OBSERVATION

Disfiguring Generalized Verrucosis in an Indonesian

Man With Idiopathic CD4 Lymphopenia
Bachti Alisjahbana, MD; Rachmat Dinata, MD; Endang Sutedja, MD; Irene Suryahudaya, MD;
Hardisiswo Soedjana, MD; Nucki N. Hidajat, MD; Rista D. Soetikno, MD; Ezra Oktaliansah, MD;
April Deng, MD, PhD; Peter Rady, PhD; Stephen Tyring, MD, PhD; Anthony A. Gaspari, MD

Background: Human papillomavirus (HPV) infec-
tions cause a spectrum of clinical disease states, depend-
ing on the causative HPV and the characteristics of the
infected host, especially the status of cell-mediated im-
munity. Generalized verrucosis is an unusual clinical pre-
sentation of a disseminated HPV infection associated with
severe immunodeficiency status.
Observations: We present a case of extreme disfigure-
ment associated with an HPV-2 (common wart virus) in-
fection. Virologic studies, immune status of the patient,
and treatment(s) are summarized.
Conclusions: The severe disfigurement of this patient
was a result of an underlying severe immunodeficiency,
permissive for a disseminated HPV-2 infection that was
allowed to progress for many years before the initiation
of therapy. Such a rare case illustrates the natural his-
tory of generalized verrucosis in the setting of severe im-
munodeficiency in the absence of sustained medical in-
terventions. Medical and surgical treatments resulted in
marked improvement in the general health of this pa-
tient, as well as improvement of the disfigurement that
resulted from the generalized verrucosis.
Arch Dermatol. 2010;146(1):69-73

Author Affiliations:
Departments of Internal
Medicine (Dr Alisjahbana),
Dermatovenereology
(Drs Dinata and Sutedja),
Anatomical Pathology
(Dr Suryahudaya), Plastic
Surgery (Dr Soedjana),
Orthopaedics and Traumatology
(Dr Hidajat), Radiology
(Dr Soetikno), and
Anesthesiology and Reanimation
(Dr Oktaliansah), Medical
Faculty, Padjadjaran University,
Dr Hasan Sadikin Hospital,
Bandung, Indonesia;
Department of Pathology,
University of Massachusetts,
Worcester (Dr Deng);
Departments of Dermatology
(Drs Rady and Tyring),
Microbiology/Molecular
Genetics (Dr Tyring), and
Internal Medicine (Dr Tyring),
The University of Texas Health
Science Center, Houston; and
Departments of Dermatology
and Microbiology/Immunology,
School of Medicine, University
of Maryland, Baltimore
(Dr Gaspari).
G
ENERALIZED VERRUCOSIS IS
a term used to describe
widespread human
papillomavirus (HPV) in-
fections. A variety of
disease states can result in such severe, po-
tentially disfiguring infections. General-
ized verrucosis is observed in patients with
underlying immunodeficiency status that are
either acquired (for example, AIDS or im-
munosuppression associated with organ
transplantation) 1,2 or rare congenital
immunodeficiency syndromes (eg, epider-
modysplasia verruciformis;3 warts, hypo-
gammaglobulinemia, infections, and myelo-
kathexis [WHIM] syndrome;4 combined
immunodeficiencies;5 and cyclic neutrope-
nia associated with chronic lymphopenia).6
We report a case of generalized verrucosis
secondary to an HPV-2 infection that re-
sulted in severe disfigurement. The under-
lying idiopathic CD4 lymphopenia re-
sulted in susceptibility to the generalized
verrucosis. The resulting skin disease was
untreated for almost 10 years, which re-
sulted in progressive, severe disfigure-
ment, including massive cutaneous horns.
METHODS
DNA EXTRACTION
From 3 wart biopsy specimens taken from the
patient, DNA was extracted by means of a DNA
extraction kit (Qiagen, Valencia, California).
The quality of the DNA extracted for polymer-
ase chain reaction (PCR) procedures was as-
sessed by amplification of the reference con-
trol gene -globin.7
HPV TYPING BY PCR
AND SEQUENCING
The HPV PCR amplification was performed by
means of 2 degenerate consensus primers,
termed CP65 and CP70, with annealing sites
located in the L1 open reading frame.8 Analy-
sis isolation, cloning, and sequencing of puta-
tive HPV PCR products were performed as de-
scribed previously.8 The obtained putative HPV
sequences were aligned and compared with
known HPV types available through the Gen-
Bank database by means of the Basic Local
Alignment Search Tool (BLAST) program (Na-
tional Center for Biotechnology Information,
National Institutes of Health, Bethesda,
Maryland).9
REPORT OF A CASE
The patient is a 39-year-old Indonesian
man who was in good health until the age
of 15 years, when a warty lesion ap-
peared on his knee. During the next 8
years, the skin lesions had spread over his
entire skin surface and prevented him from
working. At the age of 26 years (1994), he
was evaluated and treated by a dermatolo-
gist in Bandung for almost 2 years, who

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A
B
C
Figure 1. Clinical appearance of the patients warts in June 2007 before
treatment. A, Chest; B, arm and hand; and C, lower extremities.
diagnosed his condition as kutil batu (kutil meaning wart
and bart meaning stone or rock). Because his skin con-
dition continued to progress, he withdrew from further
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treatment and had been untreated since 1998. None of
his family members, neighbors, or friends have any con-
dition similar to his. Both his parents are alive, healthy,
and nonconsanguineous. The patient also has a healthy
brother and sister. He is divorced and the father of 2
healthy children. He is an unemployed construction
worker. His medical history was unremarkable, and there
were no risk factors for human immunodeficiency virus
(HIV). He was not taking any medications. He had re-
mained in his village since the onset of his disease until
June 2007, when the Discovery Channel visited him to
film a documentary about his condition.
On physical examination, widespread verrucous le-
sions were noted on his face, chest, and back (Figure 1A).
His distal extremities contained confluent verrucous le-
sions, with no visible uninvolved skin. His hands were
encased in a number of giant cutaneous horns ranging
in size from 2 to 30 cm, many of which were curved and
twisted (Figure 1B). A strong, foul odor was present. Nu-
merous cutaneous horns were present on his lower ex-
tremities, but the soles of his feet were relatively spared.
Assessment of cutaneous delayed-type hypersensitiv-
ity by intradermal skin testing with an extract of Candida
albicans (1:100 dilution; Allerderm Laboratories, Peta-
luma, California) revealed cutaneous anergy (lack of in-
duration and erythema at the skin test site at the 48-hour
and 72-hour readings). A skin biopsy specimen taken from
a lesion on his lower extremities revealed changes asso-
ciated with a viral papilloma (Figure 2A and B). The com-
puter analysis of the sequencing data obtained from the
putative HPV PCR products revealed the presence of HPV-2
infections in all 3 wart samples (Figure 3). DNA se-
quencing of the E2 region of the HPV-2 genome was com-
pleted (Table 1) and compared with a reference strain,
as well as another HPV-2 strain that was isolated from a
patient with giant cutaneous horns.10-12 The obtained se-
quencing data of the E2 region of HPV-2 from 3 clones of
3 warts were compared to the prototype HPV-2 se-
quences. Each of the 3 clones (CL1, CL2, and CL3) of the
HPV-2 E2 viral region derived from 3 warts showed a simi-
lar base change from T to C at nucleotide position 3765
(the position based on prototype HPV-2a DNA; NCBI Gen-
Bank accession number X55964). This missense muta-
tion resulted in an amino acid change at position 361 (Y
to H) of the E2 viral protein. This amino acid change within
the E2 region of HPV-2 was unique to our patient with
generalized warts and was not present in E2 protein of
HPV-2 viral isolates derived from other patients with huge
verrucae vulgaris (Lei et al,10 2007). All 3 isolates re-
vealed identical point mutations that rendered this iso-
late, as well as those isolates from another patient with gi-
ant cutaneous horns, distinct from the HPV-2 standard.
The homogeneity of the DNA sequence in the E2 region
in all 3 lesions suggested an infection with a single HPV
that was genetically stable over time.
The local Indonesian Health Ministry hospitalized the
patient in November 2007 and initiated evaluation and
treatments. During this hospitalization, he was diag-
nosed as having a pulmonary infection with Mycobacte-
rium tuberculosis (diagnosed on chest x-ray examina-
tion [not shown], Ziehl-Neelsen stain of sputum [strongly
positive], and culture) for which he was successfully
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 A
B
Figure 2. Skin biopsy specimens of warts. A, Skin biopsy specimen that
reveals acanthosis and the presence of koilocytes (original magnification
40). B, Skin biopsy specimen that reveals church spire hyperplastic
changes (original magnification 20).
treated with combination antimicrobial therapy (rif-
ampin, isoniazid, ethambutol hydrochloride, and cipro-
floxacin). He also was diagnosed as having inactive hepa-
titis B infection. He also had an episode of herpes zoster
that resolved without sequelae. His major laboratory find-
ings are summarized in Table 2 and Table 3. Of note
was a chronic CD4 lymphopenia (absolute CD4 cell count,
314/L; reference range at reference laboratory, 410-
1590/L), which was found to be reproducible when these
cell marker studies were performed on a number of sepa-
rate occasions over time (not shown).
For the treatment of his cutaneous HPV infection, he
underwent a series of surgical procedures. First, the cu-
taneous horns were debrided using a bone saw with the
patient under general anesthesia. Since the debride-
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A
M W1 W2 W3 PC NC R
603 bp
452 bp
310 bp
310 bp
268 bp
234 bp
Figure 3. Amplification of human papillomavirus (HPV) and -globin
sequences from 3 wart biopsy specimens of a patient with generalized warts.
For HPV typing, polymerase chain reaction (PCR) products were visualized
after electrophoresis in ethidium bromidestained 2% agarose gel by UV
illumination. Lanes: M, fX174 RF DNA molecular weight marker; W1 through
W3, wart samples from the patient; PC, HPV-positive DNA control;
NC, HPV-negative DNA control; and R, reagent control. A, Putative HPV PCR
fragments can be seen in specimens from the patient (W1-W3) and in the
HPV-25positive DNA control (PC). The cloning and sequencing of the
putative HPV PCR products from the wart samples revealed 452base pair
(bp) HPV-2 sequences. A faint extranon-HPVspecific PCR band can be
seen in the samples W1, W2, W3, and NC, which is described in the original
methodologic article.8 B, -Globin PCR fragments (268 bp) can be seen in
wart specimens from the patient (W1-W3) and in the control DNA specimens
(PC, NC).
ment of the cutaneous horns from his hands, he has been
using a compounded 40% salicylic acid lotion to retard
the recurrence of the massive hyperkeratosis. Second,
many of the verrucous lesions on the face and trunk were
excised (elliptical excisions with layered closures and tan-
gential plane excisions). He received a course of acitre-
tin therapy, 25 to 50 mg/d, with little noticeable effect
on growth or regression of his numerous warts. Intrave-
nous cidofovir therapy (300 mg for each infusion in nor-
mal saline solution: a gift from Gilead Pharmaceuticals,
Foster City, California) was attempted (along with hy-
dration and oral probenecid therapy), but the renal func-
tion of the patient deteriorated, and this treatment was
withdrawn after 2 intravenous infusions during a pe-
riod of 1 month. He is currently being treated with on-
going surgical procedures to excise the remaining un-
treated or recurrent warts.
COMMENT
The patient described in this report has severe immuno-
deficiency syndrome characterized by a chronic CD4
T lymphocytopenia. This patient meets the Centers for
Disease Control and Prevention criteria for this syn-
drome because he lacked serologic or virologic evi-
dence of HIV-1 or HIV-2 infection, had a CD4 cell count
of approximately 300/L on at least 2 occasions, had an
abnormally low CD4/CD8 ratio, and exhibited disease in-
dicative of impaired cellular immunity (generalized ver-
rucosis caused by HPV-2).13,14 It is noteworthy that the
CD4 lymphopenia of this patient persisted after he was
successfully treated for pulmonary tuberculosis, which
itself can be a cause of transient CD4 lymphopenias.15 A
variety of opportunistic and atypical bacterial, viral, fun-
gal, and protozoal infections can occur in patients with
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 Table 1. Missense Mutations Within the E2 Region of Human Papillomavirus 2 (HPV-2) Isolates

Nucleotide, Codon Amino Acid

Position Prototype Isolate 1a Clones 1, 2, and 3b Position Prototype Isolate 1 a Clones 1, 2, and 3 b
3037 TTA TCA 118 L S
3387 TCA CCA 235 S P
3543 TAC CAC 287 Y H
3561 AGT CGT 293 S R
3765 TAC CAC 361 Y Ha

a Data are from Lei et al.10

b From the present study.

linemia, and autosomal dominant inheritance. Other than

Table 2. Findings of Initial Laboratory Testing ( June 2007) peripheral CD4 lymphopenia, our patient lacked the fea-
tures associated with WHIM syndrome (no history of re-
Test Finding current pyogenic bacterial infections, no hypogamma-
HIV-1/2 test Nonreactive globulinemia, no myelokathexis on peripheral smear, and
Rapid plasma reagin Nonreactive no apparent autosomal dominant inheritance because both
Serum protein electrophoresis Polyclonal gammopathy his parents and all his siblings were healthy).
Gamma globulin fraction 31.6% of total 2.31 g/dL (reference
protein (reference range, 11.4%-20.4%) range, 0.6-1.2 g/dL)
Another syndrome associated with marked suscepti-
Complete blood cell count bility to disseminated HPV infection is epidermodyspla-
with differential a,b sia verruciformis, which is an autosomal recessive dis-
Hemoglobin 11.4 g/dL order with disseminated flat warts (HPV-5, HPV-8, and
Total white blood cell count 8.7/L others), an increased susceptibility to nonmelanoma skin
Comprehensive metabolic profile Within normal limits
cancer, and mutations in EVER1 and EVER2 (approxi-
Abbreviation: HIV, human immunodeficiency virus.
mately 75% of patients with this disorder exhibit muta-
a On differential counting, a low lymphocyte count of 23% was found tions of either 1 of these 2 genes).3 Our patient was in-
(reference range, 25%-40%); all other cell types were present at a normal fected exclusively with HPV-2 and did not develop any
frequency. skin cancers despite having had the HPV infection for
b SI conversion factors: To convert hemoglobin to grams per liter, multiply
by 10; total white blood cell count to 109 per liter, multiply by 0.001. almost 25 years. This reflects the benign (nononco-
genic) nature of the HPV-2 infection. However, this HPV-2
infection caused severe functional impairment and physi-
Table 3. Findings of Cell Marker Studies a cal disfigurement.
Immunodeficiency syndromes that can result in gen-
Study Finding (Reference Range) eralized verrucosis rarely present with the severe defor-
CD3 cell count, /L mity exhibited by our patient. A Chinese patient has been
Relative 40 (55-84) reported to exhibit giant cutaneous horns on his hands and
Absolute 771 (690-2540)
feet as a result of an HPV-2 infection, similar to our pa-
CD4 cell count, /L
Relative 16 (31-60) tient.10-12 There was no published information, to our
Absolute 314 (410-1590) knowledge, about the immune defect of this patient. In
CD8 cell count, /L common with our patient, the Chinese patient lived in a
Relative 22 (13-41) rural area and was eventually treated successfully with ra-
Absolute 421 (190-1184) diation therapy to his hands and feet. We compared the
CD4/CD8 ratio 0.72 (0.9-2.3)
open reading frame of the E2 region of the 3 isolates from
a Flow cytometric analysis was performed by Prodia Clinical Laboratories, our patient with that of the Chinese patient with massive
Bandung, Indonesia. cutaneous horns to a reference strain of HPV-2 and found
that all 3 isolates from our patient exhibited distinct mis-
sense mutations compared with either the reference strain
idiopathic CD4 lymphopenias, such as HPV, M tubercu- of HPV-2 or those isolates from the Chinese patient.12 This
losis, and varicella-zoster infections,14 all of which oc- finding suggests that distinct missense mutations in the
curred in our patient. The spectrum of HPV infections E2 region can result in aggressive infections, as noted in
that occurs in patients with idiopathic CD4 lymphope- these 2 patients in whom the infecting HPV exhibited dis-
nias includes juvenile laryngeal papillomatosis,16 dis- tinct open reading frame missense mutations. Functional
seminated flat and common warts,17,18 recurrent vulvar studies of the effects of the enhancing effect of the E2 re-
intraepithelial neoplasia,19 and generalized verrucosis gion from our patients isolates on HPV promoter activity
caused by HPV-2.6 There are also other immunodefi- are ongoing. Our observation that all 3 HPV isolates from
ciency diseases associated with CD4 lymphopenias and our patient exhibited identical E2 region mutations sug-
susceptibility to HPV infections, such as WHIM syn- gests a clonal origin of the infecting HPV-2, with genetic
drome.4 Such patients exhibit neutropenias, marked sus- stability of the open reading frame of the E2 region in the
ceptibility to bacterial infections, hypogammaglobu- many years of the progressive viral infection.

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 Our patient was treated with acitretin (unsuccess-
fully) and eventually cidofovir, the use of which was dis-
continued because of progressive nephrotoxicity after only
2 doses. Both acitretin (either alone or with interferon
beta)20,21 and cidofovir22-24 have been used with varying
success in treatment of other patients with generalized
verrucosis. Further characterization of his immuno-
logic defect will be critical to designing successful im-
munotherapy for his generalized verrucosis. For ex-
ample, there is a case report of a patient with generalized
verrucosis with an underlying immunodeficiency char-
acterized by chronic lymphopenia and a marked defect
in TH1-lymphocyte cytokine production (ie, interferon
gamma), who was successfully treated with granulocyte-
macrophage colony-stimulating factor to stabilize her lym-
phocyte counts during a 9-month course of interferon
gamma therapy.6 This regimen resulted in a marked re-
gression of more than 95% of her generalized wart in-
fection, with a sustained clearance of her HPV infection
during a 5-year follow-up period.
In conclusion, this case represents a rare presenta-
tion of a severe, disfiguring HPV-2 infection as a result
of an immunodeficiency associated with CD4 lympho-
cytopenia. Patients who present with massive cutane-
ous horns should be evaluated for HPV-2 infections and
an underlying associated immunodeficiency.
Accepted for Publication: July 17, 2009.
Correspondence: Anthony A. Gaspari, MD, Depart-
ments of Dermatology and Microbiology/Immunology,
University of Maryland School of Medicine, 419 W Red-
wood St, Ste 240, Baltimore, MD 21201 (agasp001
@umaryland.edu).
Author Contributions: All authors had full access to all
the data in the study and take responsibility for the integ-
rity of the data and the accuracy of the data analysis. Study
concept and design: Gaspari. Acquisition of data: Gaspari.
Analysis and interpretation of data: Alisjahbana, Dinata,
Sutedja, Suryahudaya, Soedjana, Hidajat, Soetikno, Ok-
taliansah, Deng, Rady, Tyring, and Gaspari. Drafting of the
manuscript: Alisjahbana, Dinata, Sutedja, Suryahudaya,
Soedjana, Hidajat, Soetikno, Oktaliansah, Deng, Rady, Ty-
ring, and Gaspari. Critical revision of the manuscript for im-
portant intellectual content: Alisjahbana, Dinata, Sutedja,
Suryahudaya, Soedjana, Hidajat, Soetikno, Oktaliansah,
Deng, Rady, Tyring, and Gaspari. Administrative, techni-
cal, or material support: Alisjahbana, Dinata, Sutedja, Surya-
hudaya, Soedjana, Hidajat, Soetikno, Oktaliansah, Deng,
Rady, Tyring, and Gaspari. Study supervision: Gaspari.
Financial Disclosure: None reported.
Funding/Support: This study was funded by National In-
stitute of Arthritis and Musculoskeletal and Skin Dis-
eases grant R0-1-AR46108-05 (Dr Gaspari).
Additional Contributions: The Indonesian minister of
health, Siti Fadilah Supari, MD, and the director of Dr
Hasan Sadikin Hospital, Cissy B. Sudjana Prawira, MD,
provided stimulating suggestions, help, and support.
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