Epidemiology of infections with rhinovirus types 43 and 55 in a group of university of Wisconsin student families.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
There is still controversy over the role of viruses and bacteria in rhinologic infections, especially in sinusitis. Until recently it was not fully known whether the sinuses do in fact take part in the infectious process of a common cold (viral rhinitis). CT scans show that in the vast majority of otherwise healthy volunteers with a common cold, and without a previous history of recurrent or chronic sinusitis, the sinuses are involved; there was, however, in these individuals no typical symptomatology of acute sinusitis. A viral rhinitis alone does not seem to be able to elicit a "clinical" acute otitis. Bacteria determine the clinical picture and outcome of sinusitis. There is not much controversy about the role of bacteria in acute sinusitis, S. pneumoniae, H. influenzae, and M. catarrhalis being the most frequently involved. Much more conflicting reports are published about the normal flora of the sinuses, the role of anaerobes and the microbiology of chronic sinusitis. In this paper the mechanisms of viral and bacterial infection of the nasal and sinusal mucosa are described and the results of microbiological studies in sinusitis reported by other authors and our own group are discussed. It is postulated that, although bacteria are very important in acute sinusitis, their role in chronic sinusitis is minimal, the bacteria being opportunistic colonisers.
Explore the source record for details and available documents.
Re-infection is a term used to describe a new or secondary infection by a virus that has already infected a person. In most viral diseases, re-infection with the same virus doesn't occur because once the immune system conquers the original viral infection, it creates immunity against that virus. Re-infection occurs almost constantly, however, in some types of infection, such as the cold or flu viruses, because each new version of those new viruses is substantially different from the last. This is why a person may develop immunity to the flu strain that is common in one year, but still be at risk from the strain that becomes dominant the next year.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Anti-nerve growth factor (anti-NGF) antibody has been shown to induce reactivation of latent herpes simplex virus type 1 (HSV-1) in vitro. We found that systemically administered anti-NGF induces ocular shedding of HSV-1 in vivo in rabbits harboring latent virus. Rabbits in which HSV-1 latency had been established were given intravenous injections of goat anti-NGF serum daily for 10 days beginning 42 days after primary viral infection. Tears were assayed for virus for 12 days beginning on the day of the first injection. All eight rabbits given high titer anti-NGF had infectious virus in their tears at least once during the 12-day period. Fifteen of 16 eyes were positive and the average duration of viral shedding for these eyes was 4.0 days. Latently infected rabbits receiving daily injections of nonimmune goat serum or saline for 10 consecutive days were controls. Only six of the 16 (38%) eyes from rabbits receiving nonimmune goat serum shed virus. Only one of 12 eyes from untreated rabbits shed virus. Sera from control rabbits had no detectable anti-NGF activity; titers in anti-NGF-treated rabbits ranged between 1:1000 and 1:10,000. NGF deprivation may act as a neuronal stressor and may share a common second messenger pathway with heat- or cold-stress induced reactivation of latent HSV-1.
We have studied the effect of mutations in H-2Kb on recognition of Moloney virus antigens by Kb-restricted Moloney virus-specific cytotoxic T lymphocytes (CTL) generated from H-2Db-mutant B6.C-H- 2bm13 ( bm13 ) mice. On the basis of the bm13 virus-specific recognition pattern of a series of Kb-mutant virus-infected (V+) cells, these Kb mutants could be divided into two groups that either shared the relevant H-2K restriction specificities with H-2Kb ( bm3 , bm5 , bm6 , and bm11 ) or lacked them completely (bm1) and/or almost completely ( bm8 ). In the study presented in this report, we concentrated on the alloreactive CTL included in the repertoire of bm13 Moloney-specific CTL. These CTL lysed noninfected (V-) allogeneic target cells of many H-2 types, including all Kb-mutant cells tested (bm1, bm3 , bm5 , bm6 , bm8 , and bm11 ). Recognition of V- cells of two Kb mutants, bm3 and bm11 , which share a common amino acid substitution at position 77 of the H-2K molecule with an additional change at position 89 in bm3 , was compared with recognition of the other Kb-mutant V- target cells in cold target inhibition studies. These studies showed that bm3 and bm11 cells share a determinant or determinants on the H-2K molecule recognized by alloreactive CTL among the Moloney virus-specific CTL population not present on the other Kb-mutant cells; lysis of both target cells was inhibited only by bm3 and bm11 V- cells. On the other hand, lysis of bm3 V+ target cells by bm13 virus-specific CTL was inhibited by all Kb-mutant V+ cells ( bm3 , bm5 , bm6 , and bm11 ) that were killed virus specifically by bm13 CTL. Thus, common determinants on the H-2K molecule of these Kb-mutant V+ cells are recognized by Kb-restricted Moloney virus-specific CTL. From the difference in inhibition pattern of the lytic reaction against bm3 V+ vs bm3 V- cells, we conclude that determinants on the same H-2K molecule recognized by Moloney virus-specific CTL and allocross -reactive effector cells included in the Moloney virus-specific population are not identical.
Ohio HeLa cells in multichamber slides were inoculated with nasal samples from patients presenting with common cold symptoms and incubated at 33 degrees C with gentle shaking for 48 hours. The cultures were fixed with cold acetone, and viral antigens were detected by immunofluorescence using an antirhinovirus type 2 (HRV-2) polyclonal serum. Of 158 samples, 58 (36.7%) and 57 (36%) were positive for HRV by virus isolation (confirmed by acid lability test) and by culture-amplified immunofluorescent (CAIF) test, respectively. The correlation between the two tests was highly significant (P = 0.0001). Nasal washings or nasal/throat swabs were equally suitable for detecting virus by isolation but not by CAIF. On the other hand, nasal washings were better than nasal/throat swabs for detecting HRV by CAIF. In an ELISA system, the polyclonal anti-HRV-2 serum recognized a rhinovirus antigen expressed in situ within 48 hr postinfection by all the 11 HRV serotypes investigated. However, 60 hr postinfection, the anti-HRV-2 serum recognized only homologous and closely related HRV antigens. These results suggest that a rhinovirus "common" antigen may be expressed some 48 hr after infection of Ohio HeLa cells with rhinoviruses. The CAIF test provides a sensitive, rapid and reliable procedure to detect wild-type rhinovirus infection as well as a clear alternative to detection by isolation.
Explore the source record for details and available documents.
PURPOSE: We performed a randomized, double-blind, placebo-controlled trial to evaluate the efficacy of 0.12% zinc sulfate nasal spray for reducing the duration and severity of acute upper respiratory infections. SUBJECTS AND METHODS: Patients with acute onset of upper respiratory illness of less than 24 hours' duration were eligible for the study. A nasopharyngeal swab was obtained at the time of enrollment for viral culture. Participants were randomly assigned to receive either 0.12% zinc sulfate or isotonic placebo spray. The medication was administered as two inhalations in each nostril four times a day. Each patient completed a diary card twice a day to record oral temperature, symptoms, and adverse effects. Symptoms were scored as absent (0), mild (1), moderate (2), or severe (3). RESULTS: One hundred eighty-five subjects volunteered to participate, and 160 met the criteria for enrollment. The median duration of all symptoms was 7 days in both groups (P = 0.45), and the median duration of nasal symptoms was 6 days in both groups (P= 0.12). After adjustment for baseline differences in severity, patients receiving zinc had a significant reduction in the total symptom score (P= 0.02) and the nasal symptom score (P= 0.02) on day 1, but not on any of the other days. Adverse effects were mild and had no significant association with the use of zinc. A respiratory virus was identified in 9 of the 160 participants; 6 of these were rhinovirus. CONCLUSION: A low concentration of zinc sulfate nasal spray had no effect on the duration of the common cold.
As can be seen from the preceding brief discussion, the prospects for new antiviral agents for the treatment of viral diseases ranging in severity from the common cold to AIDS appear promising. The latest advances in technologies such as crystallography, genetic engineering, and monoclonal antibodies are all being applied to the discovery of new ways to inhibit virus-specific processes. In addition, the development of diagnostic tests for viral diseases has proceeded at a rapid pace that should facilitate the proper use of the antivirals when they become available. The one lesson that has been learned in the antiviral field over the past decade is that virus-specific inhibitors do exist, and if an essential virus-specific process or protein can be identified, it is likely that a molecule can be found to inhibit or inactivate it.
Rous sarcoma virus (RSV) mainly replicates in avian fibroblasts, and the U3 enhancer region of the long terminal repeats of RSV contains the determinants for its tissue-tropic expression. We describe the cloning and characterization of an avian gene that encodes a protein capable of binding to the enhancer region of Rous sarcoma virus. A PCR-derived probe corresponding to the U3 region of RSV was used to isolate a cDNA clone by screening a chicken cDNA expression library. The cDNA is predicted to encode a polypeptide of 298 amino acids that is homologous to the Y-box (inverted CCAAT) family of DNA-binding transcription factors. This factor, which we refer to as Rous sarcoma virus enhancer factor-II (RSV-EF-II), shows 99% aa identity over a 105-amino-acid stretch that is highly conserved in all Y-box proteins, and is commonly referred to as the cold shock domain. RSV-EF-II selectively binds to single-stranded DNA, and the binding site, as determined by electrophoretic mobility shift assays, consists of the sequence 5' GTACCACC 3' located between nucleotides -112 to -119 in the noncoding strand of the RSV enhancer. Although RSV-EF-II shares considerable homology with the Y-box family of proteins, it does not bind to the inverted CCAAT boxes at positions -65 to -69 and -129 to -133 in the RSV LTR. Northern analysis indicates that RSV-EF-II-specific transcripts are expressed predominantly in avian fibroblasts and muscle tissue. The results of these binding and mRNA expression expriments suggest that RSV-EF-II may play an important role in tissue- and host-specific expression of RSV LTR-driven gene expression. Further, we show that RSV-EF-II acts as a repressor of transcription.
The detection of human herpesvirus 6 (HHV-6) DNA was carried out in throat swabs of adults and children by the polymerase chain reaction, and isolation of virus was also attempted from peripheral mononuclear cells. Although virus was isolated only from peripheral blood mononuclear cells of infants with exanthem subitum, HHV-6 DNA was detected in one of 30 healthy adults (3%), two of nine adults (22%) with common cold, two of 10 infants (20%) with exanthem subitum, four of 39 febrile children (10%) with antibody to HHV-6 (including three of 10 infants aged under 1 year old, and one of 29 children aged over 1 year old). However, HHV-6 DNA was not detected in samples from healthy neonates.
Explore the source record for details and available documents.
OBJECTIVES: A few epidemiological studies have indicated that a patient's past medical history may contribute to the risk of developing idiopathic pulmonary fibrosis (IPF). A relationship between a history of selected disorders and the risk of IPF was assessed in a multicentre hospital-based case-control study in Japan. METHODOLOGY: Included in the study were 104 patients of IPF, aged 40 years or over, who had been diagnosed within the previous 2 years, in accordance with the most recent criteria. Control subjects, aged 40 years or over, consisted of 56 hospitalized patients diagnosed as having acute bacterial pneumonia and four outpatients with the common cold. Adjustment was made for age, gender, region, pack-years of smoking, employment status, occupational exposure and BMI. RESULTS: Medical histories of hypertension, hyperlipidaemia, coronary heart disease, diabetes mellitus, hepatitis C virus infection, tuberculosis, asthma, atopic dermatitis and allergic rhinitis were not statistically significantly associated with the risk of IPF, although cases were more likely to have suffered from allergic rhinitis and less likely to have been asthmatics than control subjects. Having a child with a history of allergic rhinitis, but not of asthma or atopic dermatitis, was significantly related to an increased risk of IPF. CONCLUSIONS: These findings suggest that a genetic predisposition to allergic rhinitis may be associated with an increased risk of IPF.
Explore the source record for details and available documents.