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At least 19 recordsLinked to original sources

PubMed1976

Comparison of rhinovirus-sensitive HeLa cells and human embryo fibroblasts for isolation of rhinoviruses from patients with respiratory disease.

Rhinovirus-sensitive HeLa cells (HeLa "R") and human embryo lung fibroblasts (HEL) were compared for the isolation of rhinoviruses from patients with respiratory disease. In the period May 1970 to December 1974, 526 rhinoviruses were isolated from 517 patients, 32% in both cell types, 59% in HeLa "R" only, and 9% in HEL only. The annual isolations in HeLa "R" were between 1.7 and 4 times greater than in HEL cells and may have been due to changes in the sensitivity of the cells or the prevalence of serotypes favoring the HeLa "R" cells. Acid lability was more easily demonstrated in HeLa "R" than in HEL cells, because the infectivity titers obtained were 10- to 100-fold higher.

Cell Line↗

PubMed1977

Demonstration of dual rhinovirus infection in humans by isolation of different serotypes in human heteroploid (HeLa) and human diploid fibroblast cell cultures.

The ability to isolate rhinoviruses in human heteroploid cell cultures was investigated by inoculating HeLa cells (HeLa M) with specimens previously shown to be positive in human diploid cell cultures. The 135 positive specimens selected were representative of 22 different rhinovirus types, and 4 to 9 specimens were available for each serotype. Specimens were inoculated into human diploid fetal tonsil fibroblasts (FT), HeLa cells with 30 mM Mg2+, and HeLa cells without increased Mg2+. One hundred twelve rhinovirus strains (83%) were reisolated in FT cells, whereas 76 rhinovirus strains (56%) were recovered in HeLa cells with 30 mM Mg2+. All strains recovered in FT were the same serotype as that originally recovered in diploid cells, but five of the HeLa cell isolates (3.7% of total specimens) were different serotypes, indicating dual rhinovirus infections. Four rhinovirus serotypes, (3, 42, 48, and 70) were recovered in HeLa but not in diploid cells; these serotypes were rare in our previous studies. Isolation of rhinovirus in FT cells was usually accomplished at first passage, whereas rhinovirus cytopathic effects in HeLa cells were not observed at first passage, but required one, two, or (rarely) three blind passages. Only 28 rhinoviruses (21%) were recovered in HeLa cells without increased Mg2+; however, three serotypes, types 16, 36, and 58, were recovered as effectively in HeLa cells, with or without added Mg2+, as they were in FT cells. In general, rhinoviruses were less efficiently recovered in HeLa cells; however, certain serotypes may be detected better by HeLa cells.

Cell Line↗

PubMed1992

[Chemoprophylaxis and chemotherapy of common colds caused by rhinoviruses: overview and outlook].

Rhinoviruses are the main etiologic agents of infectious common colds, which represent about 40% of the acute respiratory infections in man. The antigenic diversity of rhinoviruses precludes any prevention by vaccination. Within the last 20 years, efforts have therefore concentrated on chemoprophylaxis or chemotherapy with antiviral agents. Interferons (alpha and beta) administered intranasally at high doses, exerted a significant prophylactic activity in volunteers inoculated with rhinoviruses or in the course of epidemics in families. By contrast, the therapeutic activity of interferons is almost nonexistent, which greatly limits their practical interest. Various synthetic chemicals exert a marked and selective inhibitory effect on the replication of various serotypes of rhinoviruses in cell cultures. In the absence of an animal model of rhinovirus infection, in vivo studies of these molecules have been performed in human volunteers, chiefly at the Common Cold Research Unit in Salisbury (Great Britain). 3 synthetic compounds (an imidazothiazole, a benzimidazole derivative and a piperazinyl-pyridazine) have exerted a significant prophylactic activity, especially marked with the latter. None of these compounds, however, was active when administered after the infectious challenge. The search for selective anti-rhinovirus compounds is still going on; it will probably be facilitated through a combination of structural studies of rhinovirus capsids (or of their cellular receptors) with computer-assisted design of synthetic molecules. The recent observation of the influence of psychological factors on the propensity of rhinovirus-infected subjects to develop clinically apparent common cold must be taken into account in future studies.

Antiviral Agents↗

PubMedDate not supplied

[Development of optimal conditions for isolation of rhinoviruses].

When 366 dispensary patients with respiratory diseases were examined in Moscow during the period December 1969--May 1971, 49 strains of rhinoviruses were isolated out of which 21 strains were identified as type 48. Using Eagle's medium with a single set of amino acids and vitamins for isolation rhinoviruses were isolated in 4.7% of cases, empdoying Eagle's medium with a double set of amino acids and vitamins in 16% of cases. Virus isolation experiments were carried out in HeLa-Bristol cell cultures and diploid strain of skin-muscle cells KM-13-70 in the presence of 30 mM MgCl2 and 2% aminopeptide. The isolation rate of rhinoviruses in both the cell cultures was approximately similar. The average duration of time for isolation of rhinoviruses in diploid cells was 13.4 days, in HeLa-Bristol cells 15 days. All rhinovirus strains were isolated within 3 passages. In addition to rhinoviruses, from the same group of patients 25 Coxsackie A-21 strains, 12 adenovirus strains and 2 herpesvirus strains were isolated using Eagle's medium with double set of amino acids and vitamins.

Adenoviridae↗

PubMed1976

Sensitivity of rhinoviruses to human leukocyte and fibroblast interferons.

Rhinoviruses were tested for sensitivity to human interferon from two sources: human leukosytes induced with Sendai virus and human diploid fibroblasts induced with polyriboinosinic-polyribocytidylic acid. Twenty-five serotypes of rhinovirus were tested against fibroblast interferon in HeLa cells, and five serotypes were evaluated in fibroblast cultures against fibroblast and leukocyte interferons. Sensitivity varied widely in the HeLa cell assay; rhinovirus type 10 was inhibited by approximately 20-40 units of interferon, whereas rhinovirus type 15 was not inhibited by 5,120 units; the significance of this observation is unclear. In contrast, when fibroblast cultures were used in the assay system, five selected serotypes, including rhinovirus types 10 and 15, had similar levels of sensitivity (0.5-5.0 units) to fibroblast or leukocyte interferon.

Cell Line↗

PubMed1979

The spread of rhinoviruses in the Soviet Union (USSR) and in Czechoslovakia (CSSR) and the role of their pathology.

Virological, serological and immunofluorescence studies revealed circulation of rhinoviruses of the strains 1A, 1B, 2, 3, 7, 9, 10, 12, 13, 14, 16-23, 27, 29-33, 42, 48, 53, 56, 60 and 69 on the territory of Czechoslovakia and the Soviet Union. According to virological results, type 48 predominated and was followed in frequency of occurrence by types 27, 14 and 16 in the USSR and 30, 1A and 31 in the CSSR. RV infection in adults with ARD diseases was the aetiology in 28.5% of cases. Among the causative agents of acute rhinitis, rhinosinusitis and otitis, rhinovirus infection makes up a large proportion. Interrelation has been found between rhinovirus infection and chronic inflammation of the mucosa of the nose, the accessory sinuses and the ears. Prolonged course of rhinovirus infection and isolation of the virus in the late stages of disease (1-4 months after its onset) support the presumption that rhinoviruses promote chronicity of inflammation. RV was isolated from patients with chronic pneumonia from the lower respiratory passages (bronchial secretion). Rhinoviraemia was found in a child who died of ARD.

Adolescent↗

PubMed2024

Rhinovirus infection of airway epithelial cells uncovers the non-ciliated subset as a likely driver of genetic susceptibility to childhood-onset asthma.

Asthma is a complex disease caused by genetic and environmental factors. Epidemiological studies have shown that in children, wheezing during rhinovirus infection (a cause of the common cold) is associated with asthma development during childhood. This has led scientists to hypothesize there could be a causal relationship between rhinovirus infection and asthma or that RV-induced wheezing identifies individuals at increased risk for asthma development. However, not all children who wheeze when they have a cold develop asthma. Genome-wide association studies (GWAS) have identified hundreds of genetic variants contributing to asthma susceptibility, with the vast majority of likely causal variants being non-coding. Integrative analyses with transcriptomic and epigenomic datasets have indicated that T cells drive asthma risk, which has been supported by mouse studies. However, the datasets ascertained in these integrative analyses lack airway epithelial cells. Furthermore, large-scale transcriptomic T cell studies have not identified the regulatory effects of most non-coding risk variants in asthma GWAS, indicating there could be additional cell types harboring these "missing regulatory effects". Given that airway epithelial cells are the first line of defense against rhinovirus, we hypothesized they could be mediators of genetic susceptibility to asthma. Here we integrate GWAS data with transcriptomic datasets of airway epithelial cells subject to stimuli that could induce activation states relevant to asthma. We demonstrate that epithelial cultures infected with rhinovirus significantly upregulate childhood-onset asthma-associated genes. We show that this upregulation occurs specifically in non-ciliated epithelial cells. This enrichment for genes in asthma risk loci, or 'asthma heritability enrichment' is also significant for epithelial genes upregulated with influenza infection, but not with SARS-CoV-2 infection or cytokine activation. Additionally, cells from patients with asthma showed a stronger heritability enrichment compared to cells from healthy individuals. Overall, our results suggest that rhinovirus infection is an environmental factor that interacts with genetic risk factors through non-ciliated airway epithelial cells to drive childhood-onset asthma.

Preprint↗

PubMed1979

Rhinoviruses: kinetics of ultraviolet inactivation and effects of UV and heat on immunogenicity.

The kinetics of ultraviolet inactivation for two human rhinoviruses and poliovirus were compared. No major differences in the rates of ultraviolet inactivation were detectable. All viral preparations inactivated by ultraviolet irradiation induced neutralizing antibody in guinea pigs. In contrast, when guinea pigs were immunized with a heat inactivated rhinovirus preparation, little or no neutralizing antibody was elicited. Immune electron microscopy of the heated rhinovirus preparations revealed the presence of particles resembling empty capsids. These results suggest that rhinoviruses and enteroviruses are affected in a similar manner when subjected to ultraviolet or heat inactivation.

Antibodies, Viral↗

PubMed1992

Model for the differential stabilities of rhinovirus and poliovirus to mild acidic pH, based on electrostatics calculations.

Previous calculations of electrostatic interactions in the rhinovirus capsid have identified a subset of histidine residues, paired with lysine or arginine, that may be involved in pH-induced conformational changes related to viral uncoating. Further calculations with the finite difference method, accounting for the dielectric environment of the ionizable groups, suggest that charge burial in the crystal conformation will prevent protonation of these histidine residues in the pentamer-pentamer interface. Calculations with a modelled pentamer-pentamer interface in which three beta-strands are removed recover mildly acidic pKa values for the histidines. These results are discussed in the context of the structural interactions of these three beta-strands, which form a beta-sheet extension from the rest of the capsid, and with regard to the conformation of the homologous beta-sheet extension in poliovirus, which also possesses homologous histidine-lysine/arginine pairs. A model is developed in which the structural stability of the beta-sheet extension is related to the difference in acid stability of rhinovirus and poliovirus. It is suggested that, for poliovirus prior to cell receptor binding, the beta-sheet extension is stable at pH 3, the pentamer-pentamer interface histidines remain buried, and the virus is acid-stable. Cell receptor binding of poliovirus destabilizes the beta-sheet extension and the acid lability that is proposed to result could be involved in viral uncoating. For rhinovirus it is suggested that the observed conformational change in the absence of cell receptor binding involves a further acidic pH-activated process or conformational fluctuations that rearrange the beta-sheet extension and expose the pentamer-pentamer interface histidine residues to the acidic medium. Sequence analysis and electrostatics calculations reveal an aspartic acid in the beta-sheet extension that may have different pKa values in rhinovirus and poliovirus.

Amino Acid Sequence↗

PubMed1992

Development of common cold symptoms following experimental rhinovirus infection is related to prior stressful life events.

Previous studies of rhinovirus infection indicate that about one third of the persons with confirmed viral infection do not show evidence of cold symptoms. Factors that determine which infected individuals will develop colds are not known. Using a rhinovirus inoculation protocol, the authors explored the possible role of recent life events, current mood, and perceived stress in the development of symptoms in individuals known to be infected. As part of a larger study, 17 subjects were exposed to a rhinovirus and were individually isolated for 5 consecutive days; cold symptoms, mucus weights, and tissue use were monitored on a daily basis during this period. Although all 17 subjects had confirmed rhinovirus infection, only 12 subjects developed clinical colds, as indicated by self-reported symptoms and by objective symptom indices. The average number of reported major life events for the previous year was significantly higher for those who developed colds than for those who did not (p < .05). Measures of affect and perceived stress before the inoculation were not different for those who did and did not develop colds. Complementing recent research demonstrating psychosocial influences on experimental infection rates, these results provide evidence that the development of cold symptomatology in experimentally infected individuals is related to prior life events.

Adolescent↗

PubMed1992

[Three cases of lower respiratory tract infection worsened after rhinovirus infection].

We experienced three cases of lower respiratory tract infections worsened after Rhinovirus infection. Case 1: A 42-year-old male with diffuse panbronchiolitis was admitted to our hospital with the complaint of dyspnea on November 21, 1988. Rhinovirus was isolated from nasal washing and P. aeruginosa was cultured from transtracheal aspiration (TTA). Case 2: A 67-year-old male, whose underlying disease was pulmonary asbestosis, was admitted to our hospital complaining of pyrexia on June 12, 1990. Rhinovirus was isolated from TTA and H. influenzae and others were cultured from TTA. Case 3: A 64-year-old male with pulmonary emphysema was admitted to our hospital with a complaint of dyspnea on August 11, 1989. On December 17, 1989 the patient developed rhinorrhea and complained of purulent sputum, pyrexia and dyspnea after five days. Rhinovirus was isolated from nasal washing and TTA and S. nonhaemolyticus and others were cultured from TTA. As indicated in this report, it is interesting to study the relationship between viral infection of the upper respiratory tract and bacterial infection of the lower respiratory tract.

Adult↗

PubMed1976

Inhibition by zinc of rhinovirus protein cleavage: interaction of zinc with capsid polypeptides.

Zinic ions rapidly inhibit virus production in HeLa cells infected with human rhinovirus type 1A and lead to the accumulation of human rhinovirus type 1A precursor polypeptides. The degree to which cleavage of these precursors is inhibited is directly dependent on the quantity of cell-associated zinc. Proteolysis resumes after the removal of zinc-containing medium, and the accumulated viral precursors are cleaved predominantly to stable virus polypeptides. The precursors stabilized at the lowest zinc levels are those that contain capsid protein sequences. Furthermore, added zinc is bound to human rhinovirus type 1A capsids and prevents them from forming crystals. Zinc-resistant mutants display antigenic alterations in coat proteins. These results suggest that zinc complexes with rhinovirus coat proteins and alters them so that they cannot function as substrates for proteases or as reactants in the assembly of the virus particles.

Capsid↗

PubMed1977

Physicochemical characterization of two serologically unrelated equine rhinoviruses.

The physicochemical properties of two serologically distinct equine rhinoviruses have been examined. Each virus sedimented at approximately 160S but co-centrifugation of the two viruses in a sucrose gradient revealed a small difference in their sedimentation coefficients. The two viruses also have different buoyant densities in cesium chloride. The equine rhinovirus type 1 equilibrated as a sharp peak at 1.45 g/ml whereas the type 2 virus equilibrated as a heterogeneous band with a peak at 1.44 g/ml but ranging in density from 1.41 to 1.45 g/ml. The relative sedimentation coefficients of the two virus RNAs were 35S for rhinovirus 1 and 37S for rhinovirus 2. A limited number of base composition analyses also showed differences between the two virus RNAs. The polypeptide profile of each serotype in polyacrylamide gels was generally similar to those of other picornaviruses but the two serotypes could be distinguished readily from each other.

Antigens, Viral↗

PubMed1976

Effects of rhinovirus infection of pulmonary function of healthy human volunteers.

The effects of experimentally induced rhinovirus and mycoplasmal respiratory tract infections on the pulmonary function of healthy, young, adult volunteers were investigated prospectively. Before inoculation, 12 volunteers were completely normal, whereas 9 had increased frequency dependence of compliance as their only abnormality of pulmonary function. Rhinovirus infection was induced in 8 of the completely normal volunteers, and 5 developed increased frequency dependence of compliance at the time of illness. These changes returned toward normal during the following 2 weeks and were not associated with concomitant changes in any other parameter of pulmonary function, including "closing volume". Three subjects with increased frequency dependence of compliance as their only abnormality before rhinovirus infection developed no significant change in dynamic compliance or any other abnormality in pulmonary function after infection. No changes in pulmonary function were detected in 3 volunteers with experimentally induced mycoplasmal infection. These finding suggest that although rhinovirus infections are associated primarily with upper respiratory illness, they can produce transient peripheral airway abnormalities in previously normal young adults; however, closing volumes, as well as routine pulmonary function studies, may not detect these changes.

Adult↗

PubMed1992

Effects of naproxen on experimental rhinovirus colds. A randomized, double-blind, controlled trial.

OBJECTIVE: To determine whether naproxen, a propionic acid inhibitor of cyclooxygenase, alters the course of experimental rhinovirus colds. DESIGN: A randomized, double-blind, controlled trial. SETTING: Rhinovirus challenge model in volunteers cloistered in individual hotel rooms. VOLUNTEERS: Eighty-seven healthy young adults with serum neutralizing antibody titers of less than or equal to 1:2 to the challenge virus; 79 were evaluable. INTERVENTION: Thirty-nine participants received naproxen (loading dose, 400 mg or 500 mg followed by 200 mg or 500 mg three times daily for 5 days). Forty participants received placebo. Treatment was started 6 hours after viral challenge. MEASUREMENTS: Daily measurement of viral titers, symptoms, nasal mucus production, and nasal tissue use; incidence of infection and illness; and measurement of homotypic serum neutralizing antibody responses. RESULTS: Viral titers and serum homotypic antibody responses were similar in the naproxen and placebo groups. Significant reductions in headache, malaise, myalgia, and cough occurred in the naproxen group. A 29% reduction was noted in the total (5-day) symptom score in the naproxen group (95% CI, 16% to 42%). CONCLUSION: Naproxen treatment did not alter virus shedding or serum neutralizing antibody responses in participants with experimental rhinovirus colds, but it had a beneficial effect on the symptoms of headache, malaise, myalgia, and cough. Prostaglandins may be among the inflammatory mediators that play a role in the pathogenesis of rhinovirus colds.

Adult↗

PubMed1978

Hand-to-hand transmission of rhinovirus colds.

Rhinovirus was transmitted from experimentally infected volunteers (donors) to susceptible recipients and the efficiencies of spread by hand-to-hand contact and large- and small-particle aerosols compared. Transmission of infection was very efficient by the hand route: 11 of 15 hand-contact exposures initiated infection, compared with one of 12 large-particle (P less than 0.005) and none of 10 small-particle (P less than 0.005) exposures. Rhinovirus was present in nine of 18 (50%) nasal swab specimens, 28 of 43 (65%) hand rinses, and seven of 18 (39%) saliva specimens of donors; geometric mean titers of positive specimens were 10(1.5), 10(1.4), and 10(1.2) tissue culture infectious dose 50/ml (TCID 50/ml), respectively. Rhinovirus was present in 20 of 43 (46%) recipient hand rinses, with a geometric mean titer of 10(1.4)TCID50/ml. Virus on donors' hands was transferred to recipients' fingers during 20 of 28 (71%) 10-second hand-contact exposures. These findings support the concept that hand contact/self-inoculation may be an important natural route of rhinovirus transmission.

Adolescent↗

PubMed1992

Internalization of a major group human rhinovirus does not require cytoplasmic or transmembrane domains of ICAM-1.

Intercellular adhesion molecule-1 (CD54), a cell adhesion molecule and the receptor for the major group of rhinoviruses, is a class 1 membrane protein with five Ig-like domains in its extracellular region, a transmembrane domain, and a short cytoplasmic domain. The amino-terminal domains (D1 and D2) are sufficient for virus binding and the first is most important (1). We have investigated whether other extracellular domains, transmembrane or cytoplasmic domains are required for virus entry as determined by postinfection virion protein biosynthesis. We demonstrate that cytoplasmic, transmembrane, and Ig-like domains 3, 4, and 5 are not essential for rhinovirus entry into transfected COS cells. The efficiency of rhinovirus infection directly correlates with the efficiency of rhinovirus binding and a form of intercellular adhesion molecule-1 that is glycophosphatidyl-inositol anchored, and thus does not extend into the inner leaflet of the membrane bilayer or the cytoplasm efficiently supports virus entry.

Cell Adhesion Molecules↗

PubMed1975

Antigenic relationships of common rhinovirus types from disabling upper respiratory illnesses.

The frequency of the common cold has been though to be due to the existence of more than 89 different serologic types of rhinoviruses. However, in the civilian and military population studied in this area from 1962 through 1970, types 1A, 1B, 2, 23, 29, 30 and 31 accounted for 81 percent of 487 rhinoviruses isolated from individuals with respiratory illnesses. Antigenic relationships between these types and others have been demonstrated by neutralization in WI-38 cell cultures and by immunodiffusion. Types 1A and 1b, 2 and 49, 23 and 30, 29 and 44 and others are related. With specific animal antisera, heterotypic antibody titers are minimal. However, following natural infection in man with one of these related types, antibody responses to the other was almost equal to the homotype and could predictably provide cross-protection. Even with inactive T13 rhinovirus vaccine in man, protective levels of neutralizing antibody to T41 were produced. It is clear that the rates of rhinovirus colds would be greatly increased if more than 89 immunologic distinct types actually existed. An effective vaccine could be easily prepared by selection of a few appropriate types, such as 1A, 2, 23, 29 and 31.

Adolescent↗