Establishment of a Mouse Model for Human Rhinovirus Infection

Yin, Fay H.; Lomax, N B

doi:10.1099/0022-1317-67-11-2335

Cited by 29 publications

(23 citation statements)

References 7 publications

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“…LDLRs are evolutionarily conserved, and HRV2 binds to cells from a number of species, e.g., mouse fibroblasts, but fails to replicate due to an intracellular block (39). Thus, the only available cell line, mouse M4 cells, which does not express any of the known minor-group HRV receptors could not be used for the present studies (27).…”

Section: Discussionmentioning

confidence: 99%

Human Rhinovirus Type 2-Antibody Complexes Enter and Infect Cells via Fc-γ Receptor IIB1

Baravalle¹,

Brabec²,

Snyers

et al. 2004

J Virol

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HeLa cells were stably transfected with a cDNA clone encoding the B1 isoform of the mouse Fc␥RII receptor (hereafter referred to as HeLa-FcRII cells). The receptor was expressed at high level at the plasma membrane in about 90% of the cells. These cells bound and internalized mouse monoclonal virus-neutralizing antibodies 8F5 and 3B10 of the subtype immunoglobulin G2a (IgG2a) and IgG1, respectively. Binding of the minor-group human rhinovirus type 2 (HRV2) to its natural receptors, members of the low-density lipoprotein receptor family, is dependent on the presence of Ca 2؉ ions. Thus, chelating Ca 2؉ ions with EDTA prevented HRV2 binding, entry, and infection. However, upon complex formation of 35 S-labeled HRV2 with 8F5 or 3B10, virus was bound, internalized, and degraded in HeLa-FcRII cells. Furthermore, challenge of these cells with HRV2-8F5 or HRV2-3B10 complexes resulted in de novo synthesis of viral proteins, as shown by indirect immunofluorescence microscopy. These data demonstrate that minor-group receptors can be replaced by surrogate receptors to mediate HRV2 cell entry, delivery into endosomal compartments, and productive uncoating. Consequently, the conformational change and uncoating of HRV2 appears to be solely triggered by the low-pH (pH < 5.6) environment in these compartments.

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Section: Discussionmentioning

confidence: 99%

Human Rhinovirus Type 2-Antibody Complexes Enter and Infect Cells via Fc-γ Receptor IIB1

Baravalle¹,

Brabec²,

Snyers

et al. 2004

J Virol

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“…Mouse-adapted HRV2 L and HRV1A grow in murine fibroblasts. We then tested whether HRV2 L , a variant of HRV2 which was adapted to replicate in mouse L cells (52,53), was able to grow in the mouse fibroblasts of the M cell collection. For control purposes, wild-type HRV2 and another minorgroup virus, HRV1A, were tested in parallel.…”

Section: Methodsmentioning

confidence: 99%

Species-Specific Receptor Recognition by a Minor-Group Human Rhinovirus (HRV): HRV Serotype 1A Distinguishes between the Murine and the Human Low-Density Lipoprotein Receptor

Reithmayer

Reischl

Snyers

et al. 2002

J Virol

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Human rhinoviruses (HRV) of the minor receptor group use several members of the low-density lipoprotein receptor superfamily for cell entry. These proteins are evolutionarily highly conserved throughout species and are almost ubiquitously expressed. Their common building blocks, cysteine-rich ligand binding repeats about 40 amino acids in length, exhibit considerable sequence similarity. Various numbers of these repeats are present in the different receptors. We here demonstrate that HRV type 1A (HRV1A) replicates in mouse cells without adaptation. Furthermore, although closely related to HRV2, it fails to bind to the human low-density lipoprotein receptor but recognizes the murine protein, whereas HRV2 binds equally well to both homologues. This difference went unnoticed due to the presence of other receptors, such as the low-density lipoprotein receptor-related protein, which allow species-independent attachment. The species specificity of HRV1A reported here will aid in defining amino acid residues establishing the contact between the viral surface and the receptor.Human rhinoviruses (HRVs) constitute a large genus within the family Picornaviridae and are the major cause of common cold infections (for a review on picornaviruses, see reference 43). Their icosahedral capsid is composed of 60 copies each of the viral proteins VP1, VP2, VP3, and VP4. The protein shell encases an RNA genome of positive polarity which is translated into a polyprotein upon arrival in the cytoplasm. The precursor protein is cleaved autocatalytically and cotranslationally by virally encoded proteases, giving rise to the capsid proteins and to the nonstructural proteins involved in replicative functions.Apart from one exception (HRV type 87 [HRV87]), the 102 serotypes are divided into a major and a minor group based on specific interaction with their cellular receptors, intercellular adhesion molecule 1 (ICAM-1; the major group) and members of the low-density lipoprotein receptor (LDLR) family (the minor group). Amino acid sequence information for the entire capsid protein region is available for 11 different serotypes (http://www.iah.bbsrc.ac.uk/virus/picornaviridae /SequenceDatabase/Index.html), and the three-dimensional structures of three major-group and two minor-group serotypes have been solved at atomic resolution (21,38,42,49,54). Medium-resolution structures from complexes of the majorgroup viruses HRV14 and HRV16 with soluble ICAM-1 (22, 39) as well as of the minor-group virus HRV2 and a soluble fragment of the very-low-density lipoprotein receptor (VLDLR) (14) have been obtained by image reconstruction from cryoelectron microscopy data. Whereas ICAM-1 binds inside the canyon, a cleft encircling the fivefold axes of icosahedral symmetry, the HRV2 receptor complex revealed that the BC loop and the HI loop of VP1 were largely covered by two of the three repeats of the recombinant VLDLR fragment VLDLR 1-3 , encompassing ligand binding repeats 1 to 3 only (41).The LDLR family comprises the LDLR proper, VLDLR, LDLR-related protein...

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“…The rat coronavirus infection is probably the animal model closest to coronavirus-induced common colds (Parker et al, 1970). Human rhionoviruses have not been adapted to rodents, except for one report in which unusual and tedious procedures were necessary to document virus replication in mice (Yin and Lomax, 1986). The EMC virus, Fig, 1.…”

Section: Introductionmentioning

confidence: 99%

Intranasal Treatment of Picornavirus and Coronavirus Respiratory Infections in Rodents Using 7-Thia-8-Oxoguanosine

Smee¹,

Alaghamandan²,

Bartlett³

et al. 1990

Antivir Chem Chemother

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SummarySince common cold viruses are responsive to interferon, we developed two animal models to test the efficacy of the interferon inducer 7-thia-8-oxoguano'" sine: (i) an intranasal coronavirus infection in suckling rats; and (ii) an intranasal encephalomyocarditis (EMC) virus infection in adult mice. Concentrations of 0.3 and 1% 7-thia-8-oxoguanosine delivered intranasally to rats 24 and 18 hours before virus inoculation were highly protective against the otherwise lethal coronavirus infection. A 1% concentration of drug administered 4 and 8 hours after virus challenge increased mean survival times of rats but did not increase numbers of survivors. Intranasal treatment of an EMC infection produced moderate improvements in mean survival times and survival. Titrations of EMC virus indicated >300-fold reductions in nasal titres in drug-treated relative to placebo control animals on days 2-4 following virus challenge. The distribution of r 4 C]-7-thia-8-oxoguanosine was determined shortly after intranasal delivery to mice and rats. Approximately 50% of total doses were deposited in the inner noses and mouths of both species. Most of the rest was found on/in the outer noses, stomachs, tracheas, oesophagi, and lungs. By analogy, the infecting viruses were deposited on/in the same organs and tissues of each species. The results suggest that containment of the viruses primarily occurred in the nasopharyngeal area prior to their spread to the lungs (rat coronavirus) or the brain (EMC), where fatal pathologies were manifest. Intranasal application of an interferon-inducing nucleoside analogue represents a new approach for the study of treatment of the common cold.

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Establishment of a Mouse Model for Human Rhinovirus Infection

Cited by 29 publications

References 7 publications

Human Rhinovirus Type 2-Antibody Complexes Enter and Infect Cells via Fc-γ Receptor IIB1

Human Rhinovirus Type 2-Antibody Complexes Enter and Infect Cells via Fc-γ Receptor IIB1

Species-Specific Receptor Recognition by a Minor-Group Human Rhinovirus (HRV): HRV Serotype 1A Distinguishes between the Murine and the Human Low-Density Lipoprotein Receptor

Intranasal Treatment of Picornavirus and Coronavirus Respiratory Infections in Rodents Using 7-Thia-8-Oxoguanosine

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