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Biomedical subjects

C J Gibbs

Publications and source records attributed to C J Gibbs.

At least 163 records · Page 9Linked to original sources
PubMed1985

Detection of picornavirus sequences in nervous tissue of amyotrophic lateral sclerosis and control patients.

We used in situ hybridization to look for picornavirus ribonucleic acid (RNA) sequences in frozen sections of central nervous system (CNS) tissue of amyotrophic lateral sclerosis (ALS) and control patients. Using reconstruction experiments, we concluded that 30 copies of viral RNA per cell could be detected with the assay. RNA which hybridized to DNAs complementary (cDNAs) to both poliovirus and Theiler's virus was found at several levels in the CNS of 2 patients, 1 ALS patient, and 1 control. In transverse sections of the spinal cord, these sequences predominated in cells of the anterior horns. We assessed the specificity of hybridization by several criteria: no hybridization was observed with heterologous visna virus cDNA probes; hybridization was abolished by pretreatment of the sections with ribonuclease; chemography artifacts were ruled out; and the results were reproduced in three independent experiments. We concluded that RNA molecules, possibly belonging to a picornavirus having sequences in common with poliovirus and Theiler's virus, were present in the CNS of these 2 patients. On the other hand, 14 cases of classic ALS, 2 cases of Guamanian parkinsonian dementia, and 5 controls had negative results. However, the presence of picornavirus sequences in our series could be underestimated because in many cases autolysis times were 10 hours or longer.

Amyotrophic Lateral Sclerosis↗
PubMed1985

Failure to detect scrapie virus in sheep at slaughter in a highly endemic region of France.

A study was carried out in a sheep slaughterhouse located in a region of France where scrapie has been endemic for several decades. Neuropathological examination of 63 randomly selected lambs and adult sheep revealed no scrapie-related abnormalities, and inoculation of mice with brain, tonsil, lateropharyngeal ganglia, and intestine from the same animals did not transmit scrapie. The failure to detect any evidence of scrapie infection in commercially-bred sheep, the absence of an increased mortality rate for human CJD in the surrounding consumer region, and the absence of a single case of CJD among slaughterhouse personnel, do not support the hypothesis that exposure to potentially scrapie-contaminated products is responsible for CJD in humans.

Abattoirs↗
PubMed1985

Differential susceptibility and resistance of immunocompetent and immunodeficient mice to fatal Hantaan virus infection.

Susceptibility and resistance to fatal Hantaan virus meningoencephalitis were studied in immunocompetent (nu/+) and congenitally T-cell deficient (nu/nu) CD-1 mice of different ages. Susceptibility of nu/+ mice to fatal infection was age-dependent, as evidenced by 100 percent mortality in mice inoculated intracerebrally with Hantaan virus (strain 76-118) during the first week of life, 60 percent mortality in mice inoculated at 9 days of age, and no disease or death in mice inoculated at 14 to 42 days of age. Deaths occurred significantly earlier in nu/+ mice inoculated at 5 and 7 days of age than in nu/+ mice less than 24 hours old. Nu/nu littermates of the same age did not exhibit a similar inverse relationship between age and survival times. Moreover, nu/nu mice 14 days or older remained susceptible, albeit with delayed onset of illness and time of death. Virus titers in brain tissues of nu/+ mice inoculated at 7 days and of nu/nu mice inoculated at 7, 9 and 14 days of age were nearly identical. In older nu/+ mice, peak virus titers were comparatively lower, but they did not seem to be influenced by the magnitude of the neutralizing antibody response. The more rapidly fatal course in nu/+ mice inoculated at a week of age than at birth, and the differential resistance between weanling nu/+ and nu/nu mice to Hantaan virus meningoencephalitis suggest that cell-mediated immunity may be responsible for both enhancement of disease and recovery from infection.

Age Factors↗
PubMed1985

Antiviral neutralizing antibody to Hantaan virus as determined by plaque reduction technique.

The 76--118 strain of Hantaan virus was titrated in E6 (Vero) cells by the plaque method using agarose overlay medium. Visible plaques, formed 10 days post-infection, were uniformly 2--3 mm in diameter. Dose-response experiments showed that a single infectious particle initiated the formation of a plaque. Infectivity titers by the plaque method were equivalent to those obtained by the endpoint method (TCID50) using the immunofluorescence antibody technique (IFA) for antigen detection. The single-cycle growth pattern of the virus showed an eclipse phase of 7 to 9 hours, with production of cell-free infectious virus 18 hours post-infection. Plaque reduction neutralization tests suggested that complement enhanced the neutralizing activity of sera; rat sera were particularly complement-dependent. The plaque reduction neutralization test was about 10 times more sensitive than the TCID50 neutralization test. Convalescent phase sera from patients with hemorrhagic fever with renal syndrome (HFRS) having higher IF antibody titers to Hantaan virus than to nephropathia epidemica (NE) virus were capable of neutralizing Hantaan virus, while sera from patients with higher IF antibody titers to NE virus than Hantaan virus did not contain neutralizing antibody to Hantaan virus.

Animals↗
PubMed1985

The 200- and 150-kDa neurofilament proteins react with IgG autoantibodies from patients with kuru, Creutzfeldt-Jakob disease, and other neurologic diseases.

Sera from 65 patients with spongiform virus encephalopathies (29 with kuru, 36 with Creutzfeldt-Jakob disease), 79 with other neurologic diseases, and 65 control subjects were examined for reactivity in immunoblots of preparations of myelinated axons and neurofilaments from mouse brain. The sera reacted most frequently with the 200-kDa and 150-kDa neurofilament proteins and less frequently with the 70-kDa neurofilament protein and a 62-kDa neurofilament-associated protein. The sera reacted with the same proteins as those which reacted with rabbit and mouse polyclonal antibodies and mouse monoclonal antibody to neurofilament proteins. Serum reactions were also seen with Trixon X-100 extracts of chimpanzee brain and bovine spinal cord but not with Triton extracts of liver, kidney, and muscle.

Alzheimer Disease↗
PubMed1985

The 200- and 150-kDa neurofilament proteins react with IgG autoantibodies from chimpanzees with kuru or Creutzfeldt-Jakob disease; a 62-kDa neurofilament-associated protein reacts with sera from sheep with natural scrapie.

Sera from 46 chimpanzees with spongiform encephalopathy (18 kuru, 28 Creutzfeldt-Jakob disease) and sera from 12 sheep with natural scrapie were tested for reactivity with immunoblots of neurofilament preparations obtained from mouse brain. The sera from the chimpanzees reacted mainly with the 200- and 150-kDa proteins of the neurofilament triplet and less frequently with the 70-kDa component of the triplet and with a 62-kDa neurofilament-associated protein. In contrast, the sera of sheep with natural scrapie reacted exclusively against the 62-kDa protein. The specificity of the reactions was established by comparison of sera reactivities with those of rabbit and mouse polyclonal antibodies and mouse monoclonal antibody to neurofilament proteins.

Animals↗
PubMed1985

Immune spleen cell-mediated protection against fatal Hantaan virus infection in infant mice.

To clarify the basis of the age-dependent susceptibility of infant mice to fatal meningoencephalitis caused by Hantaan virus, we investigated the ability of spleen cells from immune and nonimmune weanling BALB/c mice to confer protection to syngeneic infant mice. Intraperitoneal transfer of 10 X 10(7), 5 X 10(7), 2.5 X 10(7), and 1.2 X 10(7) immune spleen cells to infant mice 24 hr after intracerebral challenge with 100 50% lethal doses of Hantaan virus (strain 76-118) resulted in 100%, 70%, 64%, and 30% protection, respectively. Even as late as 48 hr after virus challenge, transfer of 10 X 10(7) immune spleen cells conferred complete protection. In contrast, nonimmune spleen cells offered no protection, even when cells were transferred 48 hr before virus challenge. The protective capacity of immune spleen cells was abolished following treatment with antibody to theta antigen and guinea pig complement, but was preserved after the depletion of B cells, a result suggesting that T cells play a crucial role in the resistance of mice to fatal Hantaan virus infection.

Aging↗
PubMed1985

Definition of three serotypes of Hantaviruses by a double sandwich ELISA with biotin-avidin amplification system.

A total of seven different isolates of Hantaviruses from five mammalian species and six geographical areas were examined by a double sandwich ELISA with biotin-avidin amplification system. Three serotypes were recognized by comparing antigen titres to homologous and heterologous antibody and blocking antibody titres to homologous and heterologous antigens. Serotype 1 included four strains: Hantaan virus isolated from Apodemus agrarius in South Korea, Hupei-I isolated from acute-phase serum from a patient with epidemic haemorrhagic fever (EHF) in China, SR-11 isolated from a laboratory rat associated with an EHF outbreak in Sapporo, Japan, and Tchoupitoulas isolated from a wharf rat (Rattus norvegicus) trapped in New Orleans, La., U.S.A. Serotype 2 included two strains of nephropathia epidemica virus, Hällnäs-I and Puumala, isolated from Clethrionomys glareolus trapped in nephropathia epidemica foci in Sweden and Finland, respectively. Serotype 3 included one strain, Prospect Hill-I, isolated from Microtus pennsylvanicus, trapped in Frederick, Md., U.S.A.

Animals↗
PubMed1985

Serotoninergic system in scrapie-infected hamsters.

Hamsters inoculated with scrapie virus show a dramatic hypersensitivity to serotoninergic drugs, developing a behavioral syndrome not unlike that obtained with pharmacologically induced lesions of the raphe nuclei. In an attempt to explain the state of hypersensitivity and to determine whether or not serotoninergic neurons were targets of the scrapie virus, pre- and postsynaptic serotoninergic sites were studied in the cerebral cortices of scrapie-infected and sham-inoculated hamsters. [3H]Imipramine binding and the uptake of endogenous 5-hydroxytryptamine (5-HT, serotonin) in synaptosomes prepared from scrapie-inoculated animals were not different from those of controls. This suggests integrity of the serotoninergic neurons in scrapie-infected hamsters. In contrast, affinity for the 5-HT1 receptor (which modulates inhibitory response) was diminished whereas that for the 5-HT2 receptor (which modulates excitatory response) was increased. This "imbalance" between the two receptors which is amplified in in vivo responses may account for the 5-HT hypersensitivity. The alteration in the affinity of the two postsynaptic 5-HT receptors supports the observation that scrapie virus alters cell plasma membranes.

Animals↗
PubMed1985

Serotypic classification of hantaviruses by indirect immunofluorescent antibody and plaque reduction neutralization tests.

Antisera prepared against 16 strains of hantaviruses isolated from patients with hemorrhagic fever with renal syndrome (HFRS) or from rodents captured in HFRS-endemic and nonendemic regions were titrated against Hantaan virus strain 76-118, Puumala virus strain Sotkamo, and Prospect Hill virus strain Prospect Hill-I by using the indirect immunofluorescent antibody and plaque reduction neutralization tests. Isolates fell into one of four distinct groups or serotypes. Serotype 1 included Apodemus-derived strains, serotype 2 included Rattus-derived strains, serotype 3 included Clethrionomys-derived strains, and serotype 4 included Microtus-derived strains. Serotypic classification of hantavirus infections was possible for humans and rodents in widely varied geographical areas, but in a few instances, sera from patients with HFRS did not conform to any of the four serotypes, suggesting the existence of as yet unidentified serotypes. A definitive serological classification of hantaviruses must await analysis of additional virus isolates.

Animals↗
PubMed1985

Attempts to implicate viruses in myasthenia gravis.

We investigated the hypothesis that a persistent viral infection of the thymus gland might trigger the autoimmune disease myasthenia gravis (MG). Thymus glands of nine patients with recent onset of MG were studied by a variety of techniques to detect the presence of occult viruses. No evidence of viral infection was found.

Adolescent↗
PubMed1984

Choline acetyltransferase activity and [3H]quinuclidinylbenzilate binding in brains of scrapie-infected hamsters.

Choline acetyltransferase (ChAT) activity and [3H]quinuclidinylbenzilate binding were studied in the brain of scrapie-infected hamsters and sham inoculated controls. Although scrapie-infected hamsters showed no reduction of ChAT activity compared to the controls, they showed a decrease in the affinity and maximum number of post-synaptic muscarinic receptors. Scrapie virus thus alters the cholinergic system at the post-synaptic rather than at the pre-synaptic level.

Animals↗
PubMed1984

Infection-specific particle from the unconventional slow virus diseases.

Scrapie-associated fibrils, first observed in brains of scrapie-infected mice, were also observed in scrapie-infected hamsters and monkeys, in humans with Creutzfeldt-Jakob disease, and in kuru-infected monkeys. These fibrils were not found in a comprehensive series of control brains from humans and animals affected with central nervous system disorders resulting in histopathologies, ultrastructural features, or disease symptoms similar to those of scrapie, kuru, and Creutzfeldt-Jakob disease. These fibrils are also found in preclinical scrapie and in the spleens of scrapie-infected mice; they are a specific marker for the "unconventional" slow virus diseases, and may be the etiological agent.

Alzheimer Disease↗