Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006277 (bronchitis)
 6,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of infectious bronchitis virus (IBV) with erythrocytes was analyzed. The binding activity of IBV was not sufficient to agglutinate chicken erythrocytes. However, it acquired hemagglutinating activity after treatment with neuraminidase to remove alpha 2,3-linked N-acetylneuraminic acid from the surface of the virion. Pretreatment of erythrocytes with neuraminidase rendered the cells resistant to agglutination by IBV. Susceptibility to agglutination was restored by resialylation of asialo-erythrocytes to contain alpha 2,3-linked sialic acid. These results indicate that IBV attaches to receptors on erythrocytes, the crucial determinant of which is sialic acid alpha 2,3-linked to galactose. In contrast to other enveloped viruses with such a binding specificity (influenza viruses and paramyxoviruses) IBV lacks a receptor-destroying enzyme.
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PMID:Neuraminidase treatment of avian infectious bronchitis coronavirus reveals a hemagglutinating activity that is dependent on sialic acid-containing receptors on erythrocytes. 132 4

Porcine transmissible gastroenteritis virus (TGEV) was found to resemble avian infectious bronchitis virus (IBV) in its interaction with erythrocytes. Inactivation of the receptors on erythrocytes by neuraminidase treatment and restoration of receptors by reattaching N-acetylneuraminic acid (Neu5Ac) to cell surface components indicated that alpha 2,3-linked Neu5Ac serves as a receptor determinant for TGEV as has been reported recently for IBV. Similar to IBV, the haemagglutinating activity of TGEV is evident only after pretreatment of virus with neuraminidase indicating that inhibitors on the virion surface have to be inactivated in order to induce the HA-activity of these viruses. A model is presented to explain why the HA-activity of untreated virus is masked and how neuraminidase treatment results in the unmasking of this activity.
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PMID:N-acetylneuraminic acid plays a critical role for the haemagglutinating activity of avian infectious bronchitis virus and porcine transmissible gastroenteritis virus. 820 48

A rapid-plate hemagglutination (HA) test to detect infectious bronchitis virus (IBV) in allantoic fluid of embryonated eggs was introduced into routine procedures for IBV identification. This system was tested in 468 diagnostic cases received by the Poultry Diagnostic and Research Center at the University of Georgia. Allantoic fluids from inoculated embryos were harvested and treated with commercially available neuraminidase enzyme. IBV in neuraminidase-treated allantoic fluid was identified by clear and consistent HA of chicken red blood cells within 1 min of incubation. The specificity of the neuraminidase rapid-plate HA assay was examined with other avian viruses in individual and dual embryonic infections. Sensitivity of this test was compared with embryo lesions and reverse transcriptase-polymerase chain reaction (RT-PCR). The rapid-plate HA assay of neuraminidase-treated allantoic fluid correlated with the RT-PCR during the early stages of IBV detection, identification, and isolation in embryonated eggs.
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PMID:A rapid-plate hemagglutination assay for the detection of infectious bronchitis virus. 1073 49

Routine batch control of licensed inactivated viral vaccines for poultry usually includes a potency assay as a measure of vaccine efficacy. Potency assays often consist of vaccination-challenge experiments in the target species or in laboratory animals. Instead of measuring the protection of vaccinated animals against virulent pathogens, the serological response after vaccination can be quantified for some vaccines. In vitro antigen quantification assays would be attractive alternatives for the current potency assays because the time and costs involved could be greatly reduced and animal use could be avoided. Such in vitro assays will only be acceptable when the correlation between results and efficacy or potency has been demonstrated convincingly. The results of our studies on antigen quantification assays indicate that, in principle, quantification of viral antigens from inactivated oil-adjuvanted vaccines is feasible and reproducible using specially developed antigen capture ELISAs in combination with specific software for statistical analysis of the ELISA data. We have developed methods to quantify the haemagglutination-neuraminidase (HN) and fusion (F) proteins of Newcastle disease virus (NDV), the viral protein 3 (VP3) of the infectious bursal disease virus (IBDV), and the spike-1 (S1) protein of the infectious bronchitis virus (IBV). Vaccination experiments with inactivated ND vaccines indicate that the in vitro quantified HN- or F-proteins of NDV are reliable indicators of the serological response after vaccination.
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PMID:Antigen quantification as in vitro alternative for potency testing of inactivated viral poultry vaccines. 1108 35

Influenza illness is an important cause of severe morbidity and mortality in the population. Oseltamivir, the first oral neuraminidase inhibitor, has proven efficacy. In children of 1 year and older (weight-dependent dosing: 30 mg, 45 mg, 60 mg or 75 mg BID for 5 days) and adults (75 mg BID for 5 days), oseltamivir reduces the duration and severity of acute influenza. Furthermore, it decreases the incidence of secondary complications such as otitis media, bronchitis, pneumonia and sinusitis. Oseltamivir has been shown to prevent influenza when given for long-term prophylaxis or for post-exposure prophylaxis. Because oseltamivir blocks the neuraminidase, an enzyme crucial to influenza virion liberation from the host cell, it is only effective during the replication phase. Clinical benefits are only seen, when oseltamivir is applied within 48 h after onset of symptoms, and clinical efficacy in acute influenza is highly dependent on the beginning of treatment. Treatment within 12 h after onset of symptoms reduces the duration of illness by an additional 74.6 h, and treatment within 24 hours an additional 53.9 h compared to the benefit seen with an intervention at 48 h. In conclusion, clinical efficacy of oseltamivir can be maximized by early start of treatment. Resistance of influenza virus against oseltamivir has rarely been observed and seems to be of no clinical relevance due to reduced transmissibility and pathogenicity of mutants. Oseltamivir is generally well tolerated. About 10% of the patients complain of transient upper gastrointestinal events, which resolved within 1-2 days, and which could be reduced when the medication was taken with a light snack.
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PMID:Early therapy with the neuraminidase inhibitor oseltamivir maximizes its efficacy in influenza treatment. 1245 53

A total of 5-7 million cases of the disease, 4.5 million medical certificates, 25,000 admissions to hospital, 15,000 mortalities and direct and indirect costs amounting to several billions - that is the outcome of a "normal" influenza season (data provided by the Influenza Study Group, AGI, of Germany on the 1998/99 season). With zanamivir (Relenza), a selective inhibitor of the influenza-specific neuraminidase, a pharmaceutical product against influenza A and B is now available in Germany for the very first time. In clinical studies, zanamivir reduced not only the duration of the illness and the severity of symptoms, but also the rate of complications and the need for antibiotics. Under practice conditions, the efficacy and tolerability of the anti-influenza product were studied during the 1999/2000 influenza season. In a large observational study in over 1,900 patients, including many patients at risk of asthma and/or chronic obstructive bronchitis, zanamivir (Relenza) improved the symptoms quickly and reliably, and was tolerated very well. The diagnosis of influenza was established clinically to discriminate the disease from colds.
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PMID:Drug under test: influenza--Relenza in daily practice. Experience during the influenza season 1999/2000. 1245 55

Nontypeable Haemophilus influenzae (NTHi) is a major cause of opportunistic respiratory tract infections, including otitis media and bronchitis. The persistence of NTHi in vivo is thought to involve bacterial persistence in a biofilm community. Therefore, there is a need for further definition of bacterial factors contributing to biofilm formation by NTHi. Like other bacteria inhabiting host mucosal surfaces, NTHi has on its surface a diverse array of lipooligosaccharides (LOS) that influence host-bacterial interactions. In this study, we show that LOS containing sialic (N-acetyl-neuraminic) acid promotes biofilm formation by NTHi in vitro and bacterial persistence within the middle ear or lung in vivo. LOS from NTHi in biofilms was sialylated, as determined by comparison of electrophoretic mobilities and immunochemical reactivities before and after neuraminidase treatment. Biofilm formation was significantly reduced in media lacking sialic acid, and a siaB (CMP-sialic acid synthetase) mutant was deficient in biofilm formation in three different in vitro model systems. The persistence of an asialylated siaB mutant was attenuated in a gerbil middle ear infection model system, as well as in a rat pulmonary challenge model system. These data show that sialylated LOS glycoforms promote biofilm formation by NTHi and persistence in vivo.
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PMID:Sialylation of lipooligosaccharides promotes biofilm formation by nontypeable Haemophilus influenzae. 1468 87

The importance of sialic acid for infection by avian Infectious bronchitis virus (IBV) has been analysed. Neuraminidase treatment rendered Vero, baby hamster kidney and primary chicken kidney cells resistant to infection by the IBV-Beaudette strain. Sialic acid-dependent infection was also observed with strain M41 of IBV, which infects primary chicken kidney cells but not cells from other species. In comparison with Influenza A virus and Sendai virus, IBV was most sensitive to pre-treatment of cells with neuraminidase. This finding suggests that IBV requires a greater amount of sialic acid on the cell surface to initiate an infection compared with the other two viruses. In previous studies, with respect to the haemagglutinating activity of IBV, it has been shown that the virus preferentially recognizes alpha2,3-linked sialic acid. In agreement with this finding, susceptibility to infection by IBV was connected to the expression of alpha2,3-linked sialic acid as indicated by the reactivity with the lectin Maackia amurensis agglutinin. Here, it is discussed that binding to sialic acid may be used by IBV for primary attachment to the cell surface; tighter binding and subsequent fusion between the viral and the cellular membrane may require interaction with a second receptor.
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PMID:Sialic acid is a receptor determinant for infection of cells by avian Infectious bronchitis virus. 1660 23

Influenza viruses represent Orthomyxoviridae family. Spherical virions are 80-120 nm in diameter and have two-layer lipid envelope. The following proteins are coded by 8 or 7 segments of the single-stranded RNA: nucleoprotein (NP), polymerase PB2, PB1 and PA, member protein--M1 and M2, glycoproteins--hemagglutinin (HA) and neuraminidase (NA). HA and NA form spikes on the virion surface. On the basis of antigenic differences there are distinguished three types of influenza virus-A, B and C. Besides, influenza A viruses occur in different subtypes, depending on the features of HA and NA. One of influenza characteristics is its antigenic changeability: antigenic drift and antigenic shift. Infection occurs by droplet route, sometimes through direct contact with infected person or surface. Influenza virus attacks epithelial cells of upper respiratory tract, where replication takes place resulting in the production of approximately 1000 of progeny virions during a single 6-12 h cycle in one cell. Necrosis of ciliary cells of mucosa facilitates invasion of bacterial pathogens. Incubation period lasts on average 1-2 days. Influenza illness without complications characterizes the sudden onset of respiratory symptoms and systemic symptoms. Regression of symptoms usually occurs after 3-5 days, but cough and malaise may be observed for over 2 weeks. Reasons for the severe course of the disease or even death are post-influenza complications, e.g. viral pneumonia and bronchitis, bronchiolitis in children, secondary bacterial pneumonia, otitis media, myocarditis and pericarditis, Reye's syndrome, myositis, myoglobinuria, neurological complications and exacerbation of existing chronic diseases. In the case of influenza there is no possible to make the unquestionable diagnosis only on the basis of clinical picture of the disease. Therefore in some circumstances there is important to make some diagnostic laboratory tests as RT-PCR, immunofluorescence assay or isolation of virus and detection of the specific antibodies. The main determinants of the immunity to influenza virus infection are antihemagglutinin (anti-HA) antibodies and antineuraminidase antibodies (anti-NA). The former play fundamental role for the protection against the infection, while anti-NA antibodies limit virus spreading and contribute to a milder course of the disease. In the response to influenza infection there are observed serum immunoglobulines IgG and IgM (after the first contact with the antigen), while immunoglobulines IgA are produced rarely. The latter are produced locally in the high concentrations on the mucus of respiratory tract. Cellular immunological response is important for recovery from influenza where a significant role of cytotoxic T lymphocytes should be emphasized. These lymphocytes are able to kill infected cells in the earliest phases of replication before the progeny virions are formed.
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PMID:[Various sides of influenza, part I--structure, replication, changeability of influenza viruses, clinical course of the disease, immunological response and laboratory diagnostics]. 1716 90

Bacteriologic examination of 1589 patients showed that, aside from C. diphtheriae, 11% of acute upper respiratory tract infections were caused by other Corynebacterium species. Such bacteria can cause infections of various localizations (bronchitis, pyelonephritis, urethritis, colpitis, dermatitis, arthritis, etc.). C. pseudodiphtheriticum and C. xerosis were isolated from clinical specimens most frequently. Corynebacterium spp. have adhesive, hemolytic, hemagglutinating, and neuraminidase activity; some of them are highly pathogenic. The most virulent, were following species: C. diphtheriae, C. pseudotuberculosis, C. urealyticum, and C. ulcerans. Corynebacterium non diphtheriae were frequently isolated from clinical specimens in association with staphylococci and streptococci. In such cases, factors of pathogenicity and resistance to antibiotics were more pronounced. Strains isolated with association with other bacteria have lost susceptibility to tetracycline, oleandomycin, penicillin, and erythromycin. It is important to be vigilant about bacteria from Corynebacterium genus in clinical settings, and thoroughly study their biologic characteristics, especially in immunocompromised patients.
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PMID:[Etiologic role of Corynebacterium non diphtheriae in patients with different pathology]. 1803 38


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