). Chicken surfactant A acids including oligodeoxynucleotides containing unmethylated
(SP-A) lacks most of the collagen domain which indicates that it CpG motifs (CpG-ODNs), such as TLR15 and the endosomal
may not be able to establish an oligomeric cluster as mammalian receptors TLR3, TLR7 and TLR21 (reviewed by Chen et al.,
SP-A. The application of IFNα in vivo resulted in a strong decrease 2013). In chicken, TLR3 is constitutively expressed in a wide
of SP-A expression (Röll et al., 2017) whereas gene expression range of tissues and similar to mammals it recognizes dsRNA and
was up-regulated during AIV infection (Reemers et al., 2010). the agonist poly-I:C and then rapidly induces type I IFN that in
The SP-A homologue chicken lung lectin (cLL), although strictly turn can up-regulate TLR3 (Karpala et al., 2008a). The expres-
not a collectin but a C-type lectin due to its lack of a collagenous sion of TLR3 during viral infections was found both up and down
domain, has moderate activity to IAV in vitro (Hogenkamp et al., regulated. Opposite changes in TLR3 expression are induced by