Association, prevalence, and

clearance of human papillomavirus

and antisperm antibodies in infected
semen samples from infertile patients
Andrea Garolla, M.D.,a Damiano Pizzol, M.D.,a Alessandro Bertoldo, B.Sc.,a Luca De Toni, B.Sc.,a
Luisa Barzon, M.D.,b and Carlo Foresta, Ph.D.a
a b
Unit for Human Reproduction Pathology, Section of Clinical Pathology; and Section of Microbiology and Medical
Biotechnologies, Department of Molecular Medicine, University of Padova, Italy

Objective: To evaluate prevalence, association, and clearance of human papillomavirus (HPV) and antisperm antibodies (ASAs) in in-
fected semen samples from infertile patients.
Design: Cross-sectional clinical study.
Setting: Andrology and microbiology sections at a university hospital.
Patient(s): Three groups of subjects: 61 infertile patients with HPV semen infection, 104 noninfected infertile subjects, and 92 control
subjects.
Intervention(s): Semen analysis, spermMar test, fluorescence in situ hybridization for sperm aneuploidy and for HPV, and immuno-
fluorescence for HPV 16-L1 and immunoglobulins (IgA, IgG, and IgM) determination.
Main Outcome Measure(s): Association of sperm procedures, HPV sperm infection, sperm aneuploidies, and sperm ASAs.
Result(s): Infertile patients with HPV semen infection showed high percentages of ASAs. In these patients HPV sperm infection was
associated with lower sperm motility, which was worse in subjects with ASAs. No alterations of sperm chromosomes were observed. To
obtain a significant clearance of both HPV sperm infection and ASAs at least 24 months of follow-up were needed.
Conclusion(s): Human papillomavirus has been recently suggested to have an important role in male infertility. This study demon-
strated that HPV sperm infection can be long lasting and frequently associated with ASAs that may further reduce male fertility. Infertile
patients with positive spermMar test results should be considered for investigation for HPV, es-
pecially if they are candidates for assisted reproduction. (Fertil SterilÒ 2013;99:125–31. Ó2013
by American Society for Reproductive Medicine.) Use your smartphone
Key Words: Antisperm antibodies, asthenozoospermia, HPV clearance, male infertility, to scan this QR code
sexually transmitted infections, sperm infection and connect to the
discussion forum for
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Discuss: You can discuss this article with its authors and with other ASRM members at http://
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S
eminal infections are widely (1, 2). Chronic viral infection of the hepatitis B virus and hepatitis C virus
accepted by clinicians and re- urogenital tract, especially HIV (HCV) semen infections are able to
searchers as significant etiologic infection, may be significant for adversely modify seminal fluid
factors of male infertility, and their pres- chronic low urethral tract inflammation parameters (5, 6). Impaired sperm
ence, even in asymptomatic males, is of- and reduced fertility (3, 4). Moreover, parameters, and in particular reduced
ten associated with poor semen quality recent studies have also shown that motility, have been observed in most of
these infections. Furthermore, viral
Received May 18, 2012; revised August 22, 2012; accepted September 5, 2012; published online semen infections have been associated
October 6, 2012. with increased frequency of sperm
A.G. has nothing to disclose. D.P. has nothing to disclose. A.B. has nothing to disclose. L.D.T. has noth-
ing to disclose. L.B. has nothing to disclose. C.F. has nothing to disclose.
aneuploidy and DNA fragmentation
Funding was provided by Master of Reproductive Medicine, University of Padua. (7, 8). Additionally, the presence of
Reprint requests: Carlo Foresta, Ph.D., University of Padova, Department of Molecular Medicine, Sec- human papillomavirus (HPV) has been
tion of Clinical Pathology, Unit for Human Reproduction Pathology, Via Gabelli 63, 35121 Pa-
dova, Italy (E-mail: carlo.foresta@unipd.it). reported in semen. Because this
infection is usually considered transient
Fertility and Sterility® Vol. 99, No. 1, January 2013 0015-0282/$36.00
Copyright ©2013 American Society for Reproductive Medicine, Published by Elsevier Inc.
in males and without detrimental
http://dx.doi.org/10.1016/j.fertnstert.2012.09.006 clinical consequences, its effects on

VOL. 99 NO. 1 / JANUARY 2013 125

ORIGINAL ARTICLE: ANDROLOGY
sperm parameters and male fertility have been inadequately
investigated (9–11). Recently our studies suggested the
possible role of HPV in male infertility, showing a reduction
of sperm motility (12). We observed a high prevalence of HPV
sperm infection in infertile patients with HPV DNA localized
in the sperm head. Moreover, we demonstrated that HPV
binding to sperm is tenacious (12, 13) and that conventional
methods of sperm washing are not able to clear the virus from
sperm surface (14). Infections are considered a risk factor for
antisperm antibodies (ASAs) development, besides being
a cause of direct damage on spermatozoa, abnormal seminal
plasma composition, and changes in mitochondrial function
(1, 2). The prevalence of ASAs is higher in infertile patients
than in the general population, and their presence is
associated with reduction of sperm motility (15–17). Although
the role of ASAs is controversial, various mechanisms have
been proposed affecting male fertility: sperm agglutination
and impaired cervical mucus penetration, complement-
mediated sperm injury through the female genital tract, and in-
terference with gametes interaction (16). Whereas some authors
have observed no strong association between chronic inflam-
matory or infectious diseases and the presence of ASAs in semen
(17, 18), other studies established that some infections are
associated with the production of ASAs and that some
antibodies are directed against so-called fertilization-related an-
tigens, leading to infertility (19–22). To date, little is known
about HPV sperm infection, its clinical consequences,
clearance time, and its association with sperm autoimmunity.
The aim of this study was both to investigate the possible
association between the presence of HPV and ASAs and to
determine their clearance time in the semen of infertile patients.
MATERIALS AND METHODS
Patients
Written informed consent was obtained from all patients, and
the study protocol was approved by the local ethics commit-
tee. We enrolled 61 consecutive infertile patients with HPV
DNA in semen detected by polymerase chain reaction, and
104 infertile patients without HPV infection who attended
the Center for Male Gamete Cryopreservation. Infertile
patients were considered those subjects with altered sperm
parameters, at least 2 years of unprotected sexual intercourse
without conception, and normal female partners (tubal, uter-
ine, cervical abnormalities, and ovarian disorders were ex-
cluded). A medical history including previous circumcision,
smoking, and sexual behavior was obtained from each pa-
tient. Exclusion criteria were history of cryptorchidism, testic-
ular trauma, or post-mumps orchitis. Varicocele and seminal
infections were excluded, respectively, by testicular Doppler
ultrasound and microbiological sperm culture. As control
subjects, a group of 92 proven fertile men who were able to
conceive during the last year and without HPV semen infec-
tion were enrolled with the same exclusion criteria. All
subjects collected semen for standard semen analysis, sperm-
Mar test, and fluorescence in situ hybridization (FISH) for
sperm aneuploidy. Additionally, sperm from infertile patients
with HPV semen infection were analyzed by FISH for HPV. On
sperm samples positive for HPV 16 and ASAs we performed
126
immunofluorescence for HPV 16-L1 protein and for immuno-
globulin determination. Subjects with HPV sperm infection
repeated FISH analysis for HPV and determination of ASAs
at 12 months and, if still infected, at 24 months.
Semen Processing
Semen samples were obtained by masturbation after 3 days of
sexual abstinence. After liquefaction at room temperature, se-
men volume, pH, sperm concentration, viability, motility, and
normal morphology were determined according to World
Health Organization guidelines for semen analysis (23). In
each sample we performed the spermMar test to exclude sperm
antibodies (as described below). Semen samples were then
washed three times with sterile phosphate-buffered saline
(PBS 1
), and the pellet was used for the subsequent analyses.
ASA Detection
Sperm antibodies were detected using the spermMar test kit
for IgG and IgA (FertiPro). Semen samples were treated ac-
cording to the kit protocol. This is an immunobead test that
used IgG- and IgA-coated latex particles, which bind to the
sperm-bound ASAs. The absence of ASAs was confirmed by
freely moving spermatozoa uncovered by latex particles.
The presence of ASAs was considered when spermatozoa re-
acted with the particles and a bunch of particles were attached
to all or at least to 50% of motile spermatozoa. The reactivity
of the test was confirmed by the formation of growing agglu-
tinates of latex particles themselves. From the evaluation of
500 motile spermatozoa, the percentage of spermatozoa
with attached latex particles represented the test result.
FISH for Sperm Aneuploidy
The study of sperm aneuploidy was performed by multicolor
FISH, as reported elsewhere (24). The DNA hybridization
was performed using a human satellite probe-specific mix
for chromosomes X, Y, and 18 (Kreatech Diagnostics). Probes
were direct-labeled with fluorochrome PlatinumBright495 for
chromosome X, resulting in a green signal and fluorochrome
PlatinumBright550 for chromosome Y, resulting in a red sig-
nal; for the detection of chromosome 18, a PlatinumBright415
direct-labeled specific probe was used, resulting in a blue sig-
nal. The DNA denaturation of sperm and probes, incubation,
posthybridization washing, and nuclear staining were per-
formed according to the Kreatech protocol. After preparation,
slides were observed using a fluorescence microscope (Nikon
Eclipse E600) equipped with a triple band-pass filter set (fluo-
rescein isothiocyanate [FITC], tetrarhodamine isothiocyanate
[TRITC], 6-diamino-2-phenylindole [DAPI]). Single spots
were evaluated as reported elsewhere (25). For each patient,
at least 2,500 cells were scored.
FISH for HPV
Glass slides containing at least 2
106 adhered sperm were
fixed in a methanol-acetic acid solution for at least 1 hour
at 20 C. To permeabilize, samples were digested with pepsin
diluted 1:25,000 in prewarmed 0.01 mol/L-1 HCl for 10 min-
utes at 37 C. Permeabilization of the specimens was stopped
VOL. 99 NO. 1 / JANUARY 2013

with 3- to 5-minute washes in PBS 1
; then samples were de-
hydrated in 70%, 80%, and absolute ethanol for 2 minutes
and finally air-dried. Samples were then overlaid with 20
mL of hybridization solution (Pan Path) containing biotin-
labeled HPV DNA probe (a mix of total genomes containing
the conserved HPV region). Each slide was covered with
a glass coverslip, and the edges were sealed with nail polish
to prevent loss of the mixture during denaturation and
hybridization. After a simultaneous denaturation of cellular
target DNA and HPV DNA probe on a heating block for 5 min-
utes at 95 C, hybridization was performed by incubating the
samples at 37 C overnight in a humidified chamber. Thereaf-
ter the coverslips were carefully removed, and the slides were
washed in PBS 1
for 10 minutes. After 15 minutes’ incuba-
tion at 37 C with the differentiation reagent (Pan Path), the
slides were washed three times in PBS 1
. The biotin-
labeled HPV probe was detected by incubation with 1:200
streptavidin Texas Red (Vector Laboratories) for 40 minutes
at room temperature. After detection the slides were washed
twice in PBS 1
/0.01% Triton and then twice in PBS 1

and mounted with a solution containing DAPI and anti-
fade (BioBlue; BioView). Samples were analyzed using a fluo-
rescence microscope (Nikon ViCo video confocal microscope)
equipped with a triple band-pass filter set (FITC, TRITC, DAPI).
For each slide at least 200 spermatozoa and 200 exfoliated
cells were analyzed. Evaluation of nuclear hybridization sig-
nals was performed by three investigators. When nuclei were
completely and homogeneously stained and multiple small
spots or single large signals were present, the sperm cells
were classified as positive. The method was tested on control
slides containing CaSki cells, a human cervical carcinoma cell
line with stably integrated and transcriptionally active HPV
genomes that served as a control for the specific probe. Cells
smeared on salinated glass slides were fixed with 4% parafor-
maldehyde in PBS for 10 minutes. After fixation, cells were
subjected to 3- to 5-minute washes in PBS 1
and then dehy-
drated with 5-minute ethanol washes (30%, 60%, and 95%).
Cell smears were then air-dried and stored at 4 C until use.
Immunofluorescence for HPV 16-L1 and
Immunoglobulin Determination
Among infertile patients with HPV semen infection, sperm
from five subjects confirmed as infected with HPV 16 were
used for this analysis. Samples were washed in PBS and fixed
in PBS/paraformaldehyde 4% for 15 minutes at room temper-
TABLE 1
Sperm parameters, FISH for sperm aneuploidy, and spermMar test results observed in the three subject groups.
Sperm
concentration Total sperm
Group (3106/mL) count (3106)
Infertile HPV-infected patients (n ¼ 61) 32.0  11.2 94.2  36.5
Infertile noninfected patients (n ¼ 104) 34.6  9.8* 108.8  44.5
Control subjects (n ¼ 92) 51.3  8.4* 156.0  42.9
* P< .01.
Garolla. Antisperm antibodies in HPV sperm infection. Fertil Steril 2013.
VOL. 99 NO. 1 / JANUARY 2013
Fertility and Sterility®
ature. Samples were then smeared on polylysinated glass
slides and air-dried. The glass slides were washed three times
in PBS for 5 minutes at room temperature and then saturated
with PBS/5% BSA/5% normal donkey serum for 30 minutes
at room temperature. Afterward, samples were incubated
with mouse monoclonal antibody HPV 16-L1 (CAMVIR-1;
0.8 mg/mL, 1:250, Santa Cruz Biotechnology) and
biotin-conjugated polyclonal anti-human IgM, IgG, or IgA
immunoglobulins (Vector Laboratories) overnight at 4 C.
Immunoreaction was detected by further incubation with
FITC-conjugated anti-mouse antibodies and streptavidin–
Texas Red (both from Vector Laboratories). Finally, nuclei
were counterstained with DAPI, and slides were mounted
with antifade buffer and 24
24-mm coverslip. Immuno-
staining was evaluated with a Nikon ViCo video confocal
microscope.
Statistical Analysis
The values shown are the averages of at least three indepen-
dent experiments (n ¼ 3) performed in triplicate. Differences
between data were determined by Fisher exact test and Welch
two-sample t test. Probability (P) values were corrected
through the Holm method, and values (two-sided) of < .01
were considered statistically significant.
RESULTS
We enrolled three groups of subjects as follows: 61 infertile
with HPV semen infection (aged 35.3  4.7 years), 104 infer-
tile without infection (aged 34.2  3.8 years), and 92 proven
fertile noninfected subjects (aged 35.5  4.2 years) used as
controls. The presence of HPV infection was detected by poly-
merase chain reaction amplification and then genotyped by
the INNO-LiPA Genotyping Extra assay, which can identify
the following HPV genotypes: HPV 6, 11, 16, 18, 26, 31, 33,
35, 39, 40, 42, 43, 44, 45, 51, 52, 53, 54, 56, 58, 59, 66, 68,
69/71, 70, 73, 74, and 82. Each of the 61 positive samples
was further evaluated by FISH analysis for HPV to determine
the percentage of infected sperm. As previously reported, only
a part of sperm cells from these samples was bound to HPV
DNA (Supplemental Fig. 1, available online). In particular,
we observed a 24.7  4.8 mean percentage of HPV-positive
sperm. Semen samples from each group were further analyzed
for semen parameters, sperm aneuploidy, and presence of
ASAs (Table 1). Seminal volume, pH (data not shown), sperm
count, normal morphology, and viability were not different in
Normal FISH Positive
Progressive morphology Viability aneuploidy spermMar test
motility (%) (%) (%) (%) result, n (%)
29.0  11.4 18.8  6.2 80.0  7.1 1.2  0.6 26 (42.6)
47.8  11.0 18.5  4.3 83.2  5.1 1.3  0.4 12 (11.5)*
53.4  11.4 21.3  4.7 83.6  5.1 0.9  0.3 2 (2.2)*
127
ORIGINAL ARTICLE: ANDROLOGY
HPV-infected and in noninfected semen samples, despite
a significant reduction of sperm number vs. control. A signif-
icant reduction of mean progressive sperm motility was found
in semen samples of infected patients vs. both controls and
infertile noninfected patients (both P< .01). The percentage
of sperm aneuploidy was not different in infected and nonin-
fected infertile patients. Sperm samples from infertile patients
more frequently showed ASAs compared with controls. Inter-
estingly, this frequency was significantly higher in infected
infertile patients than in noninfected ones (P< .01). Addition-
ally, the mean percentage of ASAs was significantly higher in
infected than in noninfected patients (mean percentage
34.7  19.8 and 15.8  9.6. respectively). Supplemental
Figure 2 shows an example of positive spermMar test. Among
infected samples, five had HPV 16, and two of them showed
a positive spermMar test result. In these samples we tested
the presence of different immunoglobulins (IgA, IgG, and
IgM). In the two samples with ASAs we observed costaining
of HPV 16-L1 with both IgA and IgG but not IgM (Fig. 1A).
FIGURE 1
Confocal microscopic analysis for HPV 16-L1 and immunoglobulins. (A) Costaining of IgA and IgG with HPV proteins in ASA-positive infected
samples. (B) Absence of immunoglobulins staining in ASA-negative infected samples.
Garolla. Antisperm antibodies in HPV sperm infection. Fertil Steril 2013.
128
No staining for any Ig was found in the other three samples
(Fig. 1B). We followed up the 61 infected patients by FISH
for HPV and ASAs, and the results are reported in Figure 2.
During a period of 24 months, infected patients (26 also had
positive spermMar test results) were advised to have protected
intercourse, to avoid smoking, and to refer to our unit in case
of warts development. After 12 months, 39 of 61 (63.9%) were
still positive for HPV, and 17 (43.6%) also for the spermMar
test, whereas 22 (36.1%) patients cleared HPV sperm infection
and all tested negative for the spermMar test. After a further
12 months, 9 patients (14.7%) still tested HPV positive and 5
(55.5%) had ASAs in semen, whereas the other 30 subjects
were negative for both HPV infection and ASAs. Table 2 re-
ports the mean values of sperm motility observed during the
follow-up period. Although there was no significant differ-
ence in sperm motility between infected patients with positive
vs. negative spermMar test results, the former group showed
lower motility through the whole follow-up period. Patients
that cleared HPV infection at 12 and 24 months showed
VOL. 99 NO. 1 / JANUARY 2013

FIGURE 2
Follow-up of 61 infertile patients with HPV sperm infection. Chart shows the prevalence and clearance of both sperm infection and ASAs at 0, 12,
and 24 months.
Garolla. Antisperm antibodies in HPV sperm infection. Fertil Steril 2013.
a mean sperm motility not significantly different from that in
infertile noninfected patients (46.8%  13.0% and
47.1%  12.1%, respectively, vs. 53.4%  11.4%).
DISCUSSION
Many reports have addressed the presence of viral semen infec-
tion such as HIV, hepatitis B virus, and HCV infections
on sperm quality (4–6). Although results have been
controversial, most authors described significant impairment
of sperm parameters in affected males. In particular, sperm
number, motility, and morphology are frequently impaired in
these patients, representing a possible cause of male
infertility (4–6). Most of the literature reporting the impact of
viruses on male fertility focused on at least three aspects: [1]
viral infections may induce an impairment of general health
and thus infertility; [2] infected patients are frequently
treated with antiretroviral therapies able to induce testicular
damage up to azoospermia; and [3] the presence of viral
DNA at sperm level may have a direct detrimental effect on
sperm parameters and gametes interaction. Recently it has
been demonstrated that HPV infection can also be present in
TABLE 2
Number of infected patients and sperm motility at baseline and during the follow-up period (12 and 24 months).
Baseline
Group n Progressive motility (%)
Infertile HPV-infected total 61 29.0  11.4
Infertile HPV-infected, spermMar þ 26 27.2  12.7
Infertile HPV-infected, spermMar  35 30.5  10.3
Infertile who cleared HPV infection – –
Garolla. Antisperm antibodies in HPV sperm infection. Fertil Steril 2013.
VOL. 99 NO. 1 / JANUARY 2013
Fertility and Sterility®
semen and that it has a relevant prevalence in some subjects
(26). This condition is frequently present in patients with
genital warts, partners of infected women, and in infertile
patients. In the latter patients we observed a significant
reduction of sperm motility that could represent the cause of
their infertility status. However, other mechanisms have been
proposed to explain the higher incidence of infertility in
HPV-infected patients. In vitro studies showed both a reduced
sperm–egg penetration when HPV-transfected spermatozoa
were used (27) and a stage-specific maturation arrest in HPV
artificially infected embryos (28). Moreover, Perino et al.
reported that, when HPV was present in semen, assisted repro-
duction techniques (ARTs) resulted in lower fertilization rate
and increased percentage of abortions (29). On this basis, we
can hypothesize that during ART, HPV may interfere with
mechanisms of sperm capacitation, acrosome reaction,
sperm–oocyte interaction, and fusion, but postfertilization ef-
fects can also be supposed. In this study we investigated a new
possible mechanism of male infertility related to HPV semen
infection. We found more than 40% of infected infertile pa-
tients had a presence of ASAs on the sperm surface. In contrast,
sperm autoimmunity was significantly lower in noninfected
12 mo 24 mo
n Progressive motility (%) n Progressive motility (%)
39 30.1  8.1 9 31.1  6.3
17 28.4  5.4 5 28.0  2.7
22 31.4  9.6 4 35.0  7.7
22 46.8  13.0 30 47.1  12.1
129
ORIGINAL ARTICLE: ANDROLOGY
infertile and in fertile control subjects, in which we found
a prevalence similar to that reported by the literature (30).
Moreover, infected patients had a higher mean percentage of
ASAs compared with noninfected ones. This finding suggests
that the presence of HPV DNA on the sperm surface may rep-
resent an antigenic stimulus for ASA formation. It is worth
noting that in all participants of this study we had previously
excluded the known causes of ASAs, such as actual and/or
previous varicocele, other viral and/or bacterial infections,
and orchitis. To confirm that sperm autoimmunity was HPV
dependent, we documented the presence of both viral proteins
and immunoglobulins in the same sperm cells in samples with
positive spermMar test results. In particular, when immunoflu-
orescence for HPV 16-L1 was present on the sperm surface, we
observed costaining for IgA and IgG. This observation suggests
that semen infection could represent a new clinical condition
associated with the presence of ASAs.
Until recently, HPV infection was considered transient and
without clinical consequences in men (31, 32). On this basis,
little has been investigated about its clinical significance and
clearance time in infertile patients. In contrast, many studies
have been done in females in whom the clearance time for
HPV infection has been reported to be approximately 1 year
(33). In infected male patients of our study a significant
viral clearance (approximately 85.3%) was obtained after
24 months. Interestingly the healing from sperm infection
paralleled the disappearance of ASAs and was significantly
related to a progressive improvement of sperm motility. The
knowledge of sperm HPV clearance time could be useful not
only in the counseling of infected males but also for their
partners and in general for infertile couples. First, this makes
possible a proper education and allows clinicians to give
advice to affected patients; second, it enables the prevention
of HPV-related cancers, especially when the partner has nega-
tive HPV test results. Moreover, considering HPV sperm infec-
tion as a possible cause of infertility, it would be helpful in the
counseling of infertile couples. If our data are confirmed by an
improvement of pregnancy rate after HPV clearance, young
couples could be advised to wait for HPV clearance before
searching natural fertility, whereas aged couples could be re-
ferred to ART cycles using sperm-washing procedures able to
remove HPV DNA from semen (13). As a limitation of this
study, we acknowledge the absence of a fertile group of sub-
jects with HPV semen infection.
In conclusion, this article confirms our previous results
showing that HPV semen infection is able to significantly im-
pair sperm motility. Unlike other viral infection, HPV seems
not to affect sperm chromosomes. Interestingly, we found
that the presence of HPV DNA at sperm level is frequently as-
sociated with ASAs of IgA and IgG classes in infertile patients.
Because autoimmune infertility is often treated by ARTs and
because these techniques can be ineffective in presence of
HPV sperm infection, we suggest screening for HPV in all
subjects with positive spermMar test results. Moreover, our
results showed that the clearance time of HPV sperm infection
in infertile patients was approximately 24 months and that
healing paralleled both the disappearance of ASAs and im-
proved sperm motility. The insights provided by this study
add new information to the sparse literature about HPV sperm
130
infection in infertile males. If our data are confirmed by fur-
ther studies, this knowledge will be very useful not only for
infected males but also for their partners and for infertile
couples.
Acknowledgments: We thank Massimo Menegazzo for
technical assistance; the staff of the Centre for Male Gamete
Cryopreservation for helpful discussion; Livio Finos, Ph.D.,
Department of Statistical Science, University of Padua for sta-
tistical analysis; and Mrs. Karyn Cecchini B.Sc., P.G.Dip., for
careful editing.
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SUPPLEMENTAL FIGURE 1

Example of FISH analysis for HPV performed on semen samples from infertile patients. (A) Noninfected sperm samples; (B) infected sperm.
Garolla. Antisperm antibodies in HPV sperm infection. Fertil Steril 2013.

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 Fertility and Sterility®

SUPPLEMENTAL FIGURE 2

Picture of positive spermMar test obtained from an infected semen sample.

Garolla. Antisperm antibodies in HPV sperm infection. Fertil Steril 2013.

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