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1 International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
2 Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
3 Department of Immunology, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan
4 Department of Molecular Pathogenesis, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kandasurugadai, Chiyoda-ku, Tokyo 101-0062, Japan
5 AIDS Research Center, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan
6 Tsukuba Primate Research Center, National Institute of Biomedical Innovation, 1 Hachimandai, Tsukuba, Ibaraki 305-0843, Japan
Correspondence
Tetsuro Matano
matano{at}m.u-tokyo.ac.jp
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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; Koup et al., 1994; Matano et al., 1998; Ogg et al., 1998; Jin et al., 1999; Schmitz et al., 1999; McMichael & Hanke, 2003; Goulder & Watkins, 2004). In a model of X4-tropic simian/human immunodeficiency virus (SHIV) 89.6P or 89.6PD infection (Reimann et al., 1996; Lu et al., 1998), which causes rapid CD4+ T-cell depletion leading to an acute crash of the host immune system in macaques, several pre-clinical trials of prophylactic AIDS vaccines have successfully shown that efficient CTL induction results in control of virus replication and prevention of acute AIDS progression (Barouch et al., 2000; Amara et al., 2001; Matano et al., 2001; Rose et al., 2001; Shiver et al., 2002; Willey et al., 2003). In contrast, most trials of such CTL-based vaccines have failed to show viraemia control in models of R5-tropic simian immunodeficiency virus (SIV) infection, which result in chronic disease progression in macaques as in human immunodeficiency virus type 1 (HIV-1) infection in humans (Feinberg & Moore, 2002; Horton et al., 2002; Casimiro et al., 2005). Comparison of vaccine effects on virus replication in the acute AIDS model of X4-tropic SHIV infection with those in the chronic model of R5-tropic SIV infection could contribute to the development of an effective prophylactic AIDS vaccine for control of persistent HIV-1 replication.
We have developed a prophylactic AIDS vaccine using a DNA-prime/Gag-expressing Sendai virus (SeV-Gag) vector boost system and have shown its potential for efficient induction of Gag-specific CTL responses in Burmese rhesus macaques (Kano et al., 2002; Matano et al., 2004). In pre-clinical trials in an acute AIDS model, all of the macaques vaccinated with the DNA-prime/SeV-Gag vector boost system controlled SHIV89.6PD replication after challenge (Matano et al., 2001; Takeda et al., 2003). Furthermore, a trial of the prophylactic DNA-prime/SeV-Gag boost vaccine showed control of SIVmac239 replication leading to undetectable set-point plasma viraemia in five out of eight vaccinees (referred to as SIV controllers), despite failure of virus control in the other three vaccinees (referred to as SIV non-controllers) (Matano et al., 2004). All of the SIV controllers showed rapid selection of viral CTL escape mutations, and analysis of the rhesus major histocompatibility complex (MHC) suggested that SIV control was associated with particular MHC haplotypes such as 90-120-Ia and ‘elite’ CTL responses specific for the MHC-restricted epitopes (Matano et al., 2004). Follow up of these SIV controllers revealed that some lost this control with accumulation of multiple viral CTL escape mutations (Kawada et al., 2006).
In this study, we followed up, for more than 2 years, rhesus macaques that showed vaccine-based control of SHIV89.6PD replication (referred to as SHIV controllers). Our results showed durable and stable virus control in the SHIV controllers, contrasting with our previous observation in SIV controllers.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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; Takeda et al., 2003) were analysed in this study. The animal list is shown in Table 1. All were Burmese rhesus macaques (Macaca mulatta) and were maintained in accordance with the Guidelines for Laboratory Animals of the National Institute of Infectious Diseases and National Institute of Biomedical Innovation.
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; Takeda et al., 2003). Of the ten macaques in the SHIV89.6PD challenge experiment, three (R00-013, R00-015 and R00-017) received a single intranasal immunization with replication-competent SeV expressing SIVmac239 Gag (SeV-Gag) (Kato et al., 1996; Kano et al., 2002) before challenge. Two (R99-007 and R99-011) received four immunizations with FMSIV DNA followed by a single SeV-Gag booster. The FMSIV plasmid DNA used in this DNA vaccination protocol (DNAv1) was constructed from an SHIVMD14YE molecular clone DNA (Shibata et al., 1997a) by replacing SHIV env with ecotropic Friend murine leukemia virus (FMLV) env (Matano et al., 2000). Two macaques (R99-005 and R99-012) received four immunizations with both the FMSIV DNA and an FMLV receptor (mCAT1)-expression plasmid DNA (Albritton et al., 1989) followed by a single SeV-Gag booster. This second DNA vaccination protocol (DNAv2) has been shown to elicit efficient CTL responses by confined mCAT1-dependent FMSIV replication (Matano et al., 2000). Three macaques (R00-020, R00-023 and R00-024) received a single immunization with CMV-SHIVdEN DNA (DNAv3) followed by a single boost with an F-deleted replication-defective SeV-Gag (F–SeV-Gag) (Li et al., 2000; Takeda et al., 2003). This CMV-SHIVdEN plasmid DNA was constructed from an env- and nef-deleted SHIVMD14YE molecular clone DNA and had the genes encoding SIVmac239 Gag, Pol, Vif and Vpx, SIVmac239/HIV-1DH12 chimeric Vpr and HIV-1DH12 Tat and Rev (Matano et al., 2004). All ten animals were challenged intravenously with 10 TCID50 SHIV89.6PD (Lu et al., 1998) approximately 3 months after the last immunization. Four unvaccinated animals were also challenged with SHIV89.6PD and all failed to control virus replication.
Quantification of plasma viral loads.
Plasma RNA was extracted using a High Pure Viral RNA kit (Roche Diagnostics). Serial fivefold dilutions of RNA samples were amplified in quadruplicate by nested RT-PCR using SIV gag-specific primers to determine the end point. Plasma SIV RNA levels were calculated according to the Reed–Muench method, as described previously (Matano et al., 2004). The lower limit of detection was approximately 4x102 RNA copies ml–1.
Sequencing of viral and proviral genomes.
Plasma RNA was extracted as described above and genomic DNA was extracted from peripheral blood mononuclear cells (PBMCs) using a DNeasy kit (Qiagen). A fragment corresponding to nt 458–2185 (containing the entire gag region) in the SHIV89.6P genome (GenBank accession no. U89134
[GenBank]
) was amplified from plasma RNA by nested RT-PCR. Alternatively, fragments corresponding to nt 458–2185, 2019–3187, 3038–4197, 4056–5213, 5079–6250, 6065–7225, 7047–8176 and 7998–9172 in the SHIV89.6P genome were amplified from proviral DNA by nested PCR. The PCR products were sequenced using dye terminator chemistry and an automated DNA sequencer (Applied Biosystems). Alternatively, PCR products were subcloned into plasmids using a TOPO cloning system (Invitrogen) and sequenced.
Measurement of virus-specific T-cell levels by intracellular cytokine staining.
We measured virus-specific T-cell levels by flow cytometric analysis of gamma interferon (IFN-
) induction after specific stimulation, as described previously (Matano et al., 2001, 2004). In brief, PBMCs were co-cultured with autologous herpesvirus papio-immortalized B lymphoblastoid cell lines (B-LCLs) infected with a vesicular stomatitis virus G (VSV-G)-pseudotyped SIVGP1 for SHIV-specific stimulation. The pseudotyped virus was obtained by co-transfection of COS-1 cells with a VSV-G-expression plasmid and the SIVGP1 DNA, an env- and nef-deleted SHIV molecular clone DNA, constructed by removing the whole FMLV env region from the FMSIV DNA. Alternatively, PBMCs were co-cultured with B-LCLs pulsed with peptide mixture (final concentration of each peptide, 0.5–2 µM) for peptide-specific stimulation. A panel of 117 overlapping peptides (15–17 aa in length and overlapping by 10–12 aa) spanning the entire SIVmac239 Gag sequence (Sigma-Aldrich) were divided into ten pools (1–10) each consisting of 11 or 12 peptides. Intracellular IFN- staining was performed using a Cytofix/Cytoperm kit (Becton Dickinson) according to the manufacturer's instructions. Fluorescein isothiocyanate-conjugated anti-human CD4, peridinin chlorophyll protein-conjugated anti-human CD8, allophycocyanin-conjugated anti-human CD3 and phycoerythrin-conjugated anti-human IFN- antibodies (Becton Dickinson) were used. Specific T-cell levels were calculated by subtracting non-specific IFN-+ T-cell frequencies from those after SHIV-specific or peptide-specific stimulation. Specific T-cell levels of <100 cells per 106 PBMCs were considered negative.
Measurement of virus-specific neutralizing titres.
We performed a neutralizing assay for the measurement of virus-specific neutralizing titres in plasma, as described previously (Shibata et al., 1997b). Serial twofold dilutions of heat-inactivated plasma were prepared in duplicate and mixed with 10 TCID50 SHIV89.6PD. In each mixture, 5 µl diluted plasma was incubated with 5 µl virus. After a 45 min incubation at room temperature, each 10 µl mixture was added to 5x104 MT4 cells in a well of a 96-well plate. After 12 days of culture, supernatants were harvested. Progeny virus production in the supernatants was examined by ELISA for detection of SIV p27 core antigen (Beckman Coulter) to determine the 100 % neutralizing end point. The lower limit of detection was a titre of 1 : 2.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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; Takeda et al., 2003), three animals received a single SeV-Gag vaccination alone, whilst the remaining seven animals were immunized with a DNA-prime/SeV-Gag boost vaccine before challenge (Table 1
). The seven animals vaccinated with the prime–boost vaccine (R99-007, R99-011, R99-005, R99-012, R00-020, R00-023 and R00-024) were able to control virus replication, with undetectable set-point plasma viraemia. Two (R00-015 and R00-017) of the three animals vaccinated with SeV-Gag alone were also able to control viraemia, but the remaining one (R00-013) failed to control virus replication and showed acute CD4+ T-cell depletion. This animal R00-013 developed AIDS and was euthanized at week 53.
In the present study, we determined the MHC class I (MHC I) haplotypes of the SHIV controllers and their viral genome sequences at around 1 or 2 months after challenge to examine whether SHIV controllers showed rapid selection of CTL escape mutations as observed in our previous analysis, in particular MHC-associated control of SIV replication. Importantly, control of SHIV89.6PD replication was observed in vaccinees with diverse MHC haplotypes (Table 1). Analysis of the proviral gag region in PBMCs at around week 8 showed a predominance of the wild-type sequence in all nine SHIV controllers (Table 2). Sequencing of the plasma viral gag region at week 5 in three of them confirmed the lack of dominant mutations (Table 2). Thus, the SHIV controllers controlled virus replication without rapid selection of CTL escape mutations.
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). All eight SHIV controllers maintained control of virus replication for more than 2 years (Fig. 1). Viraemia was undetectable and peripheral CD4+ T-cell counts were maintained during the observation period. Analysis of the gag region in PBMC-derived proviral DNA revealed that the wild-type sequence was still dominant around 1 year after challenge in all eight (Table 1). Additionally, we succeeded in amplifying almost the entire coding region of the proviral genomes from three (R00-015, R00-017 and R00-023) of the eight controllers at around 1 year for sequencing and found no dominant non-synonymous mutations except for one leading to a change in aa 401 in Env in macaque R00-015, suggesting inefficient virus replication during the period of SHIV control.
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). Thus, none of the SHIV controllers showed a significant increase in SHIV-specific T-cell levels, suggesting stable virus control without any sign of a virus replication burst in the chronic phase.
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). A similar pattern of disappearance (pool 10-specific), appearance (pool 3- and 9-specific) and maintenance (pool 6- and 8-specific) of CD8+ T-cell responses during the period of SHIV control was also observed in macaque R00-017 (Fig. 4). These results suggested that SHIV89.6PD replication was not completely contained in these macaques.
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). In contrast to such efficient induction of neutralizing antibodies in SHIV controllers, macaque R00-013, which failed to control SHIV replication, showed no neutralizing antibody induction after challenge.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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; Sadagopal et al., 2005). Whilst these vaccine regimens utilized Env as an immunogen (Amara et al., 2002), we have developed vaccine regimens not targeting Env and demonstrated their efficacies leading to control of SHIV89.6PD replication in rhesus macaques (Matano et al., 2001; Takeda et al., 2003). In the present study, we followed up these SHIV controllers for more than 2 years after challenge. All maintained this control with undetectable plasma viraemia, indicating that efficient CTL induction by a prophylactic AIDS vaccine not targeting Env can result in sustained control of virus replication and protection from AIDS progression in a model of X4-tropic SHIV infection.
X4-tropic SHIV and R5-tropic SIV target different CD4+ T-cell subsets in rhesus macaques and this difference has been indicated as resulting in their divergent clinical courses (Nishimura et al., 2004). Indeed, it has been shown that X4-tropic SHIV targets CXCR4+ naive CD4+ T cells for depletion, whereas R5-tropic SIV, like HIV-1 infection in humans, eliminates CCR5+ effector memory CD4+ T cells in rhesus macaques during the acute phase of infection (Picker et al., 2004; Li et al., 2005; Mattapallil et al., 2005; Nishimura et al., 2005; Picker & Watkins, 2005). In the latter chronic AIDS model, several CTL vaccine trials have recently shown partial reductions in viral loads with amelioration of acute memory CD4+ T-cell loss, but this partial control was transient and unstable (Letvin et al., 2006; Mattapallil et al., 2006; Wilson et al., 2006). In our previous study (Matano et al., 2004), SIV control was observed consistently in the three vaccinees possessing MHC I haplotype 90-120-Ia, but this control was not stable and two of them lost viraemia control around week 60 after challenge. In the present study showing long-term, stable SHIV control, we found several differences between X4-tropic SHIV controllers and R5-tropic SIV controllers.
First, patterns of de novo neutralizing antibody induction were completely different between the two. Although the vaccine regimens did not target Env, SHIV-specific neutralizing antibodies appeared rapidly and became detectable by week 6 post-challenge in the SHIV controllers, whereas no neutralizing antibody induction was observed in the SHIV non-controllers. Thus, SHIV-specific neutralizing antibodies can be rapidly induced if animals are protected by CTLs from complete CD4+ T-cell depletion in the acute phase and may be involved in viraemia control at the set point and after (Rasmussen et al., 2002). In contrast, SIV-specific neutralizing antibody induction in the SIV controllers was poor and less efficient than the SIV non-controllers (data not shown), indicating that neutralizing antibody responses are not involved in SIV control.
Secondly, all of the SIV controllers showed rapid selection of viral CTL escape mutations, whereas this sign of particular CTL pressure (Borrow et al., 1997; Goulder et al., 1997; Price et al., 1997; Goulder & Watkins, 2004; Matano et al., 2004) was not observed in any of the SHIV controllers. Additionally, SIV control was associated with some MHC haplotypes such as 90-120-Ia, but SHIV control was observed in vaccinees with diverse MHC haplotypes. Indeed, none of the SHIV controllers had the MHC haplotype 90-120-Ia associated with SIV control. Although the involvement of functional virus-specific CD4+ T-cell responses remains unclear, these results support the notion that multiple target-specific CTL effectors are involved in SHIV control, whereas relatively limited regions of viral antigens are targeted by effectors responsible for SIV control.
All of the SHIV controllers maintained virus control for more than 2 years. Sequencing of viral genomes revealed a predominance of the wild-type sequence around 1 year after SHIV89.6PD challenge, and analysis of SHIV-specific T-cell levels showed no signs of a burst of virus replication during the chronic phase. These results indicated stable virus control in the chronic phase in the SHIV controllers. Interestingly, however, analysis of Gag peptide-specific CD8+ T-cell responses in some of the SHIV controllers showed a shift of targeting epitopes during the period of virus control, suggesting that virus replication was inefficient but not completely contained, even in the SHIV controllers.
In summary, the present study revealed several differences in vaccine-based virus control in a model of X4-tropic SHIV compared with R5-tropic SIV infections. Our results suggest that, compared with virus control with limited effectors in SIV controllers, the control of X4-tropic SHIV89.6PD replication may be maintained more stably in the presence of multiple functional immune effectors.
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ACKNOWLEDGEMENTS |
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Received 12 August 2006;
accepted 4 October 2006.
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