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R Eberle

Publications and source records attributed to R Eberle.

81 records · Page 5Linked to original sources
PubMed1980

gA and gB glycoproteins of herpes simplex virus type 1: two forms of a single polypeptide.

Utilizing a combination of preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis and sodium dodecyl sulfate-hydroxylapatite column chromatography, we have separated and purified the gA and gB glycoproteins of the major virus-specific glycoprotein region from herpes simplex virus type 1-infected cells. By using purified antigen preparations, antisera specific to each of these glycoproteins were produced. Immunoprecipitation from detergent extracts of infected cells and radioimmune precipitation of the purified antigens have shown that the anti-gA and anti-gB sera each recognize both the gA and the gB glycoproteins. The anti-gA serum was also shown to neutralize virus despite the presence of only minute quantities of the gA glycoprotein in virions. Pulse-chase studies have indicated that the gA and gB glycoproteins are synthesized from a common precursor polypeptide. Together, these data demonstrate that the gA and gB glycoproteins of herpes simplex virus type 1 are antigenically similar but not identical and probably represent two different forms of the same polypeptide which differ in their degree of glycosylation.

Centrifugation, Density Gradient↗
PubMed1979

[On diagnosis of myocardial infarction in the polytraumatized investigation in dogs (author's transl)].

The reliability of CKMB in cases in which damage of sceletal muscles and myocardium occurred in close sequence is tested in dogs. Results show that in simultaneous damage of heart and muscles, CKMB exceeds the requested ratio of 5 to 8% of total CK, thus proving the myocardial infarction. In cases in which myocardial infarction succeeds a damage of sceletal muscle--e.g. a polytrauma --within distance of hours only, the absolutely high level of CKMB proves the infarction, even below the critical ratio of the total CK.

Animals↗
PubMedDate not supplied

Clinicopathological characterization of monkey B virus (Cercopithecine herpesvirus 1) infection in mice.

The purpose of this study was to establish a small animal model for monkey B virus (BV) infection. Mice were inoculated intramuscularly with several BV isolates. Comparisons were based upon the doses required to produce infection (ID50), non-central nervous system (CNS) clinical disease (CS50), CNS disease (CNSD50) and lethal effect (LD50). Strains differed in respect of the dose required to produce clinical disease in BALB/c mice. C57BL/6 mice were more resistant than BALB/c mice to CNS disease. Skin lesions at the inoculation site consisted of epidermal necrosis, ulceration, serocellular crusts and underlying dermatitis. CNS lesions included marked inflammation in the ipsilateral dorsal root ganglion and lumbar spinal cord (point of viral entry). The distribution of the lumbar spinal cord lesions suggested viral entry via sensory afferent neurons, ventral motor tracts, or both. The lesions in the more cranial spinal cord segments suggested ascension to the brain via bilateral spinothalamic and spinoreticular tracts. Brain lesions included encephalitis with neuronal necrosis and white matter destruction located consistently at the base of the brainstem, the reticular system, and rostrally to the thalamus and hypothalamus. Viral antigen was detected immunohistochemically in the lesions. The results indicated an ascending encephalomyelitis syndrome similar to that produced by BV in man.

Animals↗
PubMedDate not supplied

Temporal progression of viral replication and gross and histological lesions in Balb/c mice inoculated epidermally with Saimiriine herpesvirus 1 (SaHV-1).

Saimiriine herpesvirus 1 (SaHV-1), an alphaherpesvirus enzootic in squirrel monkeys, is genetically related to monkey B virus and human herpes simplex virus (HSV). To study the temporal progression of viral spread and associated lesions, Balb/c mice were inoculated epidermally by scarification with a green fluorescent protein (GFP)-expressing recombinant strain of SaHV-1 and killed sequentially. Pinpoint ulcerative lesions in the inoculated epidermis progressed over a few days to unilateral or bilateral hindlimb paresis or paralysis, urinary and faecal incontinence, abdominal distension, hunched posture and eventual depression warranting euthanasia. Viral replication was present within epidermal keratinocytes, neurons of the dorsal root ganglia and thoracolumbar spinal cord, regional autonomic ganglia, lower urinary tract epithelium and colonic myenteric plexuses, as indicated by histological lesions and GFP expression. Almost all mice inoculated with 10(5) or 10(6) plaque-forming units (PFU) of SaHV-1 developed rapidly progressive disease. Two of eight mice given 10(4)PFU developed disease, but no mice receiving less than 10(4)PFU gave evidence of infection. Mice that showed no clinical signs also failed to develop an antiviral IgG response, indicating absence of active viral infection. For SaHV-1 inoculated epidermally, the ID(50), CNSD(50) and LD(50) values were identical (10(4.38)), indicating that successful infection by this route invariably resulted in lethal CNS (central nervous system) disease. Consistently severe disease in all infected animals, with regionally extensive distribution of viral replication, constituted a marked difference from the disease produced by intramuscular inoculation.

Animals↗
PubMedDate not supplied

Comparative pathology of infections with baboon and African green monkey alpha-herpesviruses in mice.

The comparative pathology of Herpesvirus papio 2 (HVP2) of baboons and SA8 virus of African green monkeys relative to that of herpes simplex virus (HSV1) of man was investigated in young adult mice inoculated intramuscularly and observed for 21 days. The 50% infectious dose (ID(50)) for HVP2 was approximately 10(2.0) plaque-forming units (PFU), while the ID(50) for HSV1 and SA8 was 10(2.5) and 10(3.8), respectively. There were marked differences in the ability of these three viruses to invade the central nervous system (CNS) and cause clinical neurological disease. HSV1 produced neurological signs in a few animals given 10(6)PFU, but SA8 did not. In contrast, HVP2 readily invaded the CNS and produced fatal disease with doses as low as 10(2)PFU. Two isolates of HVP2 tested had a 50% CNS disease dose (CNSD(50)) of 10(2.5) and 10(3.0)PFU and an LD(50) of 10(3.8) and 10(4.3)PFU, respectively. Histopathological examination of tissue from HVP2-infected mice revealed severe lesions of inflammation and necrosis in the central, peripheral and autonomic nervous systems, as well as of other tissues including skin, adrenal glands and the gastrointestinal tract. Viral antigens were detected immunohistochemically in lesions. This study showed that while both HVP2 and SA8 could infect mice, there were marked differences in the ability of these two closely related viruses to cause clinical disease and CNS lesions. This murine model may prove useful in the investigation of viral or host determinants responsible for the varying neurovirulence of these simian alpha-herpesviruses.

Animals↗