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Journal of Clinical Microbiology, January 2000, p. 357-361, Vol. 38, No. 1
0095-1137/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Improved Amplification of Genital Human
Papillomaviruses
P. E.
Gravitt,1,*
C. L.
Peyton,2
T. Q.
Alessi,2
C. M.
Wheeler,2
F.
Coutlée,3
A.
Hildesheim,4
M. H.
Schiffman,4
D. R.
Scott,5 and
R. J.
Apple1
Department of Human Genetics, Roche Molecular
Systems, Alameda, California1;
Department of Molecular Genetics and Microbiology, University
of New Mexico, Albuquerque, New Mexico2;
Départements de Microbiologie-Infectiologíe,
CHUM, Montréal, Québec, Canada3;
Environmental Epidemiology Branch, National Cancer
Institute, Rockville, Maryland4; and
Department of Pathology, Kaiser Permanente, Portland,
Oregon5
Received 26 July 1999/Returned for modification 8 September
1999/Accepted 5 October 1999
 |
ABSTRACT |
Genital human papillomaviruses (HPVs) are commonly detected from
clinical samples by consensus PCR methods. Two commonly used primer
systems, the MY09-MY11 (MY09/11) primers and the GP5+-GP6+ (GP5+/6+)
primers, amplify a broad spectrum of HPV genotypes, but with various
levels of sensitivity among the HPV types. Analysis of the
primer-target sequence homology for the MY09/11 primers showed an
association between inefficient amplification of HPV types and the
number and position of mismatches, despite accommodation of sequence
variation by inclusion of degenerate base sites. The MY09/11 primers
were redesigned to increase the sensitivity of amplification across the
type spectrum by using the same primer binding regions in the L1 open
reading frame. Sequence heterogeneity was accommodated by designing
multiple primer sequences that were combined into an upstream pool of 5 oligonucleotides (PGMY11) and a downstream pool of 13 oligonucleotides
(PGMY09), thereby avoiding use of degenerate bases that yield
irreproducible primer syntheses. The performance of the PGMY09-PGMY11
(PGMY09/11) primer system relative to that of the standard MY09/11
system was evaluated with a set of 262 cervicovaginal lavage specimens.
There was a 91.5% overall agreement between the two systems
(kappa = 0.83; P < 0.001). The PGMY09/11 system
appeared to be significantly more sensitive than the MY09/11 system,
detecting an additional 20 HPV-positive specimens, for a prevalence of
62.8% versus a prevalence of 55.1% with the MY09/11 system
(McNemar's 
2 = 17.2; P < 0.001).
The proportion of multiple infections detected increased with the
PGMY09/11 system (40.0 versus 33.8% of positive infections). HPV types
26, 35, 42, 45, 52, 54, 55, 59, 66, 73, and MM7 were detected at least
25% more often with the PGMY09/11 system. The PGMY09/11 primer system
affords an increase in type-specific amplification sensitivity over
that of the standard MY09/11 primer system. This new primer system will
be useful in assessing the natural history of HPV infections,
particularly when the analysis requires HPV typing.
| |
INTRODUCTION |
L1 consensus primer PCR systems,
particularly the MY09-MY11 (MY09/11) and GP5+-GP6+ (GP5+/6+) primer
systems (1, 4, 9, 13), have been widely used to study the
natural history of human papillomaviruses (HPVs) and their role in the
development of genital cancer, particularly of the uterine cervix
(8, 10, 18). The MY09/11 HPV DNA detection system was used
to show convincingly for the first time that the determinants of
infection with HPV were the same as those for cervical cancer, namely,
the sexual behavior variables such as increased number of lifetime
sexual partners (11). Furthermore, both consensus primer
methods have been used in a number of important studies that show
unequivocally the associated risk of infection with certain types of
HPV with the development of cervical cancer (12, 15). The
sensitivities of these methods and their ability to amplify and detect
greater than 25 of the HPV genotypes known to infect the genital mucosa have provided researchers with an extremely valuable tool which has
been considered a "gold standard" for HPV detection for the last
several years. However, despite the progress toward the understanding of HPV-associated disease facilitated by the use of these consensus primer systems, limitations are still evident, particularly in regard
to the variability of detection sensitivity among specific HPV types
(17).
At the time that the MY09/11 primer system was designed, only 5 of the
20 or more known genital HPV genotype sequences had been reported;
specifically, HPV types 6, 11, 16, 18, and 33 (13). The
primers were thus designed in a conserved region of the L1 open reading
frame with the intent of amplifying in a single reaction both the five
genotypes whose sequences are known and, presumptively, other genital
HPVs with shared sequence homology in this region. The chosen regions
were not entirely homologous even among the five original HPV types,
and positions with nucleotide base heterogeneity were accommodated by
inclusion of degenerate base sites. The resultant degenerate primers
comprised a mixture of 24 unique oligonucleotide sequences. Over the
next decade studies with these primers for amplification and detection
of HPV from genital samples demonstrated the ability of the primers to
amplify a spectrum of more than 30 genital HPV types, albeit with
various levels of sensitivity (2). Only a single
modification to the original primer set was made, wherein an extra,
sequence-specific oligonucleotide (HMB01) directed to the minus strand
of HPV type 51 (HPV-51) was included to facilitate the amplification of
this important, cancer-associated type of HPV (7). The
MY09/11 system referred to in this paper is inclusive of the HMB01 primer.
The nature of the synthesis of a mixture of oligonucleotides with
degenerate base sequences relies on the presumed random addition of one
of two or more nucleotide bases at the position of degeneracy. The
random insertion of bases at degenerate positions is not a controlled
process, such that an equal proportion of each sequence combination
cannot be guaranteed. Furthermore, no analytical method for the
verification of sequence proportions was readily available for quality
control purposes, so that functional testing with each HPV type as a
template was required to ensure the comparability of different lots of
primers. Results from our own laboratories (P. E. Gravitt and F. Coutlée, unpublished data) indicate differences in type-specific
amplification efficiencies among separate syntheses of the MY09/11
degenerate primers (data not shown).
We sought to improve the reproducibility and sensitivity of the MY09/11
HPV amplification system by developing a set of oligonucleotide pools,
PGMY09 and PGMY11, based on the same primer binding regions used for
MY09/11. Rather than using the degenerate primer method, we grouped
virus types together by sequence homology in each of the two primer
binding regions. From these groupings, we designed a set of 5 upstream oligonucleotides comprising the PGMY11 primer pool and a set
of 13 downstream oligonucleotides comprising the PGMY09 primer pool
(PGMY09/11 primer system). These primers were used in amplification
reactions similar to the standard MY09/11 PCR protocols, and we
continued to coamplify HPV with the internal 
-globin control using
the primer pair PC04 and GH20. We compared the performance of this new
set of L1 consensus primers to that of the standard MY09/11 system for
the amplification and detection of HPV from cervical cell samples.
| |
MATERIALS AND METHODS |
HPV sequence alignment and primer design.
The L1 regions of
all sequenced HPV genotypes were obtained through the Los Alamos
National Laboratories HPV Database (http://hpv-web.lanl.gov/) and were
aligned by using the Wisconsin Package (Genetics Computer Group,
Madison, Wis.). The MY09/11 primer binding regions of each of these
sequences were sorted into groups according to 3' DNA sequence
homology. The DNA sequence mismatches remaining within selected HPVs
were chosen according to their stability (16) and were kept
near the 5' end of the oligonucleotide. Dissociation temperatures and
duplex formation of each primer sequence were determined by using Oligo
5.0 (Molecular Biologic Insights, Inc., Cascade, Colo.). The criteria
for redesigning the primers were as follows. The same primer binding
regions in the target HPV types were used so that the same detection
and genotyping methods could be retained. The broad-spectrum
amplification that defines consensus PCR was accomplished with pools of
oligonucleotides rather than the former addition of degenerate base
sites in the MY09/11 primer sequences. The number of oligonucleotides
for each primer pool (upstream and downstream primers) was kept to a
minimum, such that the maximum numbers of HPV types were matched with a single primer.
Sample acquisition.
Cervicovaginal lavage specimens (10 ml)
were collected as part of a large natural history study of HPV
infection at Kaiser Permanente in Portland, Oreg. (18). A
total of 1,421 cytologically normal women were seen twice during the
enrollment period, and two specimens were collected at different visits
for HPV testing. This convenience sample of multiply sampled women was
included in a study of persistence of HPV infection. HPV testing was
performed with all 1,421 specimens from the first visit by using
MY09/11 consensus primers (18). Two hundred sixty-two women
were positive for HPV DNA by L1 consensus PCR (MY09/11) at the time of
study enrollment (i.e., at the first visit). The second specimens from these 262 women comprised the sample set for the present analysis. No
clinical interventions were taken between the first and second samplings. This convenience sample set was selected on the basis of the
assumption that at the second sampling point many of these women would
still have detectable HPV DNA at the cervix, some would have cleared
their infection and would be HPV negative, and others would have
acquired a new HPV infection in the interim between the first and
second samplings. This maximized the probability of a high HPV
prevalence useful for meaningful HPV assay comparisons (i.e., expected
50% persistence or acquisition rate between the sampling time points,
yielding approximately equal numbers of HPV-positive and -negative
specimens). This second specimen was tested by PCR with both MY09/11
and PGMY09/11, and the results from each assay were blinded to the
operators performing the analyses. All participating women gave
informed consent.
Sample preparation.
The cervicovaginal lavage specimens were
prepared for PCR by standard protocols (1, 18). In brief,
each lavage specimen was digested for 1 h at 65°C in the
presence of 200 µg of proteinase K per ml and 1% Laureth-12. The
samples were spun briefly at maximum speed in an Eppendorf
microcentrifuge to remove all condensation from the cap of the
Eppendorf tube and were heated to 95°C for 10 min to heat denature
the residual protease. The samples were centrifuged again briefly, and
5 µl was used for each PCR assay.
Standard MY09/11 consensus PCR.
The protocol used as the
gold standard to evaluate the new system was performed as described
previously (6). Each sample was amplified with 5'
biotinylated MY09/11 (50 pmol of each primer) and HMB01, GH20, and PC04
(5 pmol of each primer) in the presence of 1× PCR Buffer II, 6 mM
MgCl2, 200 µmol (each) dATP, dCTP, and dGTP, 600 µmol
dUTP, and 7.5 U of AmpliTaq Gold DNA polymerase (Perkin-Elmer, Foster
City, Calif.). Amplifications were performed in a Perkin-Elmer TC9600
thermal cycler by using the ultrasensitive profile of AmpliTaq Gold
activation at 95°C for 9 min and 40 cycles of 95°C for 1 min,
55°C for 1 min, and 72°C for 1 min. This was followed by a final
extension at 72°C for 5 min, and the amplification reaction mixtures
were stored at 4 to 15°C.
PGMY09/11 L1 consensus PCR.
The protocol for the L1
consensus PCR assay was optimized for the new primer pools PGMY09 and
PGMY11. The MY09/11 primer set was replaced with 5' biotinylated PGMY09
and PGMY11. An equimolar mixture of each primer was added to the PCR
master mixture for a final concentration of 10 pmol of each
oligonucleotide in the primer sets. The -globin primers GH20 and
PC04 were also biotinylated, and the concentration of each of these was
reduced from 5 pmol per PCR, as in the standard L1 protocol, to 2.5 pmol per PCR mixture in the revised L1 protocol. Also, the final
concentration of MgCl2 in the PCR mixture was reoptimized
to a final concentration of 4 mM (reduced from 6 mM in the standard
protocol). Otherwise, the PCR buffers, reagents, and amplification
profiles were identical to those described above.
HPV genotyping.
The PCR products from both the standard and
revised L1 consensus PCR assays are amenable to genotype discrimination
by the recently described HPV immobilized probe assay (6).
The protocol used for detection of products from both assays was
performed as described previously (6), in which the PCR
products were denatured in 0.4 N NaOH and were hybridized to an
immobilized HPV probe array, with positive hybridization detected by
streptavidin-horseradish peroxidase-mediated color precipitation at the
probe site.
Statistical analysis.
Statistical analyses were performed
with STATA 6.0 software (STATA, College Station, Tex.). Kappa
statistics were calculated to measure the agreement between the primer
systems beyond that expected by chance (5). Significance
testing for the unequal distribution of discordant results was
performed by McNemar's chi-square test for matched pair data when
comparing dichotomous outcomes (3) and the Stuart-Maxwell
test for marginal homogeneity when comparing multiple categorical
outcomes (14).
| |
RESULTS |
In addition to the irreproducibility of the MY09/11 primer
synthesis, amplification efficiency has been shown to vary
systematically among the HPV genotypes when known target quantities of
the genotype are analyzed and when amplification with the MY09/11
primer system is compared to that with another consensus PCR system
(17). Analysis of the alignment of the MY09/11 primer
binding regions for 19 of the 23 sequenced genital HPV genotypes (Table
1) revealed more destabilizing mismatches
for the genotypes shown in our laboratories and others to amplify with
poor efficiency (e.g., HPV types 26, 52, and 55) relative to the number
of mismatches for the HPV types that amplified well (e.g., HPV types
16, 18, and 33). The efficiency of amplification appeared to be related
to the number, position, and stability of the mismatch (data not
shown). As expected, primers with greater than four mismatches to the
target sequence tended to be less efficient (e.g., HPV types 42 [MY09], 26 [MY09], and 59 [MY11]). Primers with less than four
mismatches overall but with one or more mismatches at the 3' end of the
oligonucleotide also tended to segregate with the less efficiently
amplified HPVs (e.g., types HPV 39 [MY09], 45 [MY09], and 55 [MY09]).
The MY09/11 consensus primers were redesigned in an attempt to correct
both the irreproducibility of the degenerate primer synthesis and to
increase the sensitivity of amplification to a 10-copy endpoint for
each of the HPV genotypes commonly found in the genital tract. The
primer sequences resulting from this analysis are shown in Table
2. The upstream primer pool,
designated PGMY11, contains five oligonucleotide primers. The
downstream primer pool, designated PGMY09, contains a total of 13 oligonucleotide primers. The amplification parameters were reoptimized
in the presence of the new primer pools. The overall increase in
stability of the new primers to their target sequences required a
reduction in the total final MgCl2 concentration to 4 mM.
This primer pool accommodates the efficient amplification of the
following HPV genotypes to at least a sensitivity of 10 genomes per
PCR: 6, 11, 16, 18, 26, 31, 33, 35, 40, 45, 51, 52, 56, and 59 (data
not shown). Several other HPV genotypes, including HPV types 39, 42, 53, 54, 55, 58, 61, 62, 64, 66, 67, 68, 69, 70, 71, 72, 73, IS39, CP8304, CP6108, MM4, MM7, and MM8, were amplified as well as or better with PGM09/11 than with MY09/11, as determined from comparison of endpoint dilution amplifications (data not shown).
To verify the results of the analytic analyses, we conducted a parallel
comparison of the MY09/11 and PGMY09/11 amplification systems with 262 cervical specimens. Of the 262 cervical specimens, a total of 15 were
excluded from further analysis due to poor or no -globin
amplification, indicating either a lack of sufficient cellular material
for PCR or the presence of polymerase inhibitors. Thirteen of these
samples were negative for -globin amplification by both the
PGMY09/11 and the MY09/11 amplification systems, while two samples were
excluded because of a lack of -globin amplification by the PGMY09/11
system only. The general summary results for HPV prevalence for the
remaining 247 samples are presented in Table
3. The overall percent agreement between
the two methods was 91.5%, with a kappa value of 0.83 (P < 0.001). There was an increase in overall HPV prevalence with the
PGMY09/11 system relative to that with the MY09/11 system (62.8 and
55.1%, respectively). Of the 21 samples with discordant HPV results,
20 were positive with the PGMY09/11 system only and 1 was positive with
the MY09/11 system only (McNemar's 2 = 17.19;
P < 0.001). The additional positive specimens detected by the PGMY09/11 system comprised 17 samples with single infections with HPV types 16, 18 (2 samples), 35, 42, 51, 52, 54 (2 samples), 55, 59, 66 (four samples), MM7, and MM8 and 3 samples with multiple infections containing HPV type 51 and 42, HPV types 31, 54, and 66, and
HPV types 33, 45, and 6. The one sample called positive only with the
MY09/11 system contained HPV-31. The most notable differences between
the two primer systems were seen when the abilities of the two systems
to detect specific types as part of multiple infections were compared.
The overall proportion of multiple infections detected with the MY09/11
primer system was 46 of 136 (33.8%), whereas that with the PGMY09/11
primer system was 62 of 155 (40%). A summary of the type-specific
positive results is presented in Fig. 1.
Figure 1 demonstrates graphically the absolute increase in the rate of
detection of specific HPV types. The following cancer-associated HPV
types were detected at least 25% more often with the PGMY09/11 primer
system: HPV types 26, 35, 45, 52, 55, 59, 68, 73, and MM7. The
following non-cancer-associated types were also detected at least 25%
more often with the PGMY09/11 primer system: HPV types 42, 54, and 66. Table 4 shows a comparison of HPV
detection results when categorized by cancer risk group as HPV
negative, high-risk type positive (positive for at least one of the
following HPV types: 16, 18, 26, 31, 33, 35, 39, 45, 51, 52, 55, 56,
58, 59, 68, 73, MM4, and MM7), or low-risk type positive (positive for
at least one of the following HPV types without concomitant coinfection
with high-risk HPV types: HPV types 6, 11, 40, 42, 53, 54, 57, 66, and
MM8). The agreement between the PGMY09/11 and MY09/11 amplification
systems by risk group is 88.7% (kappa = 0.81; P < 0.001). The PGMY09/11 primers were more likely to reclassify
samples into a higher risk group category compared with the risk
assignment based on HPV typing with the MY09/11 primers (Stuart-Maxwell
2 = 20.45; P < 0.001).
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TABLE 3.
Overall agreement in results for HPV with MY09/11 and
PGMY09/11 for 247 cervicovaginal
lavage specimensa
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FIG. 1.
HPV type-specific positive results with PGMY09/11 and
MY09/11. The total number of positive results by HPV type are plotted:
open bar, detected with MY09/11 only; shaded bar, detected with both
primer sets; stippled bar, detected with PGMY09/11 only. The
type-specific results include positive results for HPV types from
specimens infected with both single and multiple HPV types.
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TABLE 4.
Agreement in HPV risk group assignment with MY09/11 and
PGMY09/11 for 247 cervicovaginal
lavage specimensa
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| |
DISCUSSION |
Overall, the MY09/11 L1 consensus primer system was improved, both
practically, in terms of the elimination of the need for degenerate
primer synthesis, and functionally, as demonstrated by the increased
sensitivity of amplification across the genital HPV type spectrum. Each
oligonucleotide comprising the PGMY09/11 pools is synthesized
independently, allowing verification of the sequence of each
primer. Also, the concentration of each primer can be ascertained and
consistent proportions of primer in the PGMY09/11 pools can thus be
maintained. This represents an important improvement in the quality
assurance for the HPV consensus primers that was absent for the
degenerate primer system. The sensitivity of type-specific
amplification, particularly from samples infected with multiple HPV
types, was substantially improved. The HPV types that were most
affected in the clinical validation study were consistent with the
prediction based on the mismatch analysis with target regions and
MY09/11. There was a general increase in type-specific sensitivity
with the PGMY09/11 system that was independent of the targeted
type-specific improvements. It is not clear whether this was due to an
overall increase in sensitivity due to the redesigned HPV primers or to
less competition from -globin product amplification. The -globin
primer concentration was reduced by one-half from that in the MY09/11
protocol in response to our observations that the coamplification of
-globin reduced the endpoint sensitivity of HPV detection for
several HPV genotypes. It is clear from the plasmid amplifications that
the major improvements to the types most affected by use of PGMY09/11
were not attributable to differences in -globin primer concentrations.
The degree of the effect with the PGMY09/11 primer system is
proportional to the amount of virus in the sample (as determined by
plasmid titrations [data not shown]), reflective of the differences in sensitivities between the two primer systems. We have subsequently analyzed a set of HPV-containing swabs from women who were diagnosed by
cytological analysis with low-grade squamous intraepithelial lesions
and in whom the viral copy number is likely to be quite high, and we
have seen a less dramatic increase in the additional number of
specimens with type-specific positive results (data not shown).
However, the types most affected were consistent with those presented
here. Thus, the magnitude of the absolute differences in HPV
type-specific results will vary depending on the viral burden of the
samples being tested.
Because the increase in HPV type-specific detection with the PGMY09/11
primers is largely restricted to samples that are positive for multiple
HPV types, we have considered the possibility that our results may be
due to cross-reactivity among the HPV genotypes rather than true
additional type-specific infections. Several characteristics of the
system make this an unlikely explanation for the increase in
type-specific prevalence observed in the present study. First, the only
substantive difference between the PGMY09/11 and the MY09/11 assays is
the primer sequence change. Both primer systems are designed to
nondiscriminately amplify any genital HPV type present in the reaction
mixture (essentially favoring primer-target cross-reactivity by
design). Type-specific differences attributable to cross-reactivity
would therefore be a consequence of probe cross-hybridization at the
genotyping level. In this comparison, the detection system used for
genotyping of the PGMY09/11 and MY09/11 amplification products
was identical. There is a chance that a general increase in
sensitivity with the PGMY09/11 primers could increase the total
amount of product generated by PCR, which could in turn increase the
rate of occurrence of false-positive signals due to cross-reactivity
(as a function of total DNA concentration). However, such a result
would show characteristic patterns of multiple infections (e.g., all
strongly HPV-16-positive samples would be consistently coinfected with
HPV-31), and we see no consistent patterns in our multiple infections.
In addition, hybridization of amplification products from
>106 input targets has shown no such cross-reactivity
among the genotypes. Finally, the increase in type-specific detection
is highly correlated with the types expected to be most affected by
sequence analysis and analytic studies. We do not, therefore, attribute
the improvement seen with the PGMY09/11 primer system to a nonspecific
HPV cross-reactivity phenomenon.
Although the gross difference in HPV prevalence is only incremental,
the overall increase in the type-specific positivity could be important
in some natural history studies of HPV, particularly in terms of
gaining a better understanding of viral persistence and host responses.
Use of the PGMY09/11 system may offer a relatively simple change in
current L1 consensus primer technology that will help to minimize the
type-specific misclassification known to affect the standard HPV
broad-spectrum assays.
| |
FOOTNOTES |
*
Corresponding author. Present address: 2810 St. Paul
St., #1, Baltimore, MD 21218. Phone: (410) 889-5456. Fax: (301)
402-0916. E-mail: pgravitt{at}jhsph.edu.
| |
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Abstract
Introduction
