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Biomedical subjects

C J Gibbs

Publications and source records attributed to C J Gibbs.

At least 127 records · Page 7Linked to original sources
PubMed1988

Intrathecal synthesis of IgG antibodies to HTLV-I supports an etiological role for HTLV-I in tropical spastic paraparesis.

High titers of antibody to human T-lymphotropic virus type I (HTLV-I) have been reported in the sera and cerebrospinal fluids of patients with tropical spastic paraparesis. By means of agarose isoelectric focusing and selective immunoblotting, we demonstrated oligoclonal bands of immunoglobulin G antibodies to HTLV-I in the serum and cerebrospinal fluid of patients with tropical spastic paraparesis. Such cerebrospinal fluid-specific immunoglobulin bands indicate intrathecal synthesis of specific antibodies to HTLV-I. These findings mimic the antibody response to measles virus in subacute sclerosing panencephalitis and support an etiological role for HTLV-I in the pathogenesis of tropical spastic paraparesis.

Antibodies, Anti-Idiotypic↗
PubMed1988

Seroprevalence of antibodies to HTLV-I in patients with chronic neurological disorders other than tropical spastic paraparesis.

Human T-lymphotropic virus type I (HTLV-I), the etiological agent of adult T-cell leukemia/lymphoma, also appears to be the cause of tropical spastic paraparesis, a chronic myelopathy reported in several different regions of the world. The prevalence of antibodies to HTLV-I in patients with chronic neurodegenerative disorders other than tropical spastic paraparesis and in patients with some muscle inflammatory disorders has been investigated. IgG antibodies to HTLV-I were measured in the sera and/or cerebrospinal fluid from 82 Guamanian patients with amyotrophic lateral sclerosis and parkinsonism-dementia, 164 Guamanian normal controls, 10 patients with kuru from the Eastern Highlands of Papua New Guinea, 4 patients with Viliuisk encephalomyelitis from the Iakut region of eastern Siberia, 45 Italian patients with multiple sclerosis, and 56 patients with polymyositis (49 from the United States and 7 from Jamaica). As determined by enzyme-linked immunosorbent assay, Western immunoblot, and gelatin particle agglutination techniques, serological evidence of HTLV-I infection was found in 1 patient with amyotrophic lateral sclerosis and 1 control subject from Guam, and in 1 patient from the United States and all 7 Jamaican patients with polymyositis. Except for the high seropositivity rate among the group of Jamaican patients with polymyositis, our data indicate that HTLV-I is an unlikely causative agent in the spectrum of the neurological diseases examined. The seropositivity of the 7 Jamaican patients with polymyositis requires further study.

Adult↗
PubMed1988

Immunological findings in neurological diseases associated with antibodies to HTLV-I: activated lymphocytes in tropical spastic paraparesis.

A retrovirus involvement in the etiology of certain neurological diseases is currently an area of intense interest. Tropical spastic paraparesis and other chronic progressive myelopathies have been clearly associated with increased serum and cerebrospinal fluid antibody titers to human T-lymphotropic virus type I; however, little is known about the cellular immune response. In the present study, activated T-lymphocytes were found in the peripheral blood of patients with this disorder. There were increased numbers of large CD3-positive cells that also expressed histocompatibility leukocyte Class II (DR) and interleukin 2-receptor molecules. In addition, a significantly elevated spontaneous lymphoproliferative response was demonstrated in all patients. This is consistent with the known in vitro effects of human T-lymphotropic virus type I. In one patient, a defect in the generation of measles virus-specific cytotoxic T cells was identified. These observations indicate abnormalities of the cellular immune response in tropical spastic paraparesis.

Antibodies, Viral↗
PubMed1988

Histochemical and X-ray microanalytical localization of aluminum in amyotrophic lateral sclerosis and parkinsonism-dementia of Guam.

Histochemical staining for aluminum, using Solochrome azurine or Morin, provided a rapid, simple and reliable means of identifying areas and structures of the brain of interest for closer scrutiny by X-ray microanalysis in patients with amyotrophic lateral sclerosis and parkinsonism-dementia of Guam. Neuronal perikarya, dendritic processes, and the walls of some cerebral vessels were aluminum positive by Solochrome azurine staining. In some cases, the deposition of aluminum was rather diffuse, particularly in the white matter. Fluorescent localization of aluminum using Morin was equally sensitive and specific, but provided less morphological detail than Solochrome azurine. Confirmation of histochemical detection of aluminum was achieved by examining adjacent tissue sections using wavelength-dispersive spectrometry coupled to a computer-controlled electron beam X-ray microprobe. Although the minimum detectable limits for aluminum by these histochemical procedures are unknown, the lower detection limit of our X-ray microanalytical technique is 10-100 ppm dry weight. Solochrome and Morin staining, as verified by X-ray microanalysis, afford a useful and reliable means of surveying multiple anatomical regions for aluminum deposition in naturally occurring and experimentally induced neurodegenerative disorders.

Adolescent↗
PubMed1988

Experimental hantavirus infection in nonhuman primates.

Mild, transient proteinuria and azotemia were produced in three cynomolgus monkeys (Macaca fascicularis) and a chimpanzee (Pan troglodytes) following intravenous inoculation with Prospect Hill virus, a hantavirus isolated from meadow voles in the United States. This is the first demonstration of an acute nephropathy in nonhuman primates with the viruses causing hemorrhagic fever with renal syndrome.

Animals↗
PubMed1988

Temporal development of cross-neutralization between HTLV-III B and HTLV-III RF in experimentally infected chimpanzees.

Sera from chimpanzees inoculated respectively with HTLV-III B, LAV, HTLV-III RF and brain tissue from an AIDS patient were analysed for neutralizing activity by two methods: a cell fusion inhibition test (CFI) using HTLV-III B infected cells as inoculum and CD4+ cells as target and a replication inhibition test (RIT) using cell-free HTLV-III B as well as HTLV-III RF as inoculum and also CD4+ cells as target. All chimpanzees seroconverted for HTLV-III B antibodies within 2 months after inoculation and the ten sera included in the study recognized the HTLV-III B core proteins p17 and p24 and the transmembrane protein gp41 by immunoblotting. The HTLV-III B external envelope gp120 was recognized by eight sera with antibodies active in the CFI (CFI-Ab) or in the RIT (VN-Ab) using HTLV-III B as inoculum, while neither of two sera without such reactivity did. HTLV-III B CFI-Ab and HTLV-III B VN-Ab concurred in nine of ten serum samples. LAV and HTLV-III B infection induced HTLV-III B CFI-Ab and HTLV-III B VN-Ab within 9 months after inoculation in all four chimpanzees tested. However, only the serum of one of the four animals also neutralized HTLV-III RF. HTLV-III RF inoculation evoked only HTLV-III RF VN-Ab within nine months. Between 11 and 18 months neutralizing activity to both HTLV-III B and HTLV-III RF was found in all four sera of chimpanzees inoculated with HTLV-III B, LAV or HTLV-III RF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Human immunodeficiency virus type 1 neutralization epitope with conserved architecture elicits early type-specific antibodies in experimentally infected chimpanzees.

Chimpanzees are susceptible to infection by divergent strains of human immunodeficiency virus type 1 (HIV-1), none of which cause clinical or immunological abnormalities. Chimpanzees were inoculated with one of four strains of HIV-1: human T-lymphotropic virus (HTLV) type IIIB, lymphadenopathy virus (LAV) type 1, HTLV type IIIRF, or an isolate from the brain of a patient with acquired immunodeficiency syndrome. Within 6 months after inoculation with the closely related strains HTLV-IIIB or LAV-1, six chimpanzees developed serum antibodies to the C-terminal half (amino acids 288-467) of the HTLV-IIIB external envelope glycoprotein gp120. Sera from five of those chimpanzees had HTLV-IIIB cell-fusion-inhibiting antibody titers greater than or equal to 20 at that time, indicating that they neutralized the infecting strain of HIV-1 in vitro. No antibodies to the carboxyl terminus of HTLV-IIIB gp120 were observed in sera of chimpanzees inoculated with HTLV-IIIRF or with the brain-tissue strain, and those sera did not neutralize HTLV-IIIB. A rabbit immunized with the C-terminal portion of gp120 acquired neutralizing antibodies that bound to four domains of the HTLV-IIIB external envelope as analyzed by reactivity to 536 overlapping nonapeptides of gp120. One of these domains in the variable region V3, with the amino acid sequence IRIQRGPGRAFVTIG (amino acids 307-321), bound to all chimpanzee sera that neutralized HTLV-IIIB but not to the serum of the HTLV-IIIRF-inoculated chimpanzee that did not neutralize HTLV-IIIB. The HTLV-IIIRF sequence at the same location, ITKGPGRVIYA, was recognized by the serum of the HTLV-IIIRF-inoculated chimpanzee but not by any sera of the HTLV-IIIB-inoculated or LAV-1-inoculated chimpanzees. The HTLV-IIIB residues RIQR and AFV and the HTLV-IIIRF residues lysine and VIYA, flanking a highly conserved beta-turn (GPGR), appear to be critical for antibody binding and subsequent type-specific virus neutralization. This neutralization epitope, putatively consisting of a loop between two cysteine residues (amino acids 296 and 331) connected by a disulfide bond, is immunodominant in HIV-1-infected chimpanzees and induces antibodies restricted to the homologous viral strain.

Amino Acid Sequence↗
PubMed1988

Serological evidence of hantavirus infection in laboratory rats and personnel.

Laboratory-acquired haemorrhagic fever with renal syndrome (HFRS) has been reported in many countries. A serological survey of laboratory white rats and of laboratory personnel for antibodies to hantaviruses was conducted in Singapore. Forty-four per cent (143/329) of rats were seropositive by the indirect immunofluorescent antibody test but none had hantaviral antigens in lung tissues. Two of 74 laboratory personnel were seropositive but neither had a history of clinical illness. The high seropositivity rate among laboratory rats led to their replacement with Hantaan virus-free strains. To eliminate the hazard of laboratory-acquired HFRS, regular serological screening of laboratory rats and replacement of infected animals with seronegative stocks should be implemented. High risk techniques with laboratory rats, which are likely to generate aerosols, should be performed in biological safety cabinets. Serological surveillance of laboratory personnel and reporting of suspected HFRS cases are useful in the early detection of hantavirus infection.

Animals↗
PubMed1988

Leakey virus: a new hantavirus isolated from Mus musculus in the United States.

A hantavirus, designated Leakey virus, was isolated from a Mus musculus captured in Real County, Texas, U.S.A. in August 1986. Virus-specific fluorescence was first detected 13 days after inoculation of Vero-E6 cells with spleen tissue from the seropositive M. musculus. Ultrastructurally, the new isolate resembled other hantaviruses. Leakey virus induced a fatal meningoencephalitis in infant Fischer rats, with viral antigen detectable in brain, lung, liver, kidney and spleen. Serum dilution, plaque reduction neutralization tests indicated that Leakey virus was antigenically distinct from Hantaan, Seoul, Puumala and Prospect Hill viruses, and therefore constitutes a new serotype.

Animals↗
PubMed1988

Tubulovesicular structures in experimental Creutzfeldt-Jakob disease and scrapie.

Tubulovesicular structures, measuring 20-50 nm in diameter, were found in dilated neuronal processes in brains from mice infected with the Fujisaki strain of Creutzfeldt-Jakob disease virus. These particles were similar to those observed in brains from hamsters infected with scrapie. These structures are consistently present in naturally occurring and experimentally induced spongiform encephalopathies, irrespective of the host species or virus strain. Their role in pathogenesis is undetermined.

Animals↗
PubMed1987

Sleep abnormalities with REM disorder in experimental Creutzfeldt-Jakob disease in cats: a new pathological feature.

Alterations in sleep organization were studied during the clinical phase of experimental Creutzfeldt-Jakob disease (CJD) in cats. Twenty months after intracerebral inoculation of a CJD agent, cats developed clinical signs including behavioral changes, diminished grooming activity, dysmetria, startle reflex, myoclonus, and unusual sleep abnormalities. Rapid eye movement (REM) sleep displayed a new and irreversible organization, with a continuous and constant pseudoperiodic pattern of rapid eye movements, synchronous with diffuse bursts of cortical abnormalities and with ponto-geniculo-occipital (PGO) wave activity. Computer analysis revealed a constant morphology of cortical bursts and their temporal relationship with ocular episodes. Induction of PGO wave activity with benzoquinolizine derivative Ro 4-1284 demonstrated the PGO-dependent nature of the cortical alterations. Abnormal unresponsive states were observed during REM sleep phases and arousal thresholds were increased in CJD cats during REM sleep. The percentages of wakefulness and slow-wave sleep were reversed in these animals. Preliminary neuropathological observations included discrete to minimal spongiosis of cerebral gray matter and a remarkably focalized intracytoplasmic vacuolation in neurons of the raphé system. Our findings suggest that particular neuronal systems involved in sleep regulation are impaired in CJD cats.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1987

Serological survey of Prospect Hill virus infection in indigenous wild rodents in the USA.

We found serological evidence of infection with Prospect Hill virus, a Hantaan-like virus isolated from meadow voles (Microtus pennsylvanicus), in microtine and cricetid rodents trapped in Maryland, West Virginia, Minnesota and California, USA. Fluorescent antibodies were detected in sera from M. pennsylvanicus (74/277), M. californicus (39/185), Clethrionomys gapperi (5/51), Peromyscus maniculatus (4/22) and P. truei (1/11). Sera from seropositive P. maniculatus contained neutralizing antibodies against Prospect Hill virus, confirming that infection with Prospect Hill virus or antigenically related viruses is not restricted to microtine rodents in the USA. Despite the widespread distribution of Prospect Hill virus in indigenous rodents, the recent demonstration that American mammalogists are only rarely infected supports the view that the overall risk of Prospect Hill virus infection in man is low.

Animals↗
PubMed1987

Monoclonal antibody analysis of keratin expression in the central nervous system.

A monoclonal antibody directed against a 65-kDa brain protein demonstrates an epitope found in keratin from human epidermis. By indirect immunofluorescence, the antibody decorates intracytoplasmic filaments in a subclass of astrocytes and Purkinje cells of adult hamster brain. Double-label immunofluorescence study using antibody to glial fibrillary acidic protein and this antibody reveals the 65-kDa protein to be closely associated with glial filaments in astrocytes of fetal mouse brain cultures. Immunoblot analysis of purified human epidermal keratin and hamster brain homogenate confirms the reactivity of this antibody to epidermal keratin polypeptides. All the major epidermal keratins were recognized by this antibody. It did not bind to the remaining major intermediate filament proteins. These findings suggest that monoclonal antibody 34C9 recognizes a cytoskeletal structure connected with intermediate filaments. In addition, the monoclonal antibody demonstrates that epidermal keratins share an epitope not only among themselves but also with a "neural keratin."

Animals↗
PubMed1987

Intra-blood-brain barrier synthesis of human immunodeficiency virus antigen and antibody in humans and chimpanzees.

The presence of human immunodeficiency virus (HIV) antigens in cerebrospinal fluid (CSF) was associated with progressive encephalopathy in adult and pediatric patients with acquired immunodeficiency syndrome (AIDS). HIV antigen was detected in CSF from 6 of 7 AIDS patients with progressive encephalopathy. By contrast, HIV antigen, whether free or complexed, was detected in CSF from only 1 of 18 HIV antibody seropositive patients without progressive encephalopathy and from 0 of 8 experimentally infected chimpanzees without clinical signs. Intra-blood-brain barrier synthesis of HIV-specific antibody was demonstrated in the majority of patients with AIDS (9/12) or at risk for AIDS (8/13) as well as in the experimentally infected chimpanzees, indicating HIV-specific B-cell reactivity in the brain without apparent neurological signs. In 6 of 11 patients with HIV infection, antibodies synthesized in the central nervous system were directed against HIV envelope proteins. Active viral expression appears to be necessary for both the immunodeficiency and progressive encephalopathy associated with HIV infection.

AIDS-Related Complex↗