Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In mice, the mean serum concentration of the acute-phase reactant alpha 1-acid glycoprotein increased 34-48% over 14 days following experimental induction of pneumonitis by intranasal inoculation of influenza A virus. Inoculation of undiluted (hemagglutination titer 640) and 10(-1) dilution of virus was followed by development of maximum concentrations of alpha 1-acid glycoprotein in serum at seven days, of 334 micrograms/ml, compared to a concentration in control mice inoculated with irradiated inactivated virus of 225 micrograms/ml (P = 0.002). Infection with 10(-2) virus yielded a peak serum alpha 1-acid glycoprotein of 301 micrograms/ml at four days, 34% higher than in control mice at four days (P = 0.04). There were no differences in alpha 1-acid glycoprotein concentrations among virus-infected mice. Influenza A virus pneumonitis was confirmed histologically, by virus isolation, and by serologic testing, but no inoculum-dependent differences were observed. On day 7, there was a direct relationship demonstrated between the severity of pneumonitis evaluated histologically and the serum alpha 1-acid glycoprotein concentration (r = 0.50; P less than 0.02). Influenza A pneumonia in mice is associated with increased concentrations of alpha 1-acid glycoprotein in serum; the increase may be directly related to the severity of the pulmonary inflammation.
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PMID:Effect of acute experimental influenza A virus pneumonia on concentration of alpha 1-acid glycoprotein in mouse serum. 261 94

Infection following breast implants is an uncommon event. This is somewhat surprising, since the human breast is not a sterile anatomical structure. The flora found in the breast are derived from the nipple ducts and closely resemble those of normal skin. These organisms, predominantly S. epidermidis, may in some cases be responsible for firmness secondary to capsular contracture. Treatment of the periprosthetic infection usually involves implant removal, but salvage by systemic antibiotics is sometimes possible. Atypical mycobacteria are very rarely the cause of infection, but can be extremely difficult to eradicate when involved. Toxic shock syndrome has been reported to occur following breast implants and is a life-threatening problem requiring immediate removal of the implant. It may be significant that in some cases with effusion and infection occurring many months or years after implant placement, there has been a preceding event such as a laryngitis or flu-like illness. This suggests the possibility of a bacteremia being involved in the causation of the infection. If this were the case, then these patients should be handled in a fashion similar to those with prosthetic heart valves. Accordingly, in our own practice, we advise that penicillin "V" be given beforehand when a patient with breast implants is to have any dental procedure. It must be stressed that there is no statistical or scientific proof at the present time that this is of any value. In conclusion, when dealing with these large foreign bodies, absolute sterility is essential, and excellent surgical technique to obviate hematoma and the occurrence of tissue ischemia is mandatory. Evidence of severe infection necessitates implant removal, but in less severe cases a trial of intravenous antibiotics is permissible. Having removed an implant, further insertion should be deferred, preferably for 6 months. If the new implant can be placed in a different plane, that is, submuscular, this is desirable. Exposed implants can be salvaged but this requires considerable judgment and one should be prepared for re-exposure or frank infection.
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PMID:Infections in breast implants. 266 82

The effect of NO2 exposure and human susceptibility to respiratory virus infection was investigated in a placebo-controlled, randomized, double-blind trial conducted in an environmentally controlled research chamber over 3 yr. Healthy, nonsmoking, young adult volunteers who were seronegative to influenza A/Korea/82 (H3N2) virus were randomly assigned to breathe either filtered clean air (control group) or NO2 for 2 h/day for 3 consecutive days. The NO2 concentrations were 2 ppm (Year 1), 3 ppm (Year 2), and 1 or 2 ppm (Year 3). Live, attenuated cold-adapted (ca) influenza A/Korea/82 reassortant virus was administered intranasally to all subjects immediately after the second exposure. Only one of the 152 volunteers had any symptoms; this person had a low grade fever. Pulmonary function measurements and nonspecific airway reactivity to methacholine were unchanged after NO2 exposure, virus infection, or both. Infection was determined by virus recovery, a fourfold or greater increase in serum or nasal wash influenza-specific antibody titers, or both. The infection rates of the groups were 12/21 (2 ppm NO2) versus 15/23 (clean air) in Year 1, 17/22 (3 ppm NO2) versus 15/21 (clean air) in Year 2, and 20/22 (2 ppm) and 20/22 (1 ppm) versus 15/21 (clean air) in Year 3. Each group exposed to 1 or 2 ppm NO2 in the last year became infected more often (91%) than did the control group (71%), but the differences were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of nitrogen dioxide exposure on susceptibility to influenza A virus infection in healthy adults. 271 34

Infection of polymorphonuclear leukocytes (PMNL) with influenza virus causes depression of PMNL metabolic and bactericidal activities. The studies reported here were undertaken to determine whether the hemagglutinin (HA) glycoprotein of influenza virus mediates this depression. PMNL were incubated with purified HA and the oxidative responses to exogenous stimuli were measured. The results indicate that HA, in either liposomes or protein aggregates referred to as rosettes, depressed PMNL oxidative responses. Depression was observed within 2 min of initial interaction of HA with PMNL and lasted more than 2 h. The membrane fusion activity of HA requires proteolytic cleavage of the HA, whereas the receptor binding activity does not. There was no difference in the ability of virions with cleaved or uncleaved HA to depress PMNL responses suggesting that the fusion event is not required for PMNL dysfunction. Inasmuch as the HA glycoprotein binds to sialic acid-containing receptors on the surface of the PMNL, we tested whether other sialic acid-specific binding proteins can mediate the reduction of PMNL responses. Sialic acid-specific lectins from Limulus polyphemus or Limax flavus were incubated with PMNL before measuring their responses to secondary stimulus. Depression was observed upon incubation with the lectins similar to that seen upon incubation with the HA or influenza virus. These results suggest that attachment of influenza virus to sialic acid-containing receptors is responsible at least in part, for suppressing PMNL oxidative responses.
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PMID:Depression of polymorphonuclear leukocyte functions by purified influenza virus hemagglutinin and sialic acid-binding lectins. 272 34

We prospectively followed a group of unimmunized, immunosuppressed children with cancer to determine their relative risk of influenza and the severity of infection compared with those of siblings or matched community controls. The incidence of influenza infection was higher in children with cancer (23/73, 32%) than in control subjects (10/70, 14%, p = 0.02). A preseason hemagglutination inhibition titer greater than or equal to 1:32, generally used as a marker of successful immunization in vaccine trials, was protective for all children in the control groups, but did not prevent influenza infection in 24% of the patients with cancer. Infection rates of patients and community controls with titers greater than or equal to 1:32 differed significantly (p = 0.006). No significant differences were noted in duration of reported symptoms between groups, and clinical complications occurred too infrequently to analyze. However, 2 (11%) of 18 of the cancer patients with positive culture results were hospitalized during the illness and one patient developed a nosocomial infection. None of the control children was hospitalized. These findings suggest the need for further study of the immunologic response of immunosuppressed children to influenza infection and a clinical efficacy trial of the influenza vaccine in these patients.
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PMID:Influenza in children with cancer. 273 93

Infection by one strain of influenza type A provides some protection (cross-immunity) against infection by a related strain. It is important to determine how this influences the observed co-circulation of comparatively minor variants of the H1N1 and H3N2 subtypes. To this end, we formulate discrete and continuous time models with two viral strains, cross-immunity, age structure, and infectious disease dynamics. Simulation and analysis of models with cross-immunity indicate that sustained oscillations cannot be maintained by age-specific infection activity level rates when the mortality rate is constant; but are possible if mortalities are age-specific, even if activity levels are independent of age. Sustained oscillations do not seem possible for a single-strain model, even in the presence of age-specific mortalities; and thus it is suggested that the interplay between cross-immunity and age-specific mortalities may underlie observed oscillations.
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PMID:Epidemiological models with age structure, proportionate mixing, and cross-immunity. 274 40

We have defined some characteristics of the mouse Mx protein as a marker of biological response to interferon (IFN) and to virus infection in A2G mice. The Mx protein has been detected and quantitated by Western immunoblot analysis. Upon induction by poly(I):poly(C) or with Newcastle disease virus, the Mx protein is expressed and accumulated in a variety of organs, such as liver, lungs, spleen, kidneys, heart, and brain. In some organs the expression of the Mx protein is detected readily, as soon as 4 h after treatment. The highest protein level is reached at 24 h, and it remains stable for several days declining slowly to return to preinduced levels 2-3 weeks after treatment. Infection with an hepatotropic or a pneumotropic strain of influenza virus resulted in a systemic induction of Mx protein, the highest levels being found in the target organ for virus replication. Our results indicate that the Mx protein is a sensitive, quantitative, and stable marker to follow IFN activity or virus infection in an animal model.
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PMID:Expression and stability of the Mx protein in different tissues of mice, in response to interferon inducers or to influenza virus infection. 279 81

Infection of the retina with herpes simplex virus type 1 (HSV-1) causes devastating lesions usually leading to blindness. However, the interactions between individual retinal cell types and this virus have not been well characterized, probably because of limitations posed by the complexity of the intact retina. We have now approached this problem through the use of separate, purified populations of isolated chick embryo retinal neurons and photoreceptor cells, of glial cells, and of pigmented epithelial cells. This manuscript deals with the initial part of these studies, aimed at determining the susceptibility of different retinal types to HSV-1 infection. The different cultures were exposed to HSV-1 for 3-48 hr, and cell infection was evaluated by immunocytochemical detection of viral antigens or by autoradiographic study of viral DNA replication. Practically 100% of the retinal glial cells and pigmented epithelial cells appeared susceptible to HSV-1 infection. On the other hand, as many as 70% of the neurons present in glia-free, pigment epithelium-free cultures, also appeared infected after a 24-hr exposure to the virus. Neuronal susceptibility to HSV-1 was already present in early (2-day) cultures, was time- and concentration-dependent, and led to neuronal degeneration after 24-48 hr. Neuronal infection was also corroborated by the detection of viral particles by transmission electron microscopy. Photoreceptor cells were consistently and selectively resistant to HSV-1 infection at all the concentrations and time points investigated. Both immunocytochemical and autoradiographic studies showed similar results. Photoreceptor resistance to HSV-1 appears to be selective, since they could be readily infected with RNA viruses such as vesicular stomatitis virus and influenza virus. These cell culture preparations offer an attractive system for the investigation of cellular mechanisms involved in the differential susceptibility of retinal cells to viral infection. Moreover, they could also help in the screening of treatments potentially capable of preventing and (or) curing HSV-induced retinal infection.
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PMID:Differential sensitivity of cultured retinal neurons and photoreceptors to herpes simplex infection. 282 Jul 71

Chronic bronchitis is responsible for 20,000 deaths per annum in France, i.e. 5 per cent of the overall mortality rate. Infection of the bronchi and lung tissue is a frequent cause of death in these patients. Acute on chronic bronchitis ranks fifth among the causes of disablement and admission to hospital. Pneumococci and Haemophilus influenza are the organisms most frequently isolated. the incidence and potential severity of acute episodes of infection account for the repeated use of antibiotics which carries a risk of promotion bacterial resistance. RU 41740 is a non-specific immunomodulator agent which reinforces the non-specific means of the respiratory tract against infections. Three double-blind, drug versus placebo and therefore reliable therapeutic trials have shown that the drug is effective in preventing airway infection. In patients with moderately advanced chronic bronchitis, RU 41740 reduces the number and duration of acute infectious episodes as well as antibiotic consumption. This positive effect persists in patients with chronic respiratory failure, including those who present with extensive bronchial dystrophy. RU 41740 is particularly effective in patients with numerous previous episodes of infection, but it also acts at all stages of chronic bronchitis.
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PMID:[Chronic bronchitis. Value of RU 41740]. 297 Nov 83

Rhinovirus infections in Seattle families with schoolchildren (1975-1979) and in selected outpatients were revealed by virus shedding or antibody rise. These observations extend those in the Seattle Virus Watch (1965-1969). Analysis of rhinovirus serotype prevalence again revealed certain "common" persisting serotypes but provided no further evidence that new serotypes are continuing to emerge. Two seasonal peaks, spring higher than fall, were again evident. Infection rates, again inversely related to age, were lower overall than in the Virus Watch (0.42 vs. 0.64 per person-year), probably because there were fewer young children. Frequencies of antibody response by virus shedders again varied widely by serotype but differed greatly from those in the Virus Watch in rank order of response rate, suggesting that immunogenicity is not a stable serotype characteristic. The frequency and magnitude of antibody response of virus shedders increased with age. Antibody-related protection against infection was evident only in persons age greater than or equal to 10 years. Observations in 7 families during successive homotypic infection episodes indicate that postinfection immunity to natural challenge requires persistence of antibody. Of all reported respiratory illness, 11.9% (0.31 per person-year) were due to rhinoviruses and 6.9% to influenza viruses. Of viruses recovered from family members, rhinoviruses, herpes simplex, and influenza comprised 56%, 12.6%, and 12.4%, respectively. Although households often experienced greater than or equal to 2 concurrent or closely consecutive episodes of infection with different viruses, only 29 individuals were shown to shed 2 viruses at the same time. Most of the second viruses, include 3 rhinoviruses and 18 other nonhemadsorbing viruses, appeared when 582 rhinovirus-positive specimens were retested after treatment with homotypic antibody. These results suggest that rhinoviruses interfere with nonhemadsorbing viruses in cell culture but mostly with other rhinoviruses in humans.
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PMID:Rhinoviruses in Seattle families, 1975-1979. 299 30


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