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Results for “Coxsackievirus Infections”

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At least 19 recordsLinked to original sources
PubMed1976

The seroepidemiology of reovirus, coxsackievirus infections among Panamanian Indian children.

Rates of hepatitis B virus infection varied significantly among Panamanian Indian tribes. Chocó and Mainland Cuna Indians had a greater prevalence of antibody to hepatitis B surface antigen than Guaymi and Island Cuna Indians. The village water supply appeared to be the major environmental difference that distinguished the tribes from one another. Since contaminated water plays a role in the transmission of enterovirus, an attempt was made to assess relative exposure to contaminated water by determination of the prevalence of antibodies to reovirus and coxsackievirus B in children 10 years old or younger. Infection with coxsackievirus B occurred more frequently in Chocó and Mainland Cuna Indians than in Guaymi or Island Cuna Indians. Although essentially all children tested were exposed to reoviruses, Mainland Cuna Indians had the highest geometric mean titers of antibody, followed by Chocó, Guaymi, and Island Cuna Indians in descending order. This parallel in rates of hepatitis B and enterovirus infection supports the hypothesis that fecal-oral transmission of hepatitis B virus is important in certain populations.

Antibodies, Viral↗
PubMed1976

[The coxsackievirus-infected mouse: an animal model for the study of virus myocarditis].

Basing on the experimental infection of adult mice with coxsackie virus A9 reported by Lerner in 1965 and the successful cultivation of the virus from the hearts of experimental animals, a model for studying virus myocarditis is proposed. By a combination of factors favouring the infection (age of the animals above 1 year, physical load prior to infection by repeated swimming) a high virus re-isolation rate was achieved. Cultivation of the virus from the mouse heart was possible on the 3rd day p.i. in 81%, on the 6th day in 71%, on the 9th day in 31%, and on the 12th day in 12% of the cases. In 66% of the animals towards the end of the period of observation a significant increase in few cases is the virus isolated on the 3rd and 6th day p.i. also from the skeletal muscles. The model can be used both for pathogenetic studies on myocardites elicited by cardiotropic viruses and for in vivo testing of antiviral substances.

Animals↗
PubMed1978

Potentiation of coxsackievirus B3 infection in adult mice pretreated with a gold salt.

In mice treated with sodium aurothiomalate (myocrisin), prior to infection with Coxsackievirus B3, 90% of the animals died by the 11th day postinfection (p.i.). A mortality of 10% was noted in mice receiving myocrisin only, and no deaths occurred in animals infected with virus alone. The highest amount of virus was recovered from the pancreas of myocrisin-treated mice on day 3 p.i. This was over 500-fold higher than the virus titer found in the pancreas of mice infected with virus only. Generally the titer of virus present in different organs was higher at every point in drug-treated animals as compared to intact mice infected with the virus. A high and persistent viremia was present in myocrisin-treated mice; in contrast a low viremia followed by virus clearance from the blood was observed in intact mice infected with the virus. The antibody response was studied in intact and myocrisin-treated mice infected with the virus. In both groups, no neutralizing antibodies were detected on days 1, 2, and 3 p.i. On day 7 after infection, the titers of antibodies were 1:16 and 1:12 in intact and myocrisin-treated mice, respectively. Administration of hyperimmune anti-Coxsackievirus B3 serum 6 hours after infection protrected in myocrisin-treated group of mice against lethal disease. The results of these studies suggest that (1) antibodies alone may not be sufficient to limit the spread and persistence of virus in natural infections and (2) in the absence of any apparent histopathological differences the increased multiplication of Coxsackievirus B3 could be the cause of death in myocrisin-treated mice.

Animals↗
PubMed1977

Generation of cytotoxic T lymphocytes during coxsackievirus B-3 infection. I. Model and viral specificity1.

The production of cytotoxic cells in the spleen of adult male BALB/c mice infected with Coxsackievirus B-3 has been examined. An in vitro 51Cr release assay was used to measure cytotoxic activity against virus-infected and uninfected neonatal sygeneic fibroblasts. Cytotoxicity of immune spleen cells against virus-infected targets was detected on the 3rd day after infection, reached a peak on day 7, and then declined to low levels by days 12 and 14. Spleen cells obtained 3 and 5 days after infection also exerted cytotoxicity against uninfected fibroblasts, but by the 7th day there was little or no reactivity against uninfected target cells, although activity against infected fibroblasts was maximal at this time. Reciprocal assays performed by using Coxsackie and vaccinia viruses provided evidence of virus specificity of the cytotoxic reaction. When spleen cells were obtained 7 days after infection, the Coxsackievirus-immune population was not cytotoxic for vaccinia-infected fibroblasts, and the vaccinia-immune population was not cytotoxic for Coxsackievirus-infected targets, although each immune cell preparation caused significant lysis of fibroblasts infected with the homologous virus. Additional studies showed that primary mouse or hyperimmune rabbit anti-Coxsackieviral serum could not block immune spleen cell cytotoxicity or induce complement-mediated lysis of infected targets. The findings indicate that Coxsackievirus infection results in surface membrane alterations, but no evidence was obtained that antiviral antibody could react with the infected cells.

Animals↗
PubMed1977

Generation of cytotoxic T lymphocytes during coxsackievirus tb-3 infection. II. Characterization of effector cells and demonstration cytotoxicity against viral-infected myofibers1.

This report describes studies characterizing the virus-specific cytotoxic effector cells which are present in the spleens of mice 7 days after infection with Coxsackievirus B-3. An in vitro 51Cr assay employing eyngeneic virus-infected neonatal fibroblasts was used to measure cytotoxic activity. Treatment of immune cells with (anti-thy-1.2) and complement abolished dtheir cytotoxic activity, but no reduction occurred when B cells were removed by incubation with anti-Ig and complement or macrophages eliminated by adherence depletion. The findings therefore imply that the cytotoxic reaction was mediated by sensitized T cells and that B cells and macrophages did not play an important role. Reciprocal assays performed with BALB/c and CBA/J cells showed that Coxsackievirus-immune spleen cells lysed infected syngeneic targets but not allogeneic targets, providing further evidence that cytotoxicity was mediated by effector T cells. In addition and in vitro assay system employing neonatal myocardial cells was developed and used to demonstrate that Coxsackievirus-infected myofibers were susceptible to destruction by immune spleen cells. The evidence suggests that mice infected with Coxsackie B viruses are able to mount a cell-mediated immune response with production of cytotoxic T cells which have the capacity to damage tissues infected with these agents.

Animals↗
PubMed1979

Migration of epithelial cells in the small intestine of mice perorally infected with coxsackievirus B5.

The rate of cell migration in the small intestine during enteric viral infections has not been assessed previously. CD-1 mice (33 days old) were infected perorally with 1.0 X 10(8) plague-forming units of coxsackievirus B5 and 12 hr later were injected intraperitoneally with 2 micron Ci of [3H]thymidine/g of body weight. After 2, 12, 24, 48, 60, and 72 hr, mice were killed, and the small intestine was removed. Specimens obtained at each interval were examined by radioautography; similar specimens were titrated for virus by plaque assay in HeLa cells. In mice perorally infected with coxsackievirus B5, epithelial cells migrated from crypt to villus tip in 60 hr, as compared with 48 hr in uninfected control mice and 24 hr previously reported for mice perorally infected with enteric bacteria (e.g., Salmonella typhimurium). Virus was recovered from intestinal tissue, but no inflammatory response in the limina propria was apparent. These observations are consistent with previous report that substrate absorption rates may be altered during viral and bacterial enteric infection.

Animals↗
PubMed1977

Bacterial or nonbacterial pneumonia: accuracy of radiographic diagnosis.

The initial chest radiographs of 31 patients with laboratory-proved pneumonia were evaluated by a panel of 6 radiologists who had no prior knowledge of the clinical data. No statistical reliability was found for distinguishing bacterial from nonbacterial pneumonia. Radiographic diagnoses were 67% accurate for the 16 cases of bacterial pneumonia, and 65% accurate for the 9 viral cases. Six cases of Mycoplasma pneumonia were diagnosed as nonbacterial 19% of the time, and as "bacterial pneumonia" 81% of the time.

Adult↗
PubMed1976

[Aetiological studies on viral pneumonia (author's transl)].

401 cases of viral pneumonia diagnosed between January 1973 and August 1975 were investigated serologically by the complement-fixation test. The percentage distribution of the responsible pathogenic organism in this series of cases was as follows: influenza virus A 45.9%, Mycoplasma pneumoniae 19.5%, Coxsackie B viruses 9.2%, cytomegalovirus 7.5% and Chlamydia psittaci 8.5%. The remaining 9.4% cases were caused by adeno, parainfluenza, measles, influenza B, herpes simplex and respiratory syncytial viruses. Influenza virus was found mainly in elderly people (mean age 58.4 years), whilst pneumonia due to Mycoplasma occurred mainly in young adults (mean age 24.4 years). Infections with Coxsackie B viruses were almost entirely restriced to the warmer months; by contrast, the influenza virus was usually found in epidemic form and only during a few weeks in winter.

Adolescent↗
PubMed1977

Pathophysiological aspects of coxsackievirus B intestinal infection.

Our findings reveal that intestinal infection with coxsackie B5 results in decreased intestinal epithelial cell division in association with an increase in carbohydrate (glucose) and amino acid (leucine) absorption in the small intestine. These findings are contrasted with those occurring during Salmonella infection, which results in increased intestinal cell division rate but decreased carbohydrate (glucose) absorption. The changes in intestinal function and physiology that have been described occurred during an asymptomatic viral infection characterized by normal intestinal histology. A reasonable hypothesis is that these pathophysiological changes may be due not only to a variety of local factors but also to hormonal effects induced by systemic spread of coxsackievirus B.

Animals↗