Acquired Immunodeficiency Syndrome: Kano M

Kano M, Watanabe M, Maeda M. · Department of Neurosurgery, Chuno Hospital, Seki City, Gifu, Japan. · Brain Tumor Pathol. · Pubmed #10746967 No free full text.

Abstract: This report describes a case of streptococcal abscess in the nodules of a primary central nervous system (CNS) lymphoma. Magnetic resonance imaging (MRI) of the brain revealed multiple lesions with ringlike enhancement over the bilateral frontal, right temporal, and left parietal lobes. On admission, acute brain edema occurred following angiography, which resulted in respiratory arrest. Autopsy findings showed that the ringlike enhanced lesions on MRI were streptococcal abscesses localized in the lymphoma nodules. The lymphoma was classified as non-Hodgkin, diffuse large cells of B-cell lineage. No other lymphoma mass was found extracranially. An immunohistochemical study showed that the lymphoma cells were positive for leukocyte common antigen, Epstein-Barr virus, bax. and bcl-XL, and negative for L-26 and bcl-2. This case demonstrated that an opportunistic streptococcal abscess developed in primary CNS lymphoma in a patient without acquired immunodeficiency syndrome (AIDS), though a few similar cases have been reported in patients with AIDS.

Yanagisawa Y, Sato Y, Asahi-Ozaki Y, Ito E, Honma R, Imai J, Kanno T, Kano M, Akiyama H, Sata T, Shinkai-Ouchi F, Yamakawa Y, Watanabe S, Katano H. · Department of Clinical Informatics, Tokyo Medical and Dental University, Japan. · J Pathol. · Pubmed #16741895 No free full text.

Abstract: Lymphoma usually forms solid tumours in patients, and high expression levels of adhesion molecules are observed in these tumours. However, Kaposi's sarcoma-associated herpesvirus (KSHV)-related primary effusion lymphoma (PEL) does not form solid tumours and adhesion molecule expression is suppressed in the cells. Inoculation of a KSHV-associated PEL cell line into the peritoneal cavity of severe combined immunodeficiency mice resulted in the formation of effusion and solid lymphomas in the peritoneal cavity. Proteomics using two-dimensional difference gel electrophoresis and DNA microarray analyses identified 14 proteins and 105 genes, respectively, whose expression differed significantly between effusion and solid lymphomas. Five genes were identified as having similar expression profiles to that of lymphocyte function-associated antigen 1, an important adhesion molecule in leukocytes. Among these, coronin 1A, an actin-binding protein, was identified as a molecule showing high expression in solid lymphoma by both DNA microarray and proteomics analyses. Western and northern blotting showed that coronin 1A was predominantly expressed in solid lymphomas. Moreover, KSHV-encoded lytic proteins, including viral interleukin-6, were highly expressed in effusion lymphoma compared with solid lymphoma. These data demonstrate that effusion and solid lymphomas possess distinctive gene and protein expression profiles in our mouse model, and suggest that differences in gene and protein expression between effusion and solid lymphomas may be associated with the formation of effusion lymphoma or invasive features of solid lymphoma. Furthermore, the results obtained using this combination of proteomics and DNA microarray analyses indicate that protein synthesis partly reflects, but does not correlate strictly with, mRNA production.

Kato M, Igarashi H, Takeda A, Sasaki Y, Nakamura H, Kano M, Sata T, Iida A, Hasegawa M, Horie S, Higashihara E, Nagai Y, Matano T. · Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. · Vaccine. · Pubmed #15837216 No free full text.

Abstract: Recent prophylactic vaccine trials inducing virus-specific CD8+ T-cell responses have shown control of primary infections of a pathogenic simian-human immunodeficiency virus (SHIV) in macaques. In the chronic phase, therapeutic immunization replenishing virus-specific CD8+ T-cells is likely to contribute to sustained control of virus replication. In this study, we have administered a recombinant Sendai virus (SeV) vector into five rhesus macaques that had received prophylactic vaccinations and had controlled SHIV replication for more than 1 year after challenge. Our results indicate that virus-specific CD8+ T-cell responses can be expanded and broadened by therapeutic immunization with SeV vectors in the chronic phase after prophylactic vaccine-based control of primary immunodeficiency virus infections.

Lun WH, Takeda A, Nakamura H, Kano M, Mori K, Sata T, Nagai Y, Matano T. · AIDS Research Center, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan. · J Gen Virol. · Pubmed #15218180 links to  free full text

Abstract: Virus-specific cellular immune responses play an important role in the control of immunodeficiency virus replication. However, preclinical trials of vaccines that induce virus-specific cellular immune responses have failed to contain simian immunodeficiency virus (SIV) replication in macaques. A defective provirus DNA vaccine system that efficiently induces virus-specific CD8(+) T-cell responses has previously been developed. The vaccinated macaques showed reduced viral loads, but failed to contain SIVmac239 replication. In this study, macaques that showed partial control of SIV replication were followed up to see if or how they lost this control in the chronic phase. Two of them showed increased viral loads about 4 or 8 months after challenge and finally developed AIDS. Analysis of SIV-specific T-cell levels by detection of SIV-specific gamma interferon (IFN-gamma) production revealed that these two macaques maintained SIV-specific CD8(+) T cells, even after loss of control, but lost SIV-specific CD4(+) T cells when plasma viral loads increased. The remaining macaque kept viral loads at low levels and maintained SIV-specific CD4(+) T cells, as well as CD8(+) T cells, for more than 3 years. Additional analysis using macaques vaccinated with a Gag-expressing Sendai virus vector also found loss of viraemia control, with loss of SIV-specific CD4(+) T cells in the chronic phase of SIV infection. Thus, SIV-specific CD4(+) T cells that were able to produce IFN-gamma in response to SIV antigens were preserved by the vaccine-based partial control of primary SIV replication, but were lost with abrogation of control in the chronic phase.

Matano T, Kobayashi M, Igarashi H, Takeda A, Nakamura H, Kano M, Sugimoto C, Mori K, Iida A, Hirata T, Hasegawa M, Yuasa T, Miyazawa M, Takahashi Y, Yasunami M, Kimura A, O'Connor DH, Watkins DI, Nagai Y. · Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. · J Exp Med. · Pubmed #15210746 links to  free full text

Abstract: Recently, encouraging AIDS vaccine trials in macaques have implicated cytotoxic T lymphocytes (CTLs) in the control of the simian human immunodeficiency virus SHIV89.6P that induces acute CD4(+) T cell depletion. However, none of these vaccine regimens have been successful in the containment of replication of the pathogenic simian immunodeficiency viruses (SIVs) that induce chronic disease progression. Indeed, it has remained unclear if vaccine-induced CTL can control SIV replication. Here, we show evidence suggesting that vaccine-induced CTLs control SIVmac239 replication in rhesus macaques. Eight macaques vaccinated with DNA-prime/Gag-expressing Sendai virus vector boost were challenged intravenously with SIVmac239. Five of the vaccinees controlled viral replication and had undetectable plasma viremia after 5 wk of infection. CTLs from all of these five macaques rapidly selected for escape mutations in Gag, indicating that vaccine-induced CTLs successfully contained replication of the challenge virus. Interestingly, analysis of the escape variant selected in three vaccinees that share a major histocompatibility complex class I haplotype revealed that the escape variant virus was at a replicative disadvantage compared with SIVmac239. These findings suggested that the vaccine-induced CTLs had "crippled" the challenge virus. Our results indicate that vaccine induction of highly effective CTLs can result in the containment of replication of a highly pathogenic immunodeficiency virus.

Takeda A, Igarashi H, Nakamura H, Kano M, Iida A, Hirata T, Hasegawa M, Nagai Y, Matano T. · Department of Microbiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. · J Virol. · Pubmed #12915583 links to  free full text

Abstract: We previously demonstrated the excellent protective efficacy of DNA priming followed by Gag-expressing Sendai virus (SeV) boosting (DNA prime/SeV-Gag boost vaccine) against a pathogenic simian-human immunodeficiency virus (SHIV89.6PD) infection in macaques. Here we show that we established a practical, safer AIDS vaccine protocol, a single DNA priming followed by a single booster with a recently developed replication-defective F deletion SeV-expressing Gag, and show its protective efficacy against SHIV89.6PD infections.

Matano T, Kano M, Takeda A, Nakamura H, Nomura N, Furuta Y, Shioda T, Nagai Y. · Department of Microbiology, Graduate School of Medicine, The University of Tokyo, Japan. · AIDS. · Pubmed #12799562 No free full text.

This publication has no abstract.

Kano M, Matano T, Nakamura H, Takeda A, Kato A, Ariyoshi K, Mori K, Sata T, Nagai Y. · No affiliation provided · AIDS. · Pubmed #10894297 No free full text.

This publication has no abstract.