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Use of IgG avidity to indirectly monitor epizootic transmission of sin nombre virus in deer mice (Peromyscus maniculatus).

An IgG avidity assay was developed to differentiate deer mice that had recently acquired Sin Nombre virus (SNV) from those that were infected in the distant past. Using this procedure, low avidity antibodies were predominantly detected in experimentally infected deer mice (89.5%) within the first 30 days post-inoculation. The assay was then applied to sera from naturally infected deer mice collected during a field investigation associated with a cluster of hantavirus pulmonary syndrome cases. A higher proportion of seropositive mice collected during the outbreak had serum with low avidity antibodies (16.7%) when compared with mice trapped four months later (5.7%). Sin Nombre virus RNA was detectable in blood in a similar fraction of low- (45%) and high- (38.7%) avidity groups. Non-adult mice were more likely to contain low-avidity antibodies (44.4%) than were adults (9.6%). Our results indicate that the IgG avidity assay shows promise as a tool to better characterize epizootic intensity and to identify factors involved in SNV transmission.

Animals↗

Dehydrogenase-dependent ethanol metabolism in deer mice (Peromyscus maniculatus) lacking cytosolic alcohol dehydrogenase. Reversibility and isotope effects in vivo and in subcellular fractions.

Elimination of [2H]ethanol in vivo as studied by gas chromatography/mass spectrometry occurred at about half the rate in deer mice reported to lack alcohol dehydrogenase (ADH-) compared with ADH+ deer mice and exhibited kinetic isotope effects on Vmax and Km (D(V/K] of 2.2 +/- 0.1 and 3.2 +/- 0.8 in the two strains, respectively. To an equal extent in both strains, ethanol elimination was accompanied by an ethanol-acetaldehyde exchange with an intermolecular transfer of hydrogen atoms, indicating the occurrence of dehydrogenase activity. This exchange was also observed in perfused deer mouse livers. Based on calculations it was estimated that at least 50% of ethanol elimination in ADH- deer mice was caused by the action of dehydrogenase systems. NADPH-supported cytochrome P-450-dependent ethanol oxidation in liver microsomes from ADH+ and ADH- deer mice was not stereoselective and occurred with a D(V/K) of 3.6. The D(V/K) value of catalase-dependent oxidation was 1.8, whereas a kinetic isotope effect of cytosolic ADH in the ADH+ strain was 3.2. Mitochondria from both ADH+ and ADH- deer mice catalyzed NAD+-dependent ethanol oxidation and NADH-dependent acetaldehyde reduction. The kinetic isotope effects of NAD+-dependent ethanol oxidation in the mitochondrial fraction from ADH+ and ADH- deer mice were 2.0 +/- 0.1 and 2.3 +/- 0.3, respectively. The results indicate only a minor contribution by cytochrome P-450 to ethanol elimination, whereas the isotope effects are consistent with ethanol oxidation by the catalase-H2O2 system in ADH- deer mice in addition to the dehydrogenase systems.

Alcohol Dehydrogenase↗

Genetics, biochemistry, and developmental regulation of alcohol dehydrogenase in peromyscus and laboratory mice.

The ADH-negative deermouse and the strain-specific variation in level of ADH in liver tissue of inbred mice represent useful systems to investigate gene regulation at a molecular level. Few systems have advanced to the state where specific hybridization probes can be employed to determine if loci which control the amount of a protein in a tissue do so by controlling the concentration of a specific messenger RNA [Owerbach et al, 1981; Tukey et al, 1981]. The relatively high level of ADH in mouse liver and the tissue and developmental specificity of expression of this enzyme should provide useful tools for use in identifying specific ADH cDNA clones in a liver cDNA library Norgard et al, 1980]. In addition, the deermouse ADH is immunologically cross-reactive with the mouse enzyme [Felder, unpublished observation]; the availability of ADH-negative and ADH-positive deermice may also prove useful in developing successful cloning strategies.

Aging↗

Pathogenesis of Trypanosoma brucei infection in deer mice (Peromyscus maniculatus): light and electron microscopic studies on erythrocyte pathologic changes and phagocytosis.

Light microscopic and scanning and transmission electron microscopic studies demonstrated that Trypanosoma brucei EATRO 110 produced several alterations in RBC structure including microspherocytes, schistocytosis, vacuolation, doughnut-cell formation, and keratocytosis. Mature RBC and reticulocytes were constantly observed to adhere firmly to trypanosomes in heart blood and in blood vessels of the testes, heart, liver, and kidney, as well as in the sinuses and pulp cords of the spleen. Adhesion of RBC to trypanosomes was also observed by light microscopy in thin blood films. Except for a few platelets that adhered to trypanosomes, other blood cells were not involved. Minute pores were sometimes observed on the RBC membrane at the point of adhesion to the trypanosome, but effects were not seen on the parasite. Erythrophagocytosis was marked in the spleen and to a lesser extent in the liver; mature RBC, as well as reticulocytes, were engulfed. Erythrophagocytosis was presumed to arise from the mechanical injury to RBC, the damage caused by the adhesion phenomenon and the hyperactivity of the enormously enlarged spleen.

Animals↗