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Journal of Virology, September 2001, p. 8681-8689, Vol. 75, No. 18
Department of Epidemiology and International
Health, School of Public Health,1 and
Department of Medicine, School of Medicine, University of
Alabama at Birmingham, Birmingham, Alabama
352942; Aventis Pasteur, Marcy
l'Etoile, France3; and Duke University
Medical Center, Durham, North Carolina 277104
Received 4 January 2001/Accepted 23 June 2001
Carriers of certain human leukocyte antigen class I alleles show
favorable prognosis of human immunodeficiency virus type 1 (HIV-1)
infection, presumably due to effective CD8+ cytotoxic
T-lymphocyte responses, but close relationships between class I
variants mediating such responses to natural and to vaccine HIV-1
antigen have not been established. During 6 to 30 months of
administration and follow-up in trials of ALVAC-HIV recombinant canarypox vaccines, cells from 42% of 291 HIV-1-negative
vaccinated subjects typed at class I loci responded to an HIV-1 protein
in a lytic bulk CD8+ cytotoxic T-lymphocyte assay. By 2 weeks after the second dose, higher proportions of vaccinees carrying
one of two alleles consistently associated with slower progression of
natural HIV-1 infection reacted at least once: B*27 carriers reacted
to Gag (64%; odds ratio [OR] = 10.3, P = 0.001) and
Env (36%; OR = 4.6, P = 0.04), and B*57 carriers
reacted to Env (44%; OR = 6.6, P < 0.05). By 2 weeks after the third or fourth dose, B*27 carriers had responded (two or more reactions) to Gag (33%; OR = 4.4, P < 0.05) and B*57 carriers had responded to both Gag (39%; OR = 5.3, P = 0.013) and Env (39%; OR = 9.5, P = 0.002). Homozygosity at class I loci, although
conferring an unfavorable prognosis following natural infection, showed
no such disadvantage for vaccine response. Individual class I alleles
have not previously demonstrated such clear and consistent relationship
with both the clinical course of an infection and cellular immunity to
a vaccine against the infectious agent. This proof of principle that
class I an alleles modulate both processes has implications for
development of HIV-1 and presumably other vaccines.
Cellular immune response systems,
including those encoded by genes in the human leukocyte antigen (HLA)
complex, influence the wide variation in outcome of human
immunodeficiency virus type 1 (HIV-1) infection (8, 22, 26, 29,
30, 37, 52). Certain class I alleles have been consistently
associated with slower (B*27, B*57) or faster (B*35, B*08)
disease progression (8, 22, 26, 29, 30, 37), and
diminished diversity (i.e., homozygosity) at class I loci confers
substantial risk of accelerated infection (8, 30, 52). The
mechanisms by which class I alleles differentially bind peptides,
restrict the generation of CD8+ cytotoxic T lymphocytes
(CTLs), and govern the clinical response to HIV-1 are under intense
investigation (14b). Monkeys deficient in CD8+
T cells lack efficient control of viral replication and produce a
strong CTL response to an effective vaccine (2, 24, 41, 50). In HIV-1-positive humans, CTLs presumably destroy infected cells (7, 12, 18, 33, 34, 46) by targeting HIV-1 peptides
bound to surface-expressed class I molecules, establishing a dynamic
equilibrium between a continuously mutating virus population and
host-specific engagement with evolving virus.
In HIV-1-exposed but persistently seronegative individuals, the
importance of observed CTL responses in protecting against infection is
less clear (45, 49). The collective evidence that control
of initial viral acquisition is regulated by specific HLA class I
variants is also less convincing than for disease progression (5,
28, 36, 47).
Mechanisms of induced immunity to infection and natural immunity to
disease progression almost surely differ. Ample CTL reactivity may be
essential for protection by an HIV vaccine. Vaccine-generated CTL
response mediates protection against simian immunodeficiency virus
(1, 25, 51), but CTL-based efficacy has not yet been demonstrated for any human vaccine (43). Vaccines that
control established infection may be less protective against initial
virus acquisition.
Restriction of responses by polymorphic class I and/or class II HLA
gene products has been suggested with vaccines against other viral
pathogens (4, 21, 35), and early trials of HIV-vaccinia
virus (16) hinted at such regulation. The unequivocal influence of class I polymorphism on the natural history of HIV infection compels evaluation of how this genetic variability may modulate HIV-1 vaccine response. Here we have observed HIV-1-specific CD8+ CTLs in significantly higher proportions of
HIV-1-uninfected HIV vaccine recipients (3, 10, 13, 14, 39,
43) who carried class I alleles most consistently recognized as
advantageous in infected individuals. To our knowledge, such a direct
relationship has not previously been documented in humans for any
infectious agent.
(This work was presented in part at the 7th Conference on Retroviruses
and Opportunistic Infections, 29 January to 3 February 2000, San
Francisco, Calif.)
Subjects.
In compliance with federal guidelines and
institutional review board policies, 291 volunteers received vaccine in
four National Institute of Allergy and Infectious Diseases-sponsored
AIDS Vaccine Evaluation Group (AVEG) randomized, double-blind trials
summarized in Table 1 and below (3,
13, 14; L. Corey et al., Abstr. 12th Int. Conf. AIDS, abstr.
636, 1998; T. Evans et al., Abstr. 12th Int. Conf. AIDS, abstr. 277, 1998). The AVEG data coordinating center (The EMMES Corp, Potomac, Md.)
provided epidemiologic, clinical, and laboratory data at enrollment and
subsequent trial protocol and adherence data.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.18.8681-8689.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Polymorphisms in HLA Class I Genes Associated with both Favorable
Prognosis of Human Immunodeficiency Virus (HIV) Type 1 Infection and
Positive Cytotoxic T-Lymphocyte Responses to ALVAC-HIV Recombinant
Canarypox Vaccines
ABSTRACT
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
INTRODUCTION
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
MATERIALS AND METHODS
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
TABLE 1.
Schedule of vaccine administration and assays for CTL
response
Vaccine constructs and administration schedule. Protocols 022, 022A, and 029 (3, 13; L. Corey, unpublished data; T. Evans, unpublished data) tested the recombinant canarypox ALVAC-HIV vCP205 vector (Aventis Pasteur, Inc., Marcy l'Etoile, France) encoding HIV-1 proteins gp120MN, the membrane-spanning domain of gp41LAI, GagLAI, and proteaseLAI. Protocol 026 utilized the similar ALVAC-HIV vCP300 vector (Aventis Pasteur, Inc.) encoding the HIV-1 proteins found in vCP205 plus CTL epitope-rich regions from nefBRU and polLAI. Certain individuals were given boosters of recombinant HIV-1 envelope glycoprotein subunit rgp120SF2 (Chiron Vaccines, Inc., Emeryville, Calif.). Protocols 022, 022A, and 026 scheduled three or four immunizations within the first 6 months with vCP205 (protocols 022 and 022A) or vCP300 (protocol 026) alone or in combination with rgp120SF2 (Table 1). Protocol 029 scheduled four immunizations within the first 21 days with vCP205 and a booster at days 28 and 84 with rgp120SF2.
CTL assays.
Schedules for the lytic assay for four viral
proteins (Gag, Pol, Env, and Nef) according to standard AVEG methods
(13, 14, 39) differed by protocol (Table 1). Individual
recipient B lymphoblastoid cell lines (BLCLs) served as targets. We
stimulated peripheral blood mononuclear cells (PBMCs) with recombinant
HIV-1-vaccinia virus-infected autologous PBMCs cultured in RPMI 1640 (GIBCO BRL, Grand Island, N.Y.) with human antisera and interleukin 7 (R&D Systems, Minneapolis, Minn.). On day 7, we incubated cells with interleukin 2 (Amgen, Thousand Oaks, Calif.). On day 14 we assayed cytotoxicity using Na2CrO4-labeled BLCLs
infected with vaccinia virus control (vP1170) or vaccinia virus
recombinants expressing HIV-1 MN gp160 (vP1174), HIV-1 HXB2 Gag (vDK1),
or HIV-1 GagLAI (vP1287). Vaccinia virus vP1288-IIIB or
vP1218-MN was used for Pol or Nef BLCL targets, respectively.
Virogenetics (Troy, N.Y.) provided all vectors except vDK1 (D. Kuritzkes, University of Colorado Health Sciences Center). Inclusion of
unlabeled infected targets in excess reduced vaccinia virus background.
Generally we tested effector-to-target ratios of 25:1 and 50:1 in
triplicate with 5,000 targets/well. HIV-1-specific lysis of 
10% over
controls defined a positive result. A >50% loss of HIV-1-specific
activity following selective depletion by anti-CD8-bearing magnetic
beads (Dynabeads; Dynal, Great Neck, N.Y.) represented
CD8+-cell-specific lysis. Positivity required 10%
specific lysis for at least two separate effector-to-target ratios.
HLA typing. We identified HLA-A, -B, and -C alleles in DNA extracted from banked PBMCs with the QIAmp DNA mini-kit (Qiagen Inc., Valencia, Calif.). Typing was performed with sequence-based typing and sequence-specific primer (SSP) methods, which resolved most of the ambiguous and apparent homozygous alleles. For nested sequence-based typing, we performed a primary amplification encompassing exons 2 and 3 of each locus (9, 53). Sequencing of their secondary amplification products employed either the AutoLoad kit or the Sequenase v.2 kit on an ALFexpress automated DNA sequencer (Amersham-Pharmacia Biotech, Inc., Piscataway, N.J.) or M-280 streptavidin Dynabeads (Dynal Inc., Lake Success, N.Y.). HLA SequiTyper v.2.0 software (Pharmacia) assigned alleles. For SSP typing, class I Unitray ABC SSP kits (Pel-Freez Clinical Systems, Brown Deer, Wis.) were used.
The typing scheme achieved resolution to four digits at the A and B loci and to two or four digits at the C locus in the current HLA nomenclature (6). Full resolution was achieved for all but 3% of A and B alleles, which failed to amplify in three attempts or remained ambiguous after both techniques were applied. We defined homozygosity as identity at the four-digit level and assigned Bw4 specificity according to standard nomenclature (38).Statistical analysis. We defined a meaningful CTL response using two different criteria, either one or two positive measurements during the study interval, and calculated proportions of individuals with a CTL response using each criterion. For successive intervals following vaccination responses were examined separately for each viral protein (Gag, Pol, Env, and Nef). Data on "Any," Gag, and Env responses are presented; the sparseness of Pol and Nef data precluded meaningful analysis. "Any" refers to aggregate analysis of one or more proteins in any combination. Analyses requiring presence of both Gag and Env or requiring exclusively Gag or Env did not add enough information about differential HLA effects to present separately.
Analyses for protocols 022, 022A, and 026 focused on cumulative CTL response during three intervals: (i) from initial dose to 2 weeks after the second dose (criterion = one positive measurement), (ii) from initial dose to 2 weeks after the third or fourth dose (criterion = two positives), and (iii) from 2 to 76 weeks after last dose (criterion = two positives). These corresponded, respectively, to the 6-week, 26-week, and 2.5-year intervals from first inoculation. For protocol 029 we considered CTL measurements by 2 weeks after the fourth consecutive weekly dose (6 weeks after the first inoculation) along with the other three protocols at both 6 and 26 weeks. However, because protocol 029 subjects had also received 4 doses by week 6, analysis of their CTL measurements began with the post-third- or -fourth-dose, 26-week interval. Results for CTLs during the 26-week interval (criterion = two positives) are presented in greater detail; cumulative effects during shorter and longer intervals were quite consistent with those shown. The four protocols differed in the scheduled numbers of CTL measurements for each individual (Table 1), but the number of CTL responses closely paralleled the number of measurements, i.e., measurement and response frequencies were closely proportional. We formally excluded this potential protocol bias. We also analyzed each putative association with an allele in the presence and again in the absence of any other that might have explained the finding. Although typing resolved alleles to four digits in nearly all cases, the majority represented the principal allele in the two-digit serogroup. Relatively few four-digit alleles occurred at high enough frequency for separate statistical analysis, but when possible, we searched for such separate effects. Since no effect seen using aggregated two-digit allele designation was better captured by four-digit stratification, we have presented only data on aggregated alleles. Differences in allele frequencies and CTL responses by age, gender, or race, by vaccine study site, or by protocol were not large enough to require adjustment. About half of protocol 022A participants were at somewhat higher risk of exposure to HIV-1 prior to vaccination and could have been selectively primed for a CTL response; however, there was a negligible difference in response between the subjects in the two risk categories, the HLA allele frequencies of the two groups were comparable, and differential exposure was not a factor in the HLA relationships. All significance testing was based on Fisher's exact test. We have reported unadjusted P values because this was not an exploratory search but a test of involvement of four HLA alleles for which there is ample a priori evidence.| |
RESULTS |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
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Study population characteristics and overall response.
Vaccine recipients consisted primarily of Caucasians (88%) and males
(68%); the mean (standard deviation) age was 34.3 (9.9), with a range
of 18 to 60 years. The distributions of class I allele and phenotype
frequencies in the Caucasian vaccinees resembled those in other
North American populations (Table 2). No
significant deviation from Hardy-Weinberg equilibrium was observed for
Caucasians or the small number of African-Americans. HLA phenotype
distributions and proportions of homozygotes at each locus were
comparable among the four protocols (data not shown).
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HLA-A alleles.
Compared with individuals carrying other A
alleles, a significantly higher proportion of A*32 carriers showed
CTL responses (Any, 35%; odds ratio [OR] = 5.1, P = 0.003; Env, 31%; OR = 6.6, P = 0.006) (Fig.
1). The
A*32 effect on response to Env was already apparent by 2 weeks after
the second dose as well (OR = 5.3, P < 0.05), and it
remained strong throughout the postvaccination period, even when
vaccinees with B*27 and B*57 were excluded (see below). A*32 has
been associated with relatively slow disease progression in two related
population studies (26, 30), and a trend toward protection
was seen in a small group of transfusion recipients with long-standing
infection (15). For A*0201, the most common allele and
one prominently featured in experimental protocols, during the interval
through the third or fourth dose, positive CTL responses occurred in
somewhat lower proportions (Any and Gag) than for other A*02 or other
A allele carriers (data not shown).
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HLA-B alleles.
Distributions of CTL responses in vaccine
recipients with B alleles relatively consistently associated elsewhere
(8, 11, 22, 23, 26, 27, 29, 30, 37, 40, 42, 52) with faster or slower HIV disease progression are summarized in Table 3. In both the post-second-dose and the
post-third- or -fourth-dose intervals, vaccine recipients carrying
B*27 or B*57, the two alleles most widely observed to retard
disease progression (11, 22, 30, 37, 40, 42), differed
significantly from those with other alleles in the cumulative
proportion showing CTL positivity (Fig. 1). Proportions of B*27 and
B*57 carrier vaccinees who responded to Any, Gag, and Env during the
second interval were 35, 33, and 18% and 26, 39, and 39%,
respectively. For B*27 the differences were clear during the earliest
interval for Any (OR = 5.4, P = 0.002), Gag
(OR = 10.3, P = 0.001), and Env (OR = 4.6, P = 0.04); big differences persisted through
the second interval for Any (OR = 5.5, P = 0.001)
and Gag (OR = 5.0, P = 0.01) but not for Env. The
Gag effect was also evident for the entire 2.5-year study period. For
B*57, a higher response frequency was seen early for Env (OR = 6.6, P = 0.018) and became stronger after the third or
fourth dose for Any (OR = 3.3, P = 0.043), Gag
(OR = 5.3, P = 0.013), and Env (OR = 9.5, P < 0.002). During this 26-week interval, the CTL
assay was positive at least once in 72% of B*57 carriers (OR = 7.9, P < 5 × 10
4). The effects of
these two individual alleles persisted in analyses excluding volunteers
with the B*27/B*57 genotype or other apparently protective alleles.
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HLA-C alleles. No C allele by itself appeared to be associated with significantly stronger or weaker CTL response. A significantly increased frequency of response in Cw*01 carriers (OR = 4.6, P = 0.005) (Fig. 1) was readily explained by its strong disequilbrium with B*27. Similarly, although the proportion of Cw*07-positive subjects who mounted a CTL response to Gag and Env was low (ORs = 0.3; P = 0.02 to 0.06), the effect of the allele could not be separated from that of a Cw*07-bearing haplotype (see below).
Haplotypes. None of the associations observed with apparent two-locus (A-C and B-C) haplotypes surpassed those of their component A or B alleles alone in magnitude. For the apparent three-locus haplotype A*02-Cw*07-B*07, during the second and third intervals, lower proportions of the haplotype carriers mounted CTL responses to both major proteins (ORs = 0.3 to 0.8, P = 0.08 to 0.10). For individual carriers of A*02, Cw*07, or B*07 alone, proportions with CTL responses were less diminished.
Homozygosity.
Identity of alleles at the A, B, or C locus to
the four-digit level did not reduce the cumulative proportion of
vaccinees showing a CTL response to Any, Gag, or Env in the 6-week, the 26-week, or the 2.5-year interval; the data are shown for the 26-week
interval (Table 4). The six vaccinees who
were homozygous at the C locus and who were positive for CTL against
Env at 6 weeks actually experienced a somewhat higher response
frequency, and two carried specific A or B markers shown to account for
that higher frequency. Allele identity at two loci (six to eight
subjects) and three loci (four subjects) was likewise not associated
with relative unresponsiveness.
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Effect of sexual exposure. Among volunteers in protocol 022A, low-risk sexual exposure was reported by 60 (50.8%) and higher-risk exposure was reported by 58 (49.2%). Those at higher risk showed no appreciable difference in early CTL response. Cumulatively through the post-third- or -fourth-dose interval, very similar proportions of the 20 to 28 low-risk participants and the 18 to 28 higher-risk participants had produced CTL responses to Any, Gag, or Env viral proteins. None of the class I relationships described here showed a meaningful change when adjusted for exposure level (data not shown).
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DISCUSSION |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
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By 26 weeks after at least three doses of canarypox-HIV vaccine, 9 to 13% of recipients had mounted a meaningful response, as indicated by two positive CD8+ CTL lytic assays against Gag, Env, Pol, or Nef. The proportions responding to Gag or Env were significantly higher among those carrying HLA-B*27 or -B*57, the two B alleles repeatedly associated (11, 22, 37, 40, 42) with a more benign course of natural HIV-1 infection. For B*57, the protection against disease progression has been persuasively documented not only in homosexual clade B virus-infected Caucasians (primarily B*5701) (22, 37, 42) but also in heterosexual clade A virus-infected Africans (primarily B*5703) (11). The favorable effect on CTL response for both alleles was apparent even after the second dose of vaccine (i.e., at 6 weeks) but was particularly strong among B*27 carriers for both Gag and Env at this earlier time point. Although this distinction with B*27 is based on small numbers, it invites speculation about whether that allele differs fundamentally in the breadth or specificity of its peptide binding repertoire (31) or to a rapid response (54).
Although a remarkable coincidence could explain these identical class I allele-specific associations with both vaccine response and outcome of natural infection, they more likely reflect the particular capacity of these HLA molecules to bind conserved HIV-1 peptides, transporting them to the cell surface or displaying them effectively to the T-cell receptor. For the two protective HLA-B alleles, dominant epitopes and other features favorable for CTL response have been well documented (17, 19, 31, 42), and predicted peptide binding motifs in clade B HIV-1 may be especially plentiful (44). Whatever the precise molecular explanation, the generalizability of the advantage for B*57 across race, clade, and mode of transmission and the consistency of that advantage for response to both natural and vaccine-formulated HIV-1 antigens warrant close investigation.
As for the two class alleles previously observed in conjunction with poorer prognosis, B*08 showed a lower CTL response to vaccine Gag and B*35 showed a lower response to Env in all three intervals. However, neither of these reductions in response was as striking as the augmentation associated with the protective alleles. If that pattern represents a discrepancy between natural and vaccine-induced responses, several explanations are possible. First, the B*08 association with rapid disease progression has not remained as consistent as for B*35 in recent analyses (R. A. Kaslow, unpublished data). Second, compared with Gag and Env antigens produced by naturally replicating, mutating HIV-1 isolates, cloned HIV-1 genes in the tested vaccines may have expressed peptide motifs relatively more favorable for binding to or presentation by B*08 or B*35. Third, in contrast to the uniform findings thus far for different subtypes of B*57, some B*35 allele subtypes appear to mediate effective responses, and the lack of observed overall effect on CTL may reflect the heterogeneous influence of more effective and less effective subtypes intermingled (14b, 20, 48). Fourth, assessment of alleles accompanying B*08 or B*35 disclosed no masking of effects of these two by others mediating better responses to HIV canarypox vaccine motifs; however, compensation at the level of specific CD8+ CTL responses is still possible. The contrast between response to naturally and artificially presented peptides in the context of B*35 deserves further evaluation.
A*32, an allele inconsistently predisposing to slower disease progression (15, 30), merits further examination in light of its association with increased frequency of CTL response; it seems more difficult to justify further attention to the more transient associations of alleles not previously recognized as determinants (e.g., B*1501 and B*4901). Conversely, certain alleles occasionally associated with unfavorable or favorable prognosis elsewhere (e.g., A*24) (8, 27, 30) did not show the predicted influence on CTL response. Nonspecific (i.e., bulk PBMC) response in the lytic assay and unstable estimation of ORs for less common alleles both here and in cohorts of infected subjects preclude any simple explanation for the discrepant impact of these class I alleles on natural and vaccine-induced responses.
No C-locus polymorphism showed a specific effect that was clearly independent of a similar or stronger effect from a B allele in linkage disequilibrium. Although certain associations of the C-locus or B-C haplotypes with rapid or slow HIV disease progression have been reported (8, 22, 30, 37), so far none of the effects of C alleles seem sufficiently consistent and independent of their linked B alleles to be regarded seriously in their own right.
In contrast to the clear negative effect of class I homozygosity on the course of natural infection (8, 30, 52), responsiveness to vaccine proteins was entirely indifferent to reduced diversity (i.e., homozygosity). The advantage of higher degrees of allelic diversity may be less important in generating a detectable CTL response to the single, unchanging set of peptides artificially assembled in a vaccine than in retarding escape by evolving virus from immune containment (17, 32). While apparent irrelevance of class I homozygosity for vaccine-induced CTL does not ensure its irrelevance in the context of a live-virus challenge, confirmation that class I homozygosity is not overtly disadvantageous may simplify vaccine development and application.
We have uncovered noteworthy similarities as well as differences between class I HLA-mediated responses to natural HIV-1 and to certain immunogenic HIV-1 components incorporated into the ALVAC-HIV canarypox vaccine. Future clinical trials should clarify whether these similarities and differences are generalizable to other HIV-1 vaccine formulations. Beyond HIV-1 vaccines, dissection of the molecular interactions of B*27, B*57, and others that might be associated with favorable response to both replicating virus and stable antigenic peptides could have implications for our understanding of HLA determinants of vaccine-induced CTL response in general.
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ACKNOWLEDGMENTS |
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This work was supported by Public Health Service grant AI 45209 to M.J.M. and by grant AI 41951 (in part) to R.A.K. from the National Institute for Allergy and Infectious Diseases.
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FOOTNOTES |
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* Corresponding author. Mailing address: Department of Epidemiology and International Health, School of Public Health, University of Alabama at Birmingham, 220A Ryals Building, 1665 University Blvd., Birmingham, AL 35294-0022. Phone: (205) 975-8698. Fax: (205) 934-8665. E-mail: rkaslow{at}uab.edu.
Participants of the NIAID AIDS Vaccine Evaluation Group
who contributed to this study include: M. L. Clements-Mann and D. Schwartz (Johns Hopkins University, Baltimore, Md.); R. Belshe, G. Gorse, and S. Frey (St. Louis University School of Medicine, St. Louis,
Mo.); R. Dolin, M. Keefer, and T. Evans (University of Rochester
Medical Center, Rochester, N.Y.); L. Corey and J. McElrath (University
of Washington, Seattle, Wash.); and B. Graham, P. Wright, and P. Spearman (Vanderbilt University, Nashville, Tenn.).
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
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Journal of Virology, September 2001, p. 8681-8689, Vol. 75, No. 18
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.18.8681-8689.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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76: 2298-2305
[Abstract] [Full Text]
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