cord-000588-3wok0n21	2012	The present study was designed to investigate whether the presence of single nucleotide polymorphisms (SNPs) within DC-SIGN, Dectin-1, Dectin-2, CCL2 and CCR2 genes influence the risk of developing Invasive Pulmonary Aspergillosis (IPA). In addition, healthy individuals with this latter genotype showed a significantly decreased level of Dectin-1 mRNA expression compared to C-allele carriers, suggesting a role of the Dectin-1 (rs7309123) polymorphism in determining the levels of Dectin-1 and, consequently, the level of susceptibility to IPA infection. Based on these observations, the objective of the present study was to investigate the role of tagging and potentially functional single-nucleotide polymorphisms (SNPs) located within the DC-SIGN, Dectin-1, Dectin-2, MCP-1/CCL2 and CCR2 genes on IPA susceptibility. Of note is that two SNPs showing genetic interaction in this model were not significantly associated with an increased risk of IPA infection in the univariate analysis (CCR2 rs3918358 and Dectin-2 rs7134303 ).
cord-002058-rppsmirp	2010	The novel ligands are chaperone protein DnaK, 60 kDa chaperonin-1 (Cpn60.1), glyceraldehyde-3 phosphate dehydrogenase (GAPDH) and lipoprotein lprG. bovis BCG can bind to dendritic-cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN/CD209) to promote entry into human dendritic cells (DCs) and alveolar macrophages Maeda et al., 2003; Tailleux et al., 2003; Pitarque et al., 2005; Appelmelk et al., 2008) . However, the form of this protein identified after capture by the affinity column was not glycosylated at this position, and it is therefore very unlikely that DC-SIGN binds to this ligand via its Ca 2+ -dependent lectin activity. bovis BCG lysate incubated with either 125 I-DC-SIGN or 125 I-DC-SIGNR revealed that DC-SIGN and DC-SIGNR both bind the same protein at around 27 kDa, which corresponds to lprG in our SDS-PAGE system, and is the only ligand detected by this method. DC-SIGN and DC-SIGNR binding to lprG can therefore still occur when the mycobacterial protein has been denatured by SDS-PAGE.
cord-002372-ody77u5n	2015	Ginseng polysaccharides (GPs) are the responsible ingredient of ginseng in immunomodulation, and are classified as acidic and neutral GPs. Although GPs participate in various immune reactions including the stimulation of immune cells and production of cytokines, the precise function of GPs together with its potential receptor(s) and their signal transduction pathways have remained largely unknown. quinquefolius are mediated by PS with a molecular weight higher than 100 kDa. It was reported that acidic GPs promoted the production of cytotoxic cells against tumors and stimulated macrophages to produce helper types 1 and 2 (Th1 and Th2) cytokines [26, 27] . Because GPs were reported to significantly increase the viability of peritoneal macrophage cells [8] and ginseng was shown to inhibit degradation of long-lived proteins and to stimulate protein synthesis similar to polypeptide growth factors [41] , it was suggested that maintaining the cell viability under the condition of viral infection-induced stress might be an another alternative mechanism for the protective effects of GP.
cord-002395-goil7gjr	2016	The results demonstrate that two features characterize repeat units which form more stable tetramers: a leucine reside in the first position of the heptad pattern of hydrophobic residues that pack on the inside of the coiled coil and an arginine residue on the surface of the coiled coil that forms a salt bridge with a glutamic acid residue in the same polypeptide chain. Gel filtration revealed that this version of the neck domain forms a stable tetramer at room temperature since it elutes at the same position as a natural fragment of the neck domain of DC-SIGNR containing seven repeat units, which has been characterized as a tetramer [ Fig. 3(A) ]. The studies reported here suggest that the presence of stabilizing residues at positions 6 and 15 of the repeat units allows for the formation of stable tetramers even for shorter versions of the neck domain present in some individuals, which result from common genetic polymorphisms in the human population.
cord-009669-bcdjwpd1	2010	Trans-infection was reported to depend on DC-SIGNmediated binding and cellular uptake of HIV into dendritic cells (Geijtenbeek et al., 2000; Kwon et al., 2002) , followed by intracellular transport of virions to sites of dendritic cell-T cell contact, termed infectious synapses (McDonald et al., 2003) (Fig. 1) . Finally, signalling via TLR8 and DC-SIGN was required for NFkB-dependent recruitment of the transcription factor pTEF-b to the viral promoter, and thus for the generation of full-length HIV transcripts in dendritic cells -a prerequisite for productive infection (Gringhuis et al., 2010) (Fig. 2) . Dendritic cell-mediated trans-enhancement of human immunodeficiency virus type 1 infectivity is independent of DC-SIGN The C-type lectin surface receptor DCIR acts as a new attachment factor for HIV-1 in dendritic cells and contributes to trans-and cis-infection pathways Functionally distinct transmission of human immunodeficiency virus type 1 mediated by immature and mature dendritic cells
cord-017258-5mzr5s22	2015	Similar to the killer lectin-like receptors whose genes are clustered in this complex, most of the CLRs induce activating or regulatory signal cascades in response to distinct pathogenor self-derived components, through the immunoreceptor tyrosine-based activating or inhibitory motif, respectively. They commonly consist of an N-terminal cysteine-rich domain and a fibronectin type II domain as well as eight or ten CTLDs. In contrast, the asialoglycoprotein receptor family (group II) contains type II transmembrane proteins with a single CTLD, such as DC-specific ICAM3-grabbing nonintegrin (DC-SIGN, CD209), dectin-1, dectin-2, DC immunoreceptor (DCIR), and macrophage-inducible C-type lectin (Mincle) [4, 5, 9, 33, 69] . Notably, expression of some receptors is specific and they can be markers for distinct DC subsets; langerin (CD207) on Langerhans cells (LCs) and blood DC antigen (BDCA)-2 (CD303) on plasmacytoid DCs (pDCs) [25, 99] .
cord-018864-c1r2n17o	2007	In fact, the determinant role played by dendritic cells (DCs) in HIV-1 transmission might rely on specific interactions between gp120 and C-type lectins, of which the DC-specific intercellular adhesion molecule-3 (ICAM-3) grabbing nonintegrin (DC-SIGN) and DC-SIGNR (for DC-SIGN-related) are the best studied [10, 11]. In addition to its own virus-encoded envelope glycoproteins, the virus incorporates many different cellular proteins normally found on the cell surface (reviewed in [12] [13] [14] [15] The process of incorporation of host cell membrane proteins was found to be conserved among all tested HIV-1 subtypes and strains that were expanded in natural cellular reservoirs, such as mitogen-activated peripheral blood lymphocytes and human lymphoid tissue cultured ex vivo [27] [28] [29] [30] [31] [32] . Statin compounds reduce human immunodeficiency virus type 1 replication by preventing the interaction between virion-associated host intercellular adhesion molecule 1 and its natural cell surface ligand LFA-1 A dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN)-related protein is highly expressed on human liver sinusoidal endothelial cells and promotes HIV-1 infection
cord-021453-vf8xbaug	2007	
cord-021527-1etvgoxc	2009	• Diagnosis is based on the medical history, the physical examination findings, and a complete diagnostic work-up that includes a CBC, reticulocyte count, serum biochemical analysis, whole-body radiographs, and bone marrow cytology if indicated. M Key Point Base a presumptive diagnosis of insulinoma on the history, clinical signs, and repeated evidence of hypoglycemia in the presence of normal or elevated blood insulin levels. Lymphosarcoma (lymphoma) is common in ferrets of all ages, and is similar in presentation to the disease in cats and dogs (see Chapter 27). • Differential diagnoses include the early stages of adrenal gland disease; however, hair loss on the body typically occurs as well when this condition is present. • Ferrets with congestive heart failure (CHF) may present with clinical signs that resemble symptoms associated with other disease entities, such as anorexia, ascites, coughing, dehydration, dyspnea, exercise intolerance, generalized weakness, hindlimb weakness, hypothermia, lethargy, tachypnea, and weight loss.
cord-021555-rrverrsj	2007	These references also provide information regarding vaccination products licensed for use in ruminants and typical herd and flock vaccination parasite control schedules ("Current Veterinary Therapy," 1986 , 1999 "Council report," 1994; "Large Animal Internal Medicine," 1996; Smith and Sherman, 1994) When designing a vaccination program during qualification of a source or at the research facility, it is important to evaluate the local disease incidence and the potential for exposure. Clinical signs in chronic cases in older animals, such as adult goats, include soft stools, weight loss, anorexia, depression, and severe diarrhea, sometimes with mucus and blood. This pathogen does present a complication due to the carrier status of some animals, the likelihood of herd outbreaks, the severity of disease in younger animals, and the morbidity, possible progression to uveitis, and time and treatment costs associated with infections.
cord-022203-t2f0vr1w	2009	Clinical signs are often non-specific and include fever, anorexia and weight loss. Gastrointestinal signs are uncommon in cats compared to dogs, and include chronic diarrhea, mesenteric lymphadenopathy and anorexia. • Dysfunction of any organ system may result from granuloma formation within the tissue of that organ, e.g., liver, kidney, spleen, intestines, lungs, etc., however, organ failure producing clinical signs only rarely occurs, and most dysfunction is only detected on biochemical tests. Clinical signs in the acute, fatal form of extraintestinal disease are caused primarily by tissue damage from the rapidly dividing tachyzoites. • Young kittens are more likely to have gastrointestinal signs, although mild clinical disease has been reported in adult cats as well. Systemic signs, which are not present in all cats, include fever, anorexia, lethargy, vomiting, diarrhea and lymphadenopathy. Systemic signs such as fever, anorexia and depression are commonly reported (44% of cats) and can be seen with skin lesions.
cord-022243-lahg6xlm	2009	• By close proximity, the neurological structures associated with the middle ear may be affected leading to facial nerve paresis/paralysis, dry eye from decreased to absent lacrimation, and/or Acute to peracute non-progressive onset of a head tilt with ipsilateral falling or rolling in an otherwise healthy cat. Diagnosis is based on careful history taking (to disclose if there is somnolence or quietness of the animal), physical, neurological, otoscopic and ophthalmoscopic (including Schirmer tear test) examinations, serum protein concentration, cerebrospinal fluid analysis (CSF), CSF anti-coronavirus IgG titer, electrodiagnostic testing (brain auditoryevoked responses), bullae radiography, computed tomography (CT) and magnetic resonance imaging (MRI) scan. The history of an older cat presented with a rapid onset of neurological signs relating to the inner (vestibular signs and deafness) and middle ear (facial paralysis, decreased lacrimation and Horner''s syndrome) with pain upon jaw opening and a swollen face increases the index of suspicion.
cord-022283-8ny6j1ny	2009	Most cats with spinal cord disease have a combination of both ataxia and paresis, since most myelopathies cause disruption of both the motor and sensory systems. Cats presenting solely with ataxia and paresis/paralysis most commonly have spinal cord disease. The most common causes of spinal cord ataxia and paresis in cats are infectious (including feline infectious peritonitis virus (coronavirus)), neoplasia (lymphosarcoma) and trauma. Infectious diseases, such as feline infectious peritonitis, toxoplasmosis and cryptococcosis also may produce signs of progressive spinal cord dysfunction. Many cats with sacrococcygeal trauma also show signs of LMN paraparesis (sciatic nerve injury), consisting of dragging of the hind paws on their dorsum and a failure to flex the pelvic limb(s) when walking or when the withdrawal reflex is performed. Cats with severe myelopathy or cauda equina injury with analgesia have a very poor to hopeless prognosis since they commonly have physical or functional spinal cord or cauda equina transection. Feline polioencephalomyelitis is a chronic, progressive disease affecting the spinal cord and brain of cats.
cord-022352-yvdpj538	2009	
cord-022520-ebj51v9o	2007	Campylobacter jejuni is a gram-negative, spirally curved microaerophilic bacterium that is recognized as a significant cause of human enteritis and is as-sociated with diarrheic illness in several animal species, including dogs, cats, cows, goats, pigs, mink, ferrets, and sheep (Carter et al., 1995) . Reports of spontaneous cases in ferrets require diagnostic confirmation and differentiation from cases of proliferative bowel disease and other infectious and noninfectious causes of diarrhea. Systemic infection with the bovine strain in ferrets results in disseminated disease with weight loss, anorexia, lethargy, death, and miliary lesions involving the lungs and other viscera (Fox, 1998a) . Clinical disease may occur in kits as young as 1-4 days old or in older animals up to 6 weeks of age. Other potential etiologies that have been considered include two infectious agents that are known to cause chronic immune stimulation in affected ferrets, the Aleutian disease virus (ADV) and Helicobacter mustelae.
cord-022526-j9kg00qf	2009	Examination of the cardiovascular system (heart, peripheral pulse, and mucous membranes), lungs, and abdomen is essential to detect clinical signs of systemic inflammation from endotoxemia, coagulation disorders, dehydration, ileus, shock, and other abnormalities resulting from injury to the small or large intestine. Several reports suggest the efficacy of cisapride in managing intestinal disease in horses, including the resolution of persistent large colon impaction, treatment of equine grass sickness, and as a preventative for POI in horses after small intestinal surgery (0.1 mg/kg body mass intramuscularly during the postoperative period). 9 Primary role-players in DPJ-associated ileus include peritoneal inflammation, inflammatory cell migration/activation within the muscularis, small intestinal mechanical distention, and effects of endotoxin absorption. Diarrhea probably results from the severe ulceration and inflammation of the large intestine, causing increased secretion of water, electrolytes, and protein and decreased absorption of fluid.
cord-022555-a7ie82fs	2011	One study found that, of cats investigated for gastrointestinal disease, 9 of 33 cats (27%) had no pathology recognized proximal to the jejunum (i.e., the effective length of diagnostic endoscopes would have precluded diagnosis), and other organs were affected in 9 of 10 cats with inflammatory bowel diseases and 7 of 8 cats with intestinal small cell lymphoma. 60, 64 Quantification of serum cobalamin levels is recommended in cats with clinical signs of small bowel diarrhea, ones suspected to have an infiltrative disease of the small intestine (inflammatory bowel disease or gastrointestinal lymphoma), or ones with pancreatic dysfunction. Survey radiographs may be normal in cats with esophagitis and strictures, but are useful to rule out other causes for the clinical signs, such as a foreign body, or to detect related problems, such as aspiration pneumonia. 8, 29 Other non-neoplastic causes reported for gastric or gastroduodenal ulceration in cats include parasites (e.g., Ollulanus tricuspis, Toxocara cati, Aonchotheca putorii, Gnathostoma spp.), bacterial infections, toxins, inflammatory bowel disease, and foreign bodies.
cord-022575-ybj6lwdb	2009	1, 3 Signs of central vestibular syndrome suggest brainstem involvement and are not present in patients with inner ear disease except in cases of direct extension of the disease process, 8 such as can be seen with otitis media/interna 9 and neoplasia. Horner''s syndrome (miosis, ptosis, enophthalmos, and protrusion of the third eyelid) of the ipsilateral eye may be present with middle or inner ear disease, causing peripheral vestibular dysfunction ( Figure 56 -11). Peripheral vestibular dysfunction results from disease of the middle and inner ear affecting the receptors in the labyrinth and the vestibular portion of cranial nerve VIII. Seven such cats with otitis media/interna have been documented, in one study, with CNS dysfunction that included central vestibular signs. Peripheral vestibular disease in a cat with middle and inner ear squamous cell carcinoma Tympanic bulla osteotomy for treatment of middle-ear disease in cats: 19 cases (1984-1991)
cord-023165-f6o6owg3	2009	The most important reason for examining feces in sheep and goats is to determine the presence and relative number of nematode parasites infesting an animal or flock. Clinical signs of frothy bloat and free gas bloat from either food intake or physical obstruction of the esophagus are usually more severe and immediately life-threatening than bloat seen from rumen wall diseases and systemic influences. Rumen acidosis usually occurs in animals that have been fed predominantly forage-based rations and are suddenly given access to large amounts of highly fermentable concentrates or concentrated forms of energy. Table 4 -2 lists the agents most likely to cause diarrhea in lambs and kids, tissues or other samples required for diagnosis, and commonly employed test methods. Liver abscesses usually occur as a result of chronic rumenitis in cattle, but they are rare in sheep and goats. F. hepatica infestation usually causes acute disease in sheep and goats but can present as a chronic condition.
cord-023367-ujflw19b	2020	The cause of transformation is usually unknown; in rare cases, especially in flock outbreaks in sheep, it can be linked to exposure to the bovine leukemia virus, which has occurred experimentally and as a result of the administration of whole blood Anaplasma vaccines. C. perfringens type C in older sheep causes the disease known as "struck." Affected animals usually are found dead or with signs of toxemia. The course of the disease is usually very short (0.5-12 hours), so sudden or spontaneous death is a common clinical sign across affected small ruminant species. Additional evidence of systemic toxemia (metabolic acidosis, azotemia, and increases in liver and muscle enzymes) also may be seen; however, diagnosis of black disease is based on characteristic history (endemic liver fluke areas), clinical signs, and postmortem findings and testing.
cord-026009-rdhuc2n2	2009	This chapter provides information needed to diagnose and treat the most frequently encountered problems of mice, rats, gerbils, hamsters, guinea pigs, and chinchillas. • Diagnosis is based on clinical signs, history, visualization of parasite, skin scrape, and cellophane tape test. • Clinical signs in adults are caused by secondary bacterial infections and are similar to those in MRM. Common primary or secondary pathogens causing respiratory signs in mice are Streptococcus pneumoniae, Corynebacterium kutscheri, Pasteurella pneumontropica, Pseudomonas aeruginosa, and Klebsiella pneumoniae. • Mouse poliomyelitis/encephalomyelitis, also known as Theiler disease, causes clinical signs in 1 in 10,000 infected mice. • In contrast to mice, Sendai virus rarely causes clinical signs in rats. • Pneumonia in guinea pigs usually is caused by infection with S. • Diagnosis of scurvy is based on clinical signs, the exclusion of other causes of diarrhea, and response to vitamin C therapy (see Table 177 -10).
cord-026031-hnf5vayd	2009	Fresh whole blood Coagulopathy with active hemorrhage (disseminated intravascular coagulation, thrombocytopenia; massive acute hemorrhage; no stored blood available) Stored whole blood Massive acute or ongoing hemorrhage; hypovolemic shock caused by hemorrhage that is unresponsive to conventional crystalloid and colloid fluid therapy; unavailability of equipment required to prepare blood components Packed red blood cells Nonregenerative anemia, immune-mediated hemolytic anemia, correction of anemia before surgery, acute or chronic blood loss Fresh frozen plasma Factor depletion associated with active hemorrhage (congenital: von Willebrand''s factor, hemophilia A, hemophilia B; acquired: vitamin K antagonist, rodenticide intoxication, DIC); acute or chronic hypoproteinemia (burns, wound exudates, body cavity effusion; hepatic, renal, or gastrointestinal loss); colostrum replacement in neonates Frozen plasma Acute plasma or protein loss; chronic hypoproteinemia; (contains stable colostrum replacement in neonates; hemophilia B and clotting factors) selected clotting factor deficiencies Platelet-rich plasma* Thrombocytopenia with active hemorrhage (immune-mediated thrombocytopenia, DIC); platelet function abnormality (congenital: thrombasthenia in Bassett hounds; acquired: NSAIDs, other drugs) Cryoprecipitate
cord-253125-93r1aokh	2006	title: DC-SIGN Interacts with Mycobacterium leprae but Sequence Variation in This Lectin Is Not Associated with Leprosy in the Pakistani Population Here we sought to evaluate whether DC-SIGN interacts with the leprosy bacillus, Mycobacterium leprae, and whether DC-SIGN genetic variation influences the susceptibility and/or pathogenesis of the disease. Our most recent results show that nucleotide variation in the DC-SIGN promoter region is associated to susceptibility to tuberculosis [7] . leprae, we performed cold binding assays using fluorescently labeled bacilli and DC-SIGN-expressing recombinant HeLa cells as previously described [5, 11] . In this light, to investigate whether variation in the coding and/or the cis-regulatory regions of DC-SIGN is involved in susceptibility to and clinical outcome of leprosy, we conducted an association (case/control) study based on a sequencing/genotyping strategy in a cohort of patients presenting the two polarities of the disease and a group of healthy controls.
cord-265600-lnik974k	2011	Some PRRs located on the surface of dendritic cells (DCs) and other cells seem to play an important role in human immunodeficiency virus type 1 (HIV-1) transmission. Dendritic cell–specific intercellular adhesion molecule–3 grabbing non-integrin, CD209 (DC-SIGN) and its homolog, DC-SIGN-related (DC-SIGNR or L-SIGN) receptors are PPRs able to bind the HIV-1 gp120 envelope protein and, because alterations in their expression patterns also occur, they might play a role in both horizontal and vertical transmission as well as in disseminating the virus within the host. This review aims to explore the involvement of the dendritic cell-specific intercellular adhesion molecule-3 grabbing non-integrin, CD209 (DC-SIGN) and DC-SIGN-related C-type lectin domain family 4, member M (L-SIGN) receptors in HIV-1 transmission from mother to child. Transmission of the HIV-1 virus from mother to child via breast milk can occur by free virus particles and/or viral particles associated with cells [4] ; in this case, the expression of cellular receptors for recognition and adhesion of pathogens is required.
cord-266226-gxbrgy6g	2019	In particular, a red algae-derived griffithsin (GRFT) protein has demonstrated superior in vitro and in vivo antiviral activity with minimum host toxicity against a variety of clinically relevant, enveloped viruses. mGRFT possesses greatly reduced antiviral activity against HIV-1 in spite of its comparable association with high-mannose oligosaccharides, since mGRFT possesses all three carbohydrate-binding sites [20] . Combinations of GRFT and other carbohydrate-binding agents (CBAs) including Hippeastrum hybrid agglutinin, Galanthus nivalis agglutinin, a mannose-specific monoclonal antibody (mAb) (2G12), microvirin, and banana lectin also showed synergistic activity against HIV-1, HIV-2, and even against certain CBA-resistant HIV-1 strains [28] . In this regard, GRFT''s ability to partially block gp120 from binding to human DC-SIGN [34] and its potent inhibition of DC-SIGN-dependent transfer of HIV-1 [38] could synergize with its antiviral action by blocking viral entry. Monomerization of viral entry inhibitor griffithsin elucidates the relationship between multivalent binding to carbohydrates and anti-HIV activity
cord-267234-waz0k0ms	2015	Dendritic cell-specific ICAM-3-grabbing non-integrin (DC-SIGN/CD209) and liver/lymph node-specific ICAM-grabbing non-integrin (L-SIGN/CD299) which are homologues of DC-SIGN are important members in C-type lectin receptors family as key molecules to recognize and eliminate pathogens in the innate immune system. The sequence analysis results showed that mmDC-SIGN and mmL-SIGN have the same domains with other vertebrates except primates, and share some conserved motifs in CRD among all the vertebrates which play a crucial role in interacting with Ca(2+) and for recognizing mannose-containing motifs. In this study, we analyzed genomic organizations, gene structures, and synteny, evolutionary process and expression of miiuy croaker DC-SIGN (mmDC-SIGN) and L-SIGN (mmL-SIGN). Among these fish genomes, genes from TTC8 to ENTPD5 located downstream of L-SIGN had conserved synteny only differing in no RABEPK gene in miiuy croaker and no RABEPK and ALDH6A1 in stickleback. Another phylogenetic tree of L-SIGN genes constructed by Bayesian approach (Fig. 2C ) was used to test the positive selection in ancestral lineages of fishes.
cord-267269-05mezubh	2010	Previous studies have reported that TM-lacking encoding DC-SIGN sequences are transcribed as soluble cytoplasmic pro-teins but not secreted by the sDC-SIGN-expressing transfectant cells or immature MoDCs [19] . Thus, using our quantitative and specific ELISA, we observed the presence of potential sDC-SIGN isoforms in 10Ï« concentrated cell culture supernatants of mDC-SIGN-expressing DCs. In vitro DCs were generated from adult monocytes or CD34 Ï© CBPs, according to already well-known protocols [17, 23, 30] . Despite the use of high concentrations of Marimastat (10 M), no modification of sDC-SIGN versus mDC-SIGN expression patterns could be observed, thus weighing in favor of a sliced, sequence-derived product and not a shedding of mDC-SIGN by MMPs. Like many cell types, DCs are able to secrete 60 -80 nm membrane vesicles, called exosomes. In addition, as mDC-SIGN expression was reported to be responsible for MoDC CMV cis-infection, we assumed that FLAG-sDC-SIGN1AT1 may function as a promoter of the infection.
cord-267671-ys43n672	2015	Clinical Signs MCMV causes subclinical infection in adult immunocompetent mice, but experimental inoculation of neonates can cause lethal disease due to multisystemic necrosis and inflammation. Diagnosis Because infected mice do not manifest signs or lesions and the virus is very difficult to propagate in cell culture, detection and diagnosis rely on serology and molecular methods. Differential Diagnosis Reovirus infection must be differentiated from other diarrheal diseases of infant mice, including those caused by mouse coronaviruses, EDIM virus, Salmonella spp., or Clostridium piliforme. Epizootiology EDIM virus appears to be infectious only for mice and occurs episodically in mouse colonies, and infection is probably widespread geographically (Livingston and Riley, 2003; Pritchett-Corning LABORATORY ANIMAL MEDICINE et al., 2009) . Sentinel mouse surveillance, using soiled bedding, is an effective strategy for detecting MNV (Manuel et al., 2008) Differential Diagnosis The mild change in fecal consistency associated with MNV in adult mice may mimic rotavirus, coronavirus, Helicobacter spp., Citrobacter rodentium, or other enteric diseases.
cord-268902-npug5c8p	2015	In agreement with the findings in mosquitoes, a recent study has identified a C-type lectin in the shrimp Marsupenaeus japonicus that interacts with an envelope protein of White spot syndrome virus (WSSV) and consequently associates with a cell-surface calreticulin, which serves as a membrane receptor that facilitates viral entry in a cholesterol-dependent manner [128] . The interaction between lectins and viral glycoproteins may lead to the three following consequences: (1) lectins, such as MBL and SPs, function as pattern recognition molecules that bind a repertoire of viruses and activate antiviral immune responses; (2) lectins are employed as attachment factors that recruit viral particles to the cell membrane to enhance viral entry, e.g., some mammalian lectins (DC-SIGN, L-SIGN, MR and MPRs) or their homologs in arthropods (mosGCTLs); and (3) some intracellular lectins, such as calnexin and ERGIC-53, function as susceptibility factors associated with virus-encoded proteins to facilitate viral replication or assembly (please refer to Figures 1 and 4) .
cord-271505-eot38721	2006	
cord-275863-qos9vu3r	2011	In this report we have studied the interaction of dengue viruses produced in insect cells, tumor cell lines, and primary human dendritic cells (DCs) with DC-SIGN and L-SIGN. To formally prove that the loss of infection of DCs was a result of the loss of affinity of DC-produced virus for DC-SIGN, we went on to test infection on 3T3 cells expressing DC-SIGN and included in these assays the related C-type lectin L-SIGN ( Figure 3A ), which has also been reported to be a receptor for dengue virus. C6/36-and DC-derived viruses were incubated with increasing levels of pooled convalescent dengue immune serum and subsequently used to infect U937, a monocyte cell line that expresses the Fc receptor and which shows relatively low infectivity without the presence of enhancing antibodies. Viruses produced in both DCs and insect cells were susceptible to enhancement, over the same range of antibody concentrations, showing that DC-produced virus could exploit ADE to replicate in individuals undergoing a secondary dengue infection ( Figure 6A ).
cord-279343-ybncwweg	2005	The dendritic cell-specific ICAM-3 non-integrin (DC-SIGN) and its close relative DC-SIGNR recognize various glycoproteins, both pathogenic and cellular, through the receptor lectin domain-mediated carbohydrate recognition. On the basis of the current crystal structure and other published structures with sequence homology to the repeat domain, we generated a tetramer model for DC-SIGN/R using homology modeling and propose a ligand-recognition index to identify potential receptor ligands. [23] [24] [25] Modeling of the DC-SIGN/R tetramer A homology search was performed using sequences corresponding to various lengths of the repeat domain of DC-SIGNR against known structures in the Protein Data Bank (PDB). 21 On the basis of the current crystal structures and available biophysical data, a tetramer for the entire extracellular DC-SIGNR receptor was constructed by homology modeling in which the repeat regions form helical bundles to bring together their CRDs in a 4-fold related symmetry.
cord-287799-ridm3qd7	2012	Among those, Junin virus (JUNV) entry is enhanced in cells expressing DC-SIGN and for that reason surface-layer protein (S-layer) of Lactobacillus acidophilus ATCC 4365 was evaluated as a possible JUNV inhibitor. Experiments using 3T3 cells stably expressing DC-SIGN, showed an almost complete inhibition of JUNV infection when they were treated with S-layer in a similar extend as the inhibition shown by mannan. Since 3T3 cells are poorly infect by JUNV in the absence of expression of C-type lectins this model provides a really strong tool to study the effect of S-layer protein on the infection enhanced by DC-SIGN or L-SIGN. We presumed that the C-terminal portion of the S-layer would be responsible of the interaction with the glycan strand of DC-SIGN, since we have already shown it to interact with cell wall peptidoglycan [3] and it has been reported, that two repeats sequences in the C-terminal portion of the protein showed homology to carbohydrate binding domains (CBD) of Clostridium difficile S-layer/ toxin [27, 28] .
cord-293151-g3758oes	2015	This provides the necessary background to discuss the spontaneous diseases, including infectious and neoplastic conditions, prevalent in purpose bred as well as random source dogs used in biomedical research. Several factors that increase pressure at the site and/or affect the integrity of the skin will predispose an individual to develop pressure sores, including poor hygiene, self-trauma, low-protein diet, preexisting tissue damage, muscle wasting, inadequate bedding, and ill-fitting coaptation devices (Swaim and Angarano, 1990) . Chronic or recurrent corneal ulcers may also be associated with infection or hereditary causes in some breeds of dogs; however, these would be rare in the laboratory setting. Research Complications Treatment of early-stage or low-grade mammary tumors may be rewarding, allowing dogs to continue on study.
cord-300272-95o8yd7h	2020	In the context of the current COVID-19 pandemic, attention is now focused on the SARS-CoV-2 virus Zhou et al., 2020) .Coronaviruses use a homotrimeric glycosylated spike (S) protein protruding from their viral envelope to interact with cell membranes and promote fusion upon proteolytic activation. Additionally, in the case of SARS-CoV-2, a new paradigm is needed to untangle the complex clinical picture, resulting in a vast range of possible symptoms and in a spectrum of disease severity associated on one hand with active viral replication and cell infection through interaction with ACE2 along the respiratory tract, and, on the other hand, to the development of excessive immune activation, i.e. the so called "cytokine storm", that is related to additional tissue damage and potential fatal outcomes. These observations prompted us to investigate the potential interaction of C-type lectins receptors, notably DC/L-SIGN with SARS-CoV-2, through glycan recognition of the spike envelope glycoprotein, as well at their potential role in SARS-CoV-2 transmission.
cord-304720-0lgup7yj	2014	The industry significance, etiology, epidemiology, pathogenesis, clinical signs, postmortem and histpathologic lesions, diagnostic testing, and generic treatment, control, and prevention are described. Important history to understand from caretakers includes: age of pigs affected, duration of clinical signs, morbidity rate, mortality rate, treatments administered, response to treatments, and any other important information regarding previous diagnoses or disease in the affected group of animals. Records include but are not limited to: where the animals originated from; number in the herd; age; daily mortality; number treated; name of treatment, route of delivery and dose; feed and water usage; high-low temperatures; and vaccinations received or administered. Postweaning infections result in a high morbidity but low mortality; most significant economic losses at this time are caused by reduced average daily gain, market weights, and overall system efficiency. Postweaning infections result in a high morbidity but low mortality; most significant economic losses at this time are caused by reduced average daily gain, market weights, and overall system efficiency.
cord-308412-m4u1ax8k	2020	The following CT image features were observed for each patient: (a) the location, extent, and a number of lesions; (b) type of lesions (GGO, vascular thickening, pulmonary consolidation, pulmonary fibrous, interlobular septum, and solid nodules); (c) specific signs ("air bronchogram sign", "feather sign", "dandelion sign", "pomegranate sign", "rime sign"); (d) other signs (pleural effusion, mediastinal lymphadenectasis,etc). c A partially enlarged image at the same level as in figure b, suggesting that the GGO in the posterior basal segment of the left lower lobe showed a "pomegranate sign" (red arrow) Fig. 4 A older male patient who experienced constipation, and anorexia lasting for 1 week, and who had no epidemiological history. In the present study, we found that the most common CT imaging features in patients with COVID-19 were: bilateral, multifocal GGO, peripheral distribution; the predominant lower lobe; pleural effusion and lymphadenectasis were rare, which is consistent with previous reports [6] [7] [8] .
cord-322617-znvikfza	2005	
cord-333655-lylt7qld	2013	In sum, it appears that the dimeric lectin galectin-1 can enhance HIV-1 infection efficiency by cross-linking viral and host cell glycans and thereby promoting firmer adhesion of the virus to the target cell surface and facilitating virus-receptor interactions (Ouellet et al., 2005; Mercier et al., 2008; St-Pierre et al., 2011; Sato et al., 2012) . As has been shown for IAV, acquisition or deletion of glycosylation sites may affect crucial steps in the viral infection/replication process (e.g. receptor binding, fusion, release of newly formed virions) (Ohuchi et al., 1997; Wagner et al., 2000; Tsuchiya et al., 2002; Kim & Park, 2012) , alter the capacity of the virus to avoid induction of/recognition by virus-specific antibodies (glycan shielding) Wei et al., 2010; Wanzeck et al., 2011; Kim & Park, 2012; Job et al., 2013; Sun et al., 2013) , and modulate viral interaction with various immune system lectins (Reading et al., 2007; Vigerust et al., 2007; Reading et al., 2009; Tate et al., 2011a, b) .
cord-342936-43u7afl3	2007	Perhaps more importantly, such carbohydrate-binding agents (CBAs) may force the virus to delete at least part of its glycan shield to escape drug pressure 5 ; this might result in the initiation of an immune response against uncovered immunogenic envelope epitopes. Although such a mechanism may be efficient for a first-line inactivation of HIV, CBA-exposed HIV strains may decrease the efficiency of LCs to eliminate HIV, but at the same time may compromise the ability of the virus to be efficiently transmitted by DCs. The interactions of several CBAs have been extensively investigated, including: the prokaryotic CV-N and actinohivin; a variety of plant lectins, including Hippeastrum hybrid agglutinin (HHA) and UDA; the non-peptidic low-molecular-weight antibiotic PRM-A; and the monoclonal antibody 2G12 with the HIV-envelope gp120 and/or several glycan structures.
cord-344124-1ztyj0z4	2012	The long-sought entry receptors for rubella, sindbis and respiratory syncytial viruses (RV, SV and RSV), together with the missing measles virus (MV) receptor for infection of epithelial cells, were identified in 2011. The long-sought entry receptors for rubella, sindbis and respiratory syncytial viruses (RV, SV and RSV), together with the missing measles virus (MV) receptor for infection of epithelial cells, were identified in 2011. In addition, 2011 was rich in new information about the interactions of MV, RSV and phleboviruses with DC-SIGN during infection of dendritic cells, a crucial step allowing the virus to breach the epithelial barrier and gain access to the lymph nodes. For instance, for the arbovirus SV, which was also shown to interact with DCs via DC-SIGN for reaching the lymph nodes [47] , the studies discussed below have now identified an entry receptor -NRAMP -that is more likely to be used in these further stages of the infection, and perhaps at all stages, since it is very well conserved between humans and mosquitoes.