[Isolation of HIV-2 from AIDS patient in Ghana and analysis of sero-reactive patterns of Ghanaian sera].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Hayami.
Explore the source record for details and available documents.
The cell-mediated killer activity in cynomolgus monkeys, which were infected 2.5 yr previously with HTLV-1, was examined. With HTLV-1-infected autologous lymphoid cells as targets, HTLV-1-specific killer cells were not detected among PBL cells of infected monkeys, but in monkeys in which specific memory cells were found. These memory cells were converted to active specific killer cells by stimulation with mytomycin C (MMC)-treated HTLV-1 infected autologous cells in vitro. Target blocking by anti-HTLV-1-related Ag suggested that the target molecules recognized by the specific killer cells may be virus envelope glycoprotein gp 68 and other cellular Ag induced by HTLV-1 infection. In addition to the specific killer cells, NK cells that could kill not only NK-sensitive target cells but also target lymphoid cells with HTLV-1 Ag on their surface, were found in these monkeys. In vitro stimulation caused enhancement of NK cell activity as well as induction of antigen specific killer cells. These findings suggest that Ag-specific killer cells may work together with NK cells to eliminate HTLV-1-bearing T cells in vivo.
Some wild African green monkeys are known to be naturally infected with a retrovirus related to human immunodeficiency virus (HIV) without having any apparent symptoms of an AIDS-like disease. This simian immunodeficiency virus, designated SIVAGM, may be helpful in clarifying the evolution and pathogenicity of HIV. Some virus strains that were previously reported to be isolated from African green monkeys were shown to be laboratory contaminations of SIVMAC (SIV from a rhesus macaque) Here we report the complete DNA sequence of authentic SIVAGM, which was isolated from a naturally infected African green monkey of Kenyan origin. Comparison of the genome of SIVAGM with those of known HIV/SIVs indicates that the virus is a new simian lentivirus that is approximately equally distantly related to HIV-1 and HIV-2 in contrast to SIVMAC, which is much closer to HIV-2 than to HIV-1 (refs 5, 9).
Sixteen monoclonal antibodies (MAbs) against TA34 antigen found on the surface of human T-cell leukemia virus type-I (HTLV-I) infected cells were prepared. These MAbs and one previously prepared anti-TA34 MAb (TAG34) recognized 34-kDa peptide not only in HTLV-I-infected cells, but also in cells infected with simian T-cell leukemia virus (STLV-I), which is analogous in antigenicity and gene structure to HTLV-I. Radioimmuno-precipitation (RIP) tests with the MAbs showed that TA34 antigen had at least 3 overlapping epitope groups. The antigenicities of the TA34 antigens of HTLV-I-infected cells derived from various primates were investigated by immunofluorescence staining using 9 anti-TA34 MAbs. Cells from humans, apes and Old World monkeys reacted with all these antibodies, whereas cells from New World monkeys were stained by most of the antibodies, but little if at all by the remaining 2 (5A8 and TAG34). Similar results were obtained with various primate cells infected with STLV-I. All 17 MAbs used recognized a 22-kDa peptide in HTLV-I-infected cells cultured in the presence of tunicamycin. When incubated with 1% 2-mercaptoethanol at pH 7.2 at 37 degrees C, TA34 antigen lost its reactivity with TAG34, suggesting that the antigen has an intramolecular S-S bond. Twenty sera of adult T-cell leukemia (ATL) patients did not react with TA34 antigen in RIP tests.
Explore the source record for details and available documents.
Ley determinant (Fuc alpha 1----2Gal beta 1----4[Fuc alpha 1----3]GlcNAc beta 1----R) defined by mAb BM-1 is highly expressed in human immunodeficiency virus (HIV)-infected T cell lines and in CD3+ peripheral mature T cells of patients with acquired immune deficiency syndrome (AIDS) or with AIDS-related complex (ARC). Ley expression increased greatly in the CD3+ population in the advanced stage of AIDS when the CD4+ population decreased greatly. Six other carbohydrate antigens tested by their respective mAbs were not detected in these same cells. None of the carbohydrate antigens tested by the seven mAbs used in this study were found in noninfected T cell lines and in normal peripheral blood lymphocytes.
Sixteen isolates of simian retrovirus closely related to human immunodeficiency virus (HIV) were obtained from healthy African green monkeys (AGM) (Cercopithecus aethiops). The first isolate was obtained from a monkey seropositive for HIV, and the others were isolated from monkeys harboring antibodies to the first isolate. These simian retroviruses were referred to as simian immunodeficiency virus from AGM, SIV[AGM], due to their cross-reactivities with HIV structural proteins. These SIV[AGM] isolates were found by Western blotting analysis to have virus-specific proteins of 120, 66, 55, 32-40, 24 and 17 kDa, which were all similar in size to the analogous proteins of HIV. Putative gag proteins of p55, p24 and p17 were recognized by sera of human AIDS patients, but the corresponding env proteins of 32-40 and 120 kDa showed only weak cross-reactivity with those of HIV. The transmembrane glycoproteins of these 3 SIV[AGM] isolates showed size heterogeneity, being 32, 35 and 40 kDa. This virus had particles that were morphologically similar to those of HIV, and had Mg2+-dependent reverse transcriptase. Furthermore, the SIV[AGM] showed tropism and cytopathic effects on CD4-positive human cell lines. In a sero-epidemiological survey of SIV[AGM] in various non-human primates, 2 other African monkey species, the mandrill and de Brazza's monkey, were also found to have antibodies to SIV[AGM]. These HIV-related simian retroviruses will be important in determining the origin and transmission of HIV group viruses, and may provide useful animal models for studies on the infection and pathogenesis of HIV and AIDS.
Mouse monoclonal antibodies were produced against simian immunodeficiency virus (SIV) from the African green monkey (SIVAGM). The antibodies reacted with the transmembrane protein of all five SIVAGM isolates but not with those of SIVs from the rhesus macaque and mandrill or of human immunodeficiency virus type 1 or type 2, indicating that they recognize a species-specific epitope strongly conserved in SIVAGM. The transmembrane proteins of several SIVAGM isolates were found to vary in molecular size, even in the deglycosylated form after N-glycanase treatment, indicating heterogeneity of the SIVAGM isolates.
Mouse hepatitis virus (MHV)-specific T-lymphocyte clones were established from MHV-infected BALB/c mice. They expressed Thy1 and Lyt2 antigens but lacked L3T4 and NK1 antigens. The clones killed MHV-infected but not uninfected or influenza virus-infected J774.1 cells. The specificity was further defined by a cold-target competition test.
Spleen cells from mice, 4 to 60 days after infection with mouse hepatitis virus type 4, produced interleukin-2, as well as interleukin-3, in the absence of exogenous stimulants in vitro. This unique lymphokine production by mouse hepatitis virus type 4 infection was controlled by host genes.
We reported previously that homopolysaccharides with sulfate groups revealed immunomodulating activities--lymphocyte mitogens. We further investigated the role of homopolysaccharides in a different system--cultivation of Molt-4. clone no.8 with supernatant from human T cell lymphotropic virus type III (HTLV-III)-infected TALL-1, utilizing cytopathic effects (CPE), fluorescence antibody technique (FAT), reverse transcriptase (RT) assay and cell proliferation assay. Sulfated homopolysaccharides such as fucoidan, dextran sulfate with three different molecular weights, cellulose sulfate and k-carrageenan showed most potent anti-HTLV-III activities at mitogenic doses. However, neutral homopolysaccharides had no effects on anti-HTLV-III activities Sulfated heteropolysaccharides such a heparin and heparan sulfate had a little effect on anti-HTLV-III activities. It is suggested that sulfate group is most important in inhibiting growth of HTLV-III, but the structure of the polysaccharides is also important, because homopolysaccharides are more potent anti-HTLV-III agents than heteropolysaccharides.
Explore the source record for details and available documents.
Tumor cells of feline leukemia were examined for structural abnormality and expression of the myc gene. Four of 12 spontaneous leukemia cases showed structural abnormalities of the myc gene detected by Southern blotting analysis. Of these 4 cases, one (Case 1) showed a DNA rearrangement in the 5' portion of the c-myc locus associated with integration of feline leukemia virus (FeLV) genome. Another case had a newly inserted myc gene which was transduced by FeLV. In the 2 other cases, no relation of abnormalities of the myc gene to FeLV was detected. One case of experimental leukemia induced by inoculation of a cell line, FT-1, established from Case 1 showed a c-myc gene rearrangement similar to that observed in Case 1. Expression of myc RNA was examined in 3 leukemia T-cell lines, FT-1, FL74 and F422, by Northern blotting analysis. A high level of myc transcript was detected in all 3 cell lines. The size of myc RNAs in FT-1 and FL74 was the same as that of normal myc RNA, while in F422 which had myc-containing FeLV (myc-FelV), the full genome and spliced form of myc-FeLV viral RNA were detected.
Protection against human T-cell leukemia virus type-I (HTLV-I) infection in cynomolgus monkeys, achieved by immunizing the animals with env gene products of HTLV-I produced in Escherichia coli, was evaluated. Four monkeys that had been immunized with the env product produced antibody against HTLV-I gp68 and gp46, and their sera were found to cause strong inhibition of syncytium formation of a cat fibroblast cell line induced by HTLV-I. Immunized and non-immunized monkeys were challenged with live MT-2 cells, a high HTLV-I-producer cell line. After challenge, all the control non-immunized monkeys were infected with HTLV-I, as judged by the frequent detection of HTLV-I-antigens in cultures of their peripheral blood mononuclear cells (PBMC), whereas no antigens were recovered from PBMC of immunized monkeys. These results indicate that humoral immunity against HTLV-I-envelope protein elicited by immunization with the polypeptides synthesized in bacteria protected the monkeys against primary infection with HTLV-I.
Proviral integration of a simian retrovirus highly homologous to human T-cell leukemia virus type I was examined in cellular DNAs extracted from primary peripheral blood lymphocytes of 31 adult African green monkeys (Cercopithecus aethiops) that were seropositive for simian T-cell leukemia virus type I (STLV-I). Among these monkeys, one case with overt leukemia, showing pleomorphic leukemia cells similar to those in human adult T-cell leukemia (ATL), and five cases in a preleukemic state of ATL-like disease were found. Judging from the integration site of the provirus genome, primary lymphocytes of these leukemic or preleukemic cases contained monoclonally proliferated STLV-I-infected cells, whereas lymphocytes of other seropositive monkeys without hematological abnormalities were polyclonal, and those of seronegative monkeys did not contain the provirus. The restriction patterns with PstI ans SstI of most STLV-I proviruses were identical to those of the previous isolate from this species, but in three monkeys there was a deletion of one PstI site. From the correlation of the development of simian ATL-like disease with the monoclonal integration of the STLV-I provirus genome, it should be indicated that STLV-I has similar leukemogenicity to human T-cell leukemia virus type I, and so STLV-I infection in African green monkeys will be useful as an animal model of human ATL.
Explore the source record for details and available documents.
An in-vitro system for infection of cat T lymphocytes with feline leukemia virus (FeLV) was developed. For establishment of this system, FeLV was inoculated in vitro into concanavalin-A stimulated primary lymphoid cells and long-term cultured T cells grown with interleukin-2 (IL-2) from various feline lympho-hematopoietic organs. During serial cultivation with IL-2, FeLV group-specific antigen (GSA) was detected 5-6 weeks after infection in the primary cultures, and 1 week after infection in the long-term cultures of T cells. The percentage of FeLV-GSA-positive cells gradually increased with passages and reached more than 80% in several cultures of lymphoid cells, that became persistently infected and produced FeLV. These FeLV-infected lymphoid cells expressed T-cell markers, but showed no obvious differences in growth or cytological characteristics from FeLV-free feline lymphoid cells during the observation period of 60 weeks.
Explore the source record for details and available documents.