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J Lycke

Publications and source records attributed to J Lycke.

23 records · Page 2Linked to original sources

Use of immunoreactive synthetic HTLV-1 peptides in the search for antibody reactivity in multiple sclerosis.

The possible association between multiple sclerosis (MS) and antibodies to human T-cell lymphotropic virus type 1 (HTLV-1) was studied. Five synthetic and highly immunoreactive HTLV-1 peptides, four from the envelope (env) region and one from the core (gag) region, were used in an indirect enzyme-linked immunosorbent assay (ELISA). Presence of HTLV-1-specific antibodies in paired serum and cerebrospinal fluid (CSF) samples from 41 MS patients were investigated. No antibody reactivity was demonstrable in samples from 40 of them, whereas one reacted in one serum sample against the gag-peptide. Serum and CSF specimens from 15 with other neurologic diseases (OND), and negative control specimens, i.e. serum and CSF from 9 non-neurologic controls and CSF from 9 healthy controls, did not demonstrate any reactivity in the peptide-ELISAs. Our results do not support involvement of HTLV-1 infection in the etiology of MS.

Adolescent↗

Identification of type-specific linear epitopes in the glycoproteins gp46 and gp21 of human T-cell leukemia viruses type I and type II using synthetic peptides.

Synthetic peptides of 20-25 amino acids were employed in enzyme-linked immunosorbent assays to identify linear epitopes in the external glycoprotein gp46 and the transmembrane glycoprotein gp21 of human T-cell leukemia/lymphotropic viruses type I (HTLV-I) and II (HTLV-II). Ten linear epitopes were identified in the HTLV-I glycoproteins, seven in gp46 and three in gp21. Three major linear epitopes were identified in the gp46 of HTLV-II. Peptides representing linear epitopes of gp46 were found to be sensitive and specific for the detection of antibody and permit serological identification and differentiation of HTLV-I and HTLV-II infections.

Amino Acid Sequence↗

Incidence of MS during two fifteen-year periods in the Gothenburg region of Sweden.

The average annual incidence of definite and probable MS in Gothenburg was re-investigated. For 1950-1954, 1955-1959 and 1960-1964 it was 4.2, 4.2 and 4.3/100,000/year. For the five-year periods between 1974 and 1988 it was 3.0, 2.7 and 2.0/100,000/year. If possible MS was included, the corresponding incidence for 1950-1964 was 5.2, 5.3 and 5.1, and for 1974-1988 it was 3.9, 3.9 and 4.3/100,000/year. Neurological methods and diagnostic criteria were constant throughout the period. The 1950-1964 incidence was based on personally investigated cases, while the 1974-1988 incidence was based partly on review of Gothenburg neurology records. It is concluded that there has been a significant decrease in the incidence of MS in this area. However, the notified decrease may partly be explained by alterations in the case ascertainment procedure. Since the Swedish measles vaccination program started in 1971, the occurrence of measles has been declining and has practically ceased during the 1980s. The time when a possible influence of mass vaccinations against childhood diseases on MS incidence can be monitored is discussed.

Adolescent↗

Acyclovir concentrations in serum and cerebrospinal fluid at steady state.

A long-term clinical trial of acyclovir, 800 mg tid, as a therapeutic agent in multiple sclerosis (MS) is in progress. In three patients paired serum and cerebrospinal fluid (CSF) specimens were sampled after one, four, eight and twelve months of continuous treatment. These samples were collected 1.5 h before or 1.5 h after an oral dose. Acyclovir concentrations were assessed by radioimmunoassay. In the CSF, the acyclovir concentration was relatively stable, with a mean of 0.83 microM, while the serum acyclovir concentration was variable with mean peak and trough concentrations of 4.08 and 2.47 microM, respectively. In two other MS patients the acyclovir concentration time profile in serum and CSF was studied at steady state during the 8 h dose interval. In this study the acyclovir concentration in the CSF was only slightly affected by the fluctuations in serum and the acyclovir CSF/acyclovir serum ratio was apparently not influenced by the blood-brain barrier function. We found no indication of an accumulation of acyclovir in cerebrospinal fluid after one to twelve months of oral treatment.

Acyclovir↗

Herpes simplex virus infection of the human sensory neuron. An electron microscopy study.

Herpes simplex virus (HSV) type 1 was used to infect cultures of human embryonic dorsal root ganglion cells. Infected cultured were studied by electron microscopy. Viral nucleocapsids were observed to be internalized into neuronal cells bodies and neuritic extensions by fusion of the viral envelope and the plasma membrane. No signs of internalization by endocytosis were noted. Nucleocapsids were transported in neurites and were within 2 hrs postinfection found located near the microtubules and close to the nuclear pores in the perikaryon. A primary envelopment of nucleocapsids occurred at the inner lamina of the nuclear membrane and virions appeared between the two laminae. Presence of non-enveloped nucleocapsids outside the nuclear membrane and in close contact with the endoplasmic reticulum suggested that nucleocapsids could pass to the cytoplasmic side probably by de-envelopment at the outer nuclear membrane. A secondary envelopment occurred at the endoplasmic reticulum where the virions also became enclosed in transport vesicles. Enveloped virus appearing in the cytoplasm of neurons and neuritic extensions was always found only inside these transport vesicles. During their passage through the cytoplasm the virion-transport vesicle complexes were surrounded by smaller lysosome-like vesicles possibly derived from the Golgi apparatus. Fusion reactions between vesicles with virions and the smaller vesicles seemed to occur. We discuss if in this way the virion-transport vesicle complexes might be provided with glycosyl transferases and substrates necessary for maturation and completion of glycosylation of the viral envelope glycoproteins. The transport vesicles seemed essential for egress of virions from the infected cell by releasing virus when fusing with the plasma membrane.

Capsid↗