Disease relevance of Rhinovirus

• This observation indicates that, subsequent to attachment to the PVR-binding domain, poliovirus can use the same pathway as the major receptor group rhinoviruses to enter cells [1].
• Human rhinoviruses, like other picornaviruses, encode a cysteine protease (designated 3C) which cleaves mainly at viral Gln-Gly pairs [2].
• Proteinase 2A of human rhinovirus serotype 2 (HRV2 2A) was expressed in Escherichia coli and partially purified; the preparation was used to study various enzymatic parameters [3].
• Rhinovirus 2A protease and foot-and-mouth-disease virus L protease were used to analyze the association of eIF4G with eIF4A, eIF4E, and eIF3 [4].
• Coxsackievirus A21 (CAV21), like human rhinoviruses (HRVs), is a causative agent of the common cold [5].

High impact information on Rhinovirus

• Structure of human rhinovirus 3C protease reveals a trypsin-like polypeptide fold, RNA-binding site, and means for cleaving precursor polyprotein [6].
• The ICAM-1 binding site is distinct from those recognized by LFA-1, Mac-1, and the human major-type rhinoviruses [7].
• Plasmodium falciparum-infected erythrocytes bind ICAM-1 at a site distinct from LFA-1, Mac-1, and human rhinovirus [7].
• The arrangement of the immunoglobulin-like domains of ICAM-1 and the binding sites for LFA-1 and rhinovirus [8].
• ICAM-1 sequences important to binding LFA-1, rhinovirus, and four monoclonal antibodies were identified through the characterization of chimeric ICAM-1 molecules and mutants [8].

Chemical compound and disease context of Rhinovirus

• The glycoprotein intercellular adhesion molecule-1 (ICAM-1) has recently been identified as the cellular receptor for the subgroup of rhinoviruses known as the major groups [9].
• From the structure of sodium chloride to that of a human rhinovirus complexed with its receptor--X-ray crystal analysis has taken an extraordinarily fruitful path since its inception 80 years ago [10].
• We hypothesized that rhinovirus colds might increase asthma by augmenting airway allergic responses (histamine release and eosinophil influx) after antigen challenge [11].
• The activity of enviroxime against rhinovirus infection in man [12].
• Sodium cromoglicate inhibits the ICAM-1 molecule, which is the receptor for human rhinoviruses [13].

Biological context of Rhinovirus

• Analysis of a series of chimeric exchanges between human and murine ICAM-1 shows that two distinct epitopes recognized by monoclonal antibodies that block rhinovirus attachment and cell adhesion map to the N-terminal first domain of ICAM-1 [14].
• Polyadenylate sequences of human rhinovirus and poliovirus RNA and cordycepin sensitivity of virus replication [15].
• A full-length cDNA clone of the human rhinovirus type 14 genome RNA was assembled and transcribed in vitro by using the SP6 transcription system [16].
• The domain structure of ICAM-1 and the kinetics of binding to rhinovirus [17].
• Results from this study demonstrate that a large majority of emergent wheezing illnesses during childhood (2 to 16 yr of age) can be linked to infection with rhinovirus, and that these wheezing attacks are most likely in those who have rhinovirus together with evidence of atopy or eosinophilic airway inflammation [18].

Anatomical context of Rhinovirus

• In addition, ICAM-1 MAb block the cytopathic effect in HeLa cells mediated by representative major but not minor group rhinoviruses [19].
• Finally, we demonstrate that rhinovirus infection induced increased production of IL-8, IL-6, and GM-CSF from epithelial cells [20].
• Here it is shown that the Apaf-1 IRES is active in rabbit reticulocyte lysates, provided that the system is supplemented with polypyrimidine tract binding protein (PTB) and upstream of N-ras (unr), two cellular RNA binding proteins previously identified to be required for rhinovirus IRES activity [21].
• We hypothesized that rhinovirus infection of lower airway epithelium might induce ICAM-1 expression, promoting both inflammatory cell infiltration and rhinovirus infection [22].
• Moreover, the antibody fragment inhibits infection of human fibroblasts deficient in LDL-R but expressing LRP/alpha 2MR by human rhinovirus [23].

Gene context of Rhinovirus

• The loops are considerably different in structure to those of human ICAM-2 or murine ICAM-1, which do not bind rhinoviruses [24].
• Very-low-density lipoprotein receptor fragment shed from HeLa cells inhibits human rhinovirus infection [25].
• Mononuclear cells obtained at birth (umbilical cord blood) and at 1 year of age were incubated with phytohemagglutinin, respiratory syncytial virus, or rhinovirus, and supernatants were analyzed for IL-5, IL-10, IL-13, and IFN-gamma [26].
• RESULTS: Epithelial infection with rhinovirus specifically stimulated mRNA expression and release of VEGF, but not angiopoietins, in a time-dependent and dose-dependent manner [27].
• Human rhinovirus attenuates the type I interferon response by disrupting activation of interferon regulatory factor 3 [28].

Analytical, diagnostic and therapeutic context of Rhinovirus

• Seven allergic rhinitis patients and five normal volunteers were infected with rhinovirus type 16 (RV16) and evaluated by segmental bronchoprovocation and bronchoalveolar lavage [11].
• Site-directed mutagenesis suggests close functional relationship between a human rhinovirus 3C cysteine protease and cellular trypsin-like serine proteases [2].
• Studies using nasal provocation followed by nasal lavage have demonstrated that histamine plays an important role in the mediation of allergic rhinitis but not of rhinovirus infection [29].
• Twenty-four human rhinovirus serotypes were grown and purified by centrifugation in metrizamide density gradients [30].
• When crystals of human rhinovirus 16 (HRV16) and HRV14 are incubated with pleconaril, drug occupancy in the binding pocket is lower than when pleconaril is introduced during assembly prior to crystallization [31].

References