Highly conserved epitope domain in major core protein p24 is structurally similar among human, simian and feline immunodeficiency viruses

Matsuo, Kazuhiro; Nishino, Yoshinori; Kimura, Takeshi; Yamaguchi, Ryuji; Yamazaki, Akihiro; Mikami, Takeshi; Ikuta, Kazuyoshi

doi:10.1099/0022-1317-73-9-2445

Cited by 29 publications

(15 citation statements)

References 29 publications

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“…These observations indicate that the CA cross-reactivity does not map to linear peptide sequences encompassing the carboxylterminal segments of the CA protein, but most likely is correlated with non-linear or conformational determinants in this portion of the protein molecule. In contrast to the findings described above, previous studies using MAbs suggested that the M H R constitutes a linear group-specific determinant for primate immunodeficiency viruses (Niedrig et al, 1991;Matsuo et al, 1992). To investigate whether our inability to identify a linear cross-reactive determinant within the EIAV CA reflects differences in cross-reactivity between diverse lentiviruses or species-specific differences in specificity of antibody responses, we examined MAbs specific for the M H R regions of EIAV, HIV-2 and simian immunodeficiency virus macaque strain (SIVmae) for their relative ability to recognize peptide homologues of the M H R region of primate lentiviruses (HIV-1, SIVtyo, SIV ...... ) and non-primate lentiviruses (EIAV and FIV) by ELISA (Fig.…”

contrasting

confidence: 51%

“…Nevertheless, for the primate immunodeficiency viruses, including HIV-2, HIV-1, SIVma o and SIV~gm, the M H R segment within the carboxyl-terminal domain of their respective CA proteins has been established as a cross-reactive site as previously suggested (Niedrig et al, 1991;Matsuo et al, 1992). Studying the cross-reactivity between distinct members of the lentivirus subgroup, such as EIAV and HIV, we could not identify the site of cross-reactivity by using a panel of synthetic peptides, suggesting that cross-reactive antibodies are directed towards non-linear sites in the EIAV CA protein.…”

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confidence: 99%

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Equine infectious anaemia

2006

Veterinary Record

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In this study we used immune sera from equine infectious anaemia virus (EIAV)-infected horses which uniquely display broad reactivity with different lentivirus capsid proteins (CA) to characterize the cross-reactive determinants of lentivirus CA proteins. In particular, the role of the major homology region (MHR) of lentivirus CA proteins in this serological cross-reactivity was evaluated using both equine immune serum and murine monoclonal antibodies (MAbs) directed against the MHR segment of different lentiviruses. The results of our studies indicate that about 80 % of sera from long-term experimentally infected ponies or naturally infected horses react with human immunodeficiency virus type 1 CA in Western immunoblot assays. In addition, the cross-reactive determinants on the EIAV CA were localized within the immunodominant carboxyl terminus of the protein (residues 277 to 367). However, the crossreactive determinants recognized by the equine sera do not appear to correlate with linear peptides from the carboxyl terminus of the EIAV CA, including the MHR. These results suggest cross-reactivity between more distant lentiviruses is associated with non-linear determinants. In contrast, MHR-specific MAbs did react with linear peptides by ELISA and distinguished the primate lentiviruses from EIAV and feline immunodeficiency virus. These data support the concept of a highly conserved structural and antigenic organization among the CA proteins of lentiviruses from different species.

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confidence: 51%

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confidence: 99%

Equine infectious anaemia

2006

Veterinary Record

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“…Methods for virus detection, culturing the recombinant clones, and Western blotting of cell lysate were performed as previously described (15,23,24,26,41). The anti-SIV Gag monoclonal antibody (MAb) IB6 was kindly supplied by T. Sata, Department of Pathology, NIID, and by K. Ikuta, Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan (21). Primers used for PCR amplification were synthesized according to published sequences (15) and were designed to avoid destruction of any open reading frames.…”

Section: Methodsmentioning

confidence: 99%

Intravenous Inoculation of Replication-DeficientRecombinant Vaccinia Virus DIs Expressing Simian ImmunodeficiencyVirus Gag Controls Highly Pathogenic Simian-HumanImmunodeficiency Virus inMonkeys

Izumi

Ami²,

Matsuo

et al. 2003

J Virol

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To be effective, a vaccine against human immunodeficiency virus type 1 (HIV-1) must induce virus-specific T-cell responses and it must be safe for use in humans. To address these issues, we developed a recombinant vaccinia virus DIs vaccine (rDIsSIVGag), which is nonreplicative in mammalian cells and expresses the full-length gag gene of simian immunodeficiency virus (SIV). Intravenous inoculation of 10 6 PFU of rDIsSIVGag in cynomologus macaques induced significant levels of gamma interferon (IFN-␥) spot-forming cells (SFC) specific for SIV Gag. Antigen-specific lymphocyte proliferative responses were also induced and were temporally associated with the peak of IFN-␥ SFC activity in each macaque. In contrast, macaques immunized with a vector control (rDIsLacZ) showed no significant induction of antigen-specific immune responses. After challenge with a highly pathogenic simian-human immunodeficiency virus (SHIV), CD4؉ T lymphocytes were maintained in the peripheral blood and lymphoid tissues of the immunized macaques. The viral set point in plasma was also reduced in these animals, which may be related to the enhancement of virus-specific intracellular IFN-␥ ؉ CD8 ؉ cell numbers and increased antibody titers after SHIV challenge. These results demonstrate that recombinant DIs has potential for use as an HIV/AIDS vaccine.

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“…Each virion preparation was purified by sucrose density ultracentrifugation and stored at Ϫ120°C. The expression of a 55-kDa protein corresponding to SIV Gag was confirmed by Western blotting with extracts from CEF infected with rDIsSIVgag/pol and anti-SIV Gag-specific monoclonal antibodies (IB6 or V10) (35).…”

Section: Animalsmentioning

confidence: 99%

A Consecutive Priming-Boosting Vaccination of Mice with Simian Immunodeficiency Virus (SIV)gag/polDNA and Recombinant Vaccinia Virus Strain DIs Elicits Effective Anti-SIV Immunity

Someya

Xin

Matsuo

et al. 2004

J Virol

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To evaluate immunity induced by a novel DNA prime-boost regimen, we constructed a DNA plasmid encoding the gag and pol genes from simian immunodeficiency virus (SIV) (SIVgag/pol DNA), in addition to a replication-deficient vaccinia virus strain DIs recombinant expressing SIV gag and pol genes (rDIsSIVgag/pol). In mice, priming with SIVgag/pol DNA, followed by rDIsSIVgag/pol induced an SIV-specific lymphoproliferative response that was mediated by a CD4؉ -T-lymphocyte subset. Immunization with either vaccine alone was insufficient to induce high levels of proliferation or Th1 responses in the animals. The prime-boost regimen also induced SIV Gag-specific cellular responses based on gamma interferon secretion, as well as cytotoxic-T-lymphocyte responses. Thus, the regimen of DNA priming and recombinant DIs boosting induced Th1-type cell-mediated immunity, which was associated with resistance to viral challenge with wild-type vaccinia virus expressing SIVgag/pol, suggesting that this new regimen may hold promise as a safe and effective vaccine against human immunodeficiency virus type 1.

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Highly conserved epitope domain in major core protein p24 is structurally similar among human, simian and feline immunodeficiency viruses

Cited by 29 publications

References 29 publications

Equine infectious anaemia

Equine infectious anaemia

Intravenous Inoculation of Replication-DeficientRecombinant Vaccinia Virus DIs Expressing Simian ImmunodeficiencyVirus Gag Controls Highly Pathogenic Simian-HumanImmunodeficiency Virus inMonkeys

A Consecutive Priming-Boosting Vaccination of Mice with Simian Immunodeficiency Virus (SIV)gag/polDNA and Recombinant Vaccinia Virus Strain DIs Elicits Effective Anti-SIV Immunity

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