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S Nick

Publications and source records attributed to S Nick.

29 records · Page 2Linked to original sources
PubMed1990

Isolation and characterization of HIV-2ben obtained from a patient with predominantly neurological defects.

A HIV-2 strain named HIV-2ben was isolated from peripheral blood lymphocytes of a patient who, since 1984, had developed neurological symptoms such as Raynaud's syndrome, followed by paresthesia of extremities and ataxia, and finally paraparesis of the legs and incontinence. This new isolate could be distinguished from HIV-2rod by antibody-binding epitopes, peptide maps of core p24 and p18 polypeptides and restriction endonuclease cleavage pattern.

Animals↗
PubMed1990

Experimental infection of macaques with HIV-2ben, a novel HIV-2 isolate.

Ten rhesus (Macaca mulatta) and six fascicularis (Macaca fascicularis) macaques were inoculated with HIV-2ben using three different virus preparations and two routes of inoculation. Thirteen of the 16 inoculated macaques seroconverted 2-6 weeks after infection. Three M. mulatta remained seronegative. The seroconverted animals developed antibody titres from 80 to 40,000. Their antibodies reacted with gp160 and gp130 and, in varying degrees, with gp32 and core proteins. Virus could be re-isolated from 11 of the 16 macaques. M. mulatta were transiently viraemic 6-14 weeks after infection whereas all M. fascicularis were persistently viraemic 2-7 weeks after infection onwards. In the 6-18 months after infection one M. mulatta lost 20% of its body weight and two M. fascicularis showed transient lymphadenopathy and splenomegaly; the other animals remained clinically normal. A re-isolated virus from a M. mulatta was indistinguishable from the inoculated HIV-2ben by genomic restriction enzyme analysis. M. mulatta and M. fascicularis are infectable by a single intravenous injection of cell-free HIV-2ben. Persistent viraemia in M. fascicularis represents a valuable and reliable parameter for studies on antivirals and vaccines.

Animals↗
PubMed1990

Virus neutralizing and enhancing epitopes characterized by synthetic oligopeptides derived from the feline leukaemia virus glycoprotein sequence.

Synthetic peptides that mimic antigenic determinants of viral proteins were used in vaccine studies of feline leukaemia virus (FeLV) infection. Immunoreactive epitopes on FeLV gp70 and p15E were predicted according to the criteria of their terminal position, hydrophilicity and the probability of them constituting helical structures. Nineteen peptides, consisting of seven to 19 amino acid residues, were synthesized, of which two peptides were derived from the FeLV subtype A, 16 from subtype B and one from subtype C. Rabbits were immunized with individual peptides coupled to keyhole limpet haemocyanin and the specificity and biological activities of these hyperimmune sera were determined by ELISA, Western blotting, virus neutralization and cytotoxicity assays. All sera reacted specifically with the immunizing peptide. Twelve of the 19 peptides induced antibodies against purified gp85 and antibodies to 11 peptides reacted with the whole virus. One peptide representing the carboxy terminus of the transmembrane protein p15E, and two peptides derived from the external glycoprotein gp70 elicited neutralizing antibodies, whereas antisera against four peptides enhanced virus infection in vitro. None of the peptide antisera mediated complement lysis of FeLV-infected cells.

Amino Acid Sequence↗
PubMed1987

Suppression of humoral antibody formation against sheep red blood cells by infections with HSV-2 and the influence of mouse cytomegalovirus. Brief report.

HSV-2 infections suppress the antibody response to HSV-1 but do not impair the mouse cytomegalo virus (MCMV) antibody generating system. In contrast, the sheep red blood cell (SRBC) IgM response is impaired by preinfections with HSV-2 but not with HSV-1. From the time kinetics of this suppression it can be concluded that only a certain submechanism "spills over" to the SRBC system. MCMV suppresses the antibody formation induced by HSV-1.

Animals↗
PubMed1987

Virus-specific IgM and IgG antibody production by B cells during herpes simplex virus type 2-induced immunosuppression as analysed by an immunospot assay.

The mechanism of herpes simplex virus (HSV)-2-induced immunosuppression was analysed by determination of the number of IgM and IgG antibody-secreting B cells in female BALB/c mice using an immunospot assay. Primary HSV-1 or -2 as well as homologous or heterologous booster infections at different times were performed. In accordance with earlier results on humoral antibody generation, in contrast to HSV-1, HSV-2 induced only very low numbers of antibody-producing B cells in dose-response experiments. They appeared late after infection compared to HSV-1. Despite a homologous humoral booster reaction against HSV-1 at day 8 no IgM- or IgG-secreting cells in the spleen could be detected. This non-reactivity of the spleen had vanished 10 days later, when secondary reactions of B cells could be observed. Secondary infections with a high homologous dose of HSV-2 after a low primary dose produced only a low booster response of IgG-secreting B cells. Suppression of humoral antibody production induced by HSV-2 (high dose) waned after more than 50 days, indicating that the HSV-2-induced suppression did not impair antigen presentation or memory cell generation.

Animals↗
PubMed1986

Histamine augments interleukin-2 production and the activation of cytotoxic T lymphocytes.

Histamine (0.5 g/kg) was found to augment the activation of cytotoxic T lymphocytes in vivo, if injected in the late phase (day 4) of the response. The production of interleukin-2 in concanavalin A-activated spleen cell cultures was also strongly augmented by 1 X 10(-2) M histamine or by a combination of 2 X 10(-3) M histamine and histaminase (diamine oxidase). This suggests the possibility that the augmentation in vivo is mediated by the oxidized histamine derivative imidazolylacetaldehyde, since diamine oxidase occurs in many tissues. The interleukin-2-dependent proliferation of a T cell clone, on the other hand, was not affected by histamine with or without diamine oxidase. The experiments suggest that histamine supports the late phase of the cytotoxic T lymphocyte response by augmenting the interleukin-2 production.

Animals↗
PubMed1986

Glutathione augments the activation of cytotoxic T lymphocytes in vivo.

The activation of cytotoxic T lymphocytes (CTL) in vivo was found to be augmented by glutathione if injected i.p. in the late phase but not in the early phase of the response. The effect of glutathione possibly resembles the augmenting effect of 2-mercaptoethanol in lymphocyte cultures.

Animals↗
PubMed1986

Suppression and enhancement of humoral antibody formation by herpes simplex virus types 1 and 2.

Intraperitoneal infection of mice and rats by herpes simplex virus type 2 (HSV-2) but not type 1 (HSV-1) resulted in suppression of antibody formation on subsequent challenge with HSV-1 or HSV-2. Application of silica considerably enhanced antibody formation after primary HSV-1 infection, but only slightly after primary HSV-2 infection. Suppression induced by HSV-2 was, however, reduced significantly by injection of silica 21 days later, on the day of the second injection of HSV-2. Suppression could be detected soon after infection by HSV-2. The degree of this suppression depended on the dose of the injected virus and was abolished by u.v. irradiation of the virus prior to inoculation. Likewise the weak antibody response induced by HSV-2 was abolished for both neutralizing and ELISA antibodies. Infections with HSV-1 evoked considerable numbers of HSV-specific antibody-producing B cells, when assessed by an enzyme-linked immunospot assay. The B cell response to HSV-2, however, was very weak. Silica considerably enhanced the number of specific antibody-producing B cells only during primary HSV-1 infections. The present results in combination with earlier data demonstrate the central role of macrophages, which seem to be the primary target affected by silica, for enhancement and suppression of HSV-induced antibody generation.

Animals↗
PubMed1985

Suppression of cytotoxic T lymphocyte activation by L-ornithine.

The effect of L-ornithine on several types of immune reactions was analyzed. L-ornithine was found to suppress the activation of cytotoxic T lymphocytes (CTL) in vivo and in vitro. This suppressive effect was not observed with the structural analogues D-ornithine, L-lysine, or putrescine or with the amino acids L-histidine or L-alanine. The concentration of 9 X 10(-3) M L-ornithine was found to mediate a practically complete suppression of the cytotoxic response in vitro if applied on day 0 or day 1 of the culture, but a comparably weak suppression if applied on day 3. The same concentration of L-ornithine had no effect on the production of the lymphokines interleukin 2 (IL 2) and gamma-interferon (IFN-gamma). This concentration of ornithine had also no substantial effect on several types of proliferative responses, including the allogeneic mixed lymphocyte reaction, the concanavalin A-activated IL 2-dependent proliferation of thymocytes, and IL 2-dependent proliferation of the T cell clone W-2. These observations suggest that L-ornithine inhibits selectively the differentiation of CTL effector cells. By the criteria tested, the immunosuppressive effect of L-ornithine is more selective than that of cyclosporine A, which was previously found to suppress not only the activation of cytotoxic activity but also proliferative responses and the production of the lymphokines IL 2 and IFN-gamma.

Animals↗