IMMUNOHISTOCHEMICAL LOCALIZATION OF AN HIV EPITOPE
IN CEREBRAL ANEURYSMAL ARTERIOPATHY IN PEDIATRIC
ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)

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Katsuhiro Kure, M D 0 Department of Pathology (Neuropathology), Albert Einstein
College of Medicine, Bronx, New York 10461; and The Rose F. Kennedy Center for
Research in Mental Retardation and Human Development, Albert Einstein College of
Medicine, Bronx, New York 10461
Yong D. Park, M D

0 Department of Neurology, Duke University Medical Center,
Durham, North Carolina 27710

Tai-Seung Kim, M D

0 Department of Pathology (Neuropathology), Albert Einstein
College of Medicine, Bronx, New York 10461; and The Rose F. Kennedy Center for
Research in Mental Retardation and Human Development, Albert Einstein College of
Medicine, Bronx, New York 10461

William D. Lyman, PhD

0 Department of Pathology (Neuropathology), Albert
Einstein College of Medicine, Bronx, New York 10461

George Lantos, M D

Department of Radiology, Albert Einstein College of Medicine,

0

Bronx, New York 10461

Sunhee Lee, MD 0 Department of Pathology (Neuropathology), Albert Einstein
College of Medicine, Bronx, New York 10461; and the Rose F. Kennedy Center for
Research in Mental Retardation and Human Development, Albert Einstein College of
Medicine, Bronx, New York 10461
Sangho Cho, M D

0

Department of Pathology, Albert Einstein College of Medicine,

Bronx, New York 10461

Anita L. Belman, M D

0

Department of Neurology, SUNY at Stony Brook, Stony

Brook, New York 11794

Karen M . Weidenheim, MD, and Dennis W. Dickson, MD' 0 Department of
Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, New York 10461;
and The Rose F. Kennedy Center for Research in Mental Retardation and Human
Development, Albert Einstein College of Medicine, Bronx, New York 10461

Pediatric Patholou, 9t655-667, 1989
Copyr*ht @ 1989 by Hemisphere Publishing Corporation

655

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656

K . KURE E T AL.

A 6-year-old boy with acquired immunodeficiency syndrome (AIDS) developed aphasia and quadriplegia 3 months before his death. Cerebral vascular ectasia and multiple cerebral infarcts were noted on
prernortem radiological studies. Postmortem evaluation revealed diffuse aneurysmal dilatation of the circle
a j Willis associated with fresh and organizing thrombi, destruction of the elastic lamina, and marked
intimal fibroplasia. Multiple cerebral infarcts and subacute A I D S encephalitis with basal ganglia calcijcation &ere also present Immunohistochemistry with a monoclonal antibody (anti-gp41) to human
immunod<ficiency virus ( H I V ) demonstrated positively stained cells in the arterial wall of the circle a j
Willis and in the cerebral parenchyma. Double immunostaining demonstrated that gp41-positive cells in
the circle of Willis were also positive for a macrophage marker or leukocyte-common antigen, but not with
an endothalial marker. Some macrophages or rnicroglia in the cerebrum were also colabeled with antigp41 These results suggest that HIV may be directb involved in vascular pathology associated with
pediatric AIDS.
K E Y WORDS: AIDS, cerebral arteritis, aneurysm, immunohistochemktry, pediatrii, subacute encephalitis.

INTRODUCTION
Neurological complications have been increasingly reported in children
with AIDS (1). Clinical manifestations, varying from developmental delay
with progressive long-tract signs to focal neurological deficits, are seen in
over 30% of children with AIDS-related complex or AIDS (1, 2). Postmortem findings consisting of microcephaly (1, 2), subacute AIDS encephalitis,
and basal ganglia calcification (1, 3), have been described. Adult patients
with AIDS exhibit focal neurologic signs from either toxoplasmosis or lymphoma. In children, toxoplasmosis is rare, and focal lesions are a result of
lymphoma or cerebrovascular accidents (CVA) (1, 4). Hemorrhagic CVA
are often associated with coagulopathies (immune thrombocytopenia),
whereas nonhemorrhagic CVA are a result of intrinsic primary vascular diseases (4). Cerebral vasculitis affecting small parenchymal arteries and systemic vasculopathy affecting medium to large arteries are among the primary vascular diseases reported in children with AIDS (5). This report
describes a child with AIDS and a previously undescribed HIV-associated
arteriopathy affecting the circle of Willis, and discusses a possible role for
HIV in this condition.
Presented in part at the Society for Pediatric Pathology Interim Meeting, Buffalo, New York, September 29, 1988, Yediatr Pathol 1988;8:665.
Supported by NIA AG06803. DA 04583, and NS 11920.
Part of Herpes zoster imniunohistochemistry was performed by Dr. Marc Rosenblum (Department of
Parhology, Sloan-Kettering Memorial Cancer Center, New York). The authors also thank Pablo Garcia,
Lola Leon, Grace Gong, and Louis Mendez for their technical support, and Lynn Goldstein (Genetic
Systems, Seattle, WA) for anti-gp41.
Address reprint requests to Dennis W. Dickson, M . D . , Department of Pathology (Neuropathology),
K-438, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461

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CEREBRAL VASCULOPATHY IN PEDIATRIC AIDS

657

CASE REPORT
This 6-year-old boy with AIDS was the 2,700-g product of a pregnancy to a
mother with AIDS. Both parents were intravenous drug abusers and died of
AIDS before this patient’s death. The autopsy of his father showed end-stage
heroin nephropathy and subacute AIDS encephalitis. This patient’s sibling also
has AIDS and is currently hospitalized. The early childhood development of
this patient was unremarkable. He received normal childhood vaccines and had
an uncomplicated chicken pox infection at 5 years of age.
He was first hospitalized at 5’/iz years of age with Salmonella septicemia,
aphasia, and right hemiparesis. Two months later he was hospitalized for the
final time with new focal neurologic signs and oral thrush. The physical examination at that time revealed spastic diparesis, mutism, and response only to
deep pain. The pupils were unequal. Truncal petechiae and jaundice were also
noted. Computed tomographic (CT) scans of the head revealed multiple bilateral cerebral infarcts. Contrast-enhanced C T scans and cerebral angiogram
revealed markedly tortuous and dilated arteries of the circle of Willis (Fig. l a
and b).
His hospital course was complicated by pulmonary infiltrates seen on a
chest x-ray, gastrointestinal bleeding, and possible disseminated intravascular
coagulation. He developed cardiac and renal failure with anasarca, as well as
respiratory insufficiency and diarrhea. Platelet transfusions were required for
recurrent bleeding episodes. A urine viral culture grew adenovirus. A sputum
smear had acid fast bacteria. He died on the 25th hospital day.

METHODS
Tissue

The autopsy was performed within 2 hours postmortem. Samples of the left
anterior cerebral artery and cerebral tissue were fixed in 4% glutaraldehyde
and embedded in Epon for electron microscopic study. The reminder of the
brain and spinal cord were fixed by immersion in 10% buffered formaldehyde
for 2 weeks. Sections of the circle of Willis, cerebrum, midbrain, cerebellum,
pons, medulla, and spinal cord were studied with hematoxylin and eosin. Sections were also studied with elastic van Gieson, Masson’s trichrome, Alcian
blue, Luxol fast-blue, periodic acid-Schiff, Ziehl-Neelsen carbolfuchsin, and
Bodian stains.
lmmunohistochemistry

Unstained, 6-pm thick paraffin sections from the circle of Willis and the
cerebrum were mounted on gelatin-coated glass slides for immunohistochemical studies. After deparaffinization, the sections were immersed in 3 % H202

K. KURE ET AL.

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658

FIGURE 1. Contrast-enhanced CT scan of the head (a) and cerebral angiogram (b). Note marked tortuosity and dilatation of the arteries of the circle of Willis. (c) Arteries at the base of the brain show irregular
nodular ectasia and focal aneurysmal dilatation with thrombi. (d) Multiple areas of bland or hemorrhagic
infarction of different ages in the cerebral hemispheres.

CEREBRAL VASCULOPATHY IN PEDIATRIC AIDS

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for 10 minutes. Nonspecific staining was blocked with 5 % crystalline grade
bovine serum albumin (20 minutes). The sections were incubated with primary antibodies for 2 to 18 hours, and thereafter processed by the ABC
method with peroxidase (Vector, Burlingame, California) or @-galactosidase
labelled complex (Vector). The chromogen used for peroxidase was aminoethylcarbazole (AEC; bright red reaction product), and for P-galactosidase,
X-gal (BRL, Gaithersburg, Maryland; bright blue reaction product).

Viral Antibodies

HIV antibody: The detection of HIV-associated epitopes was performed
with a mouse monoclonal anti-gp41 antibody (Table 1). This antibody was
raised against the HIV envelope protein and gave reproducible and consistent
staining of HIV antigen on paraffin sections. Results using this antibody have
been previously reported (6, 7). Herpesvirus antibodies: Commercially available
anti-herpes zoster virus antibody (HZV) and anti-herpes simplex virus antibody (HSV) were used in the presence of known positive tissue controls.
Sections were independently tested with human herpes zoster convalescent
serum with high-titer, anti-HZV activity (8).

Cell Markers
The following markers were used to define cell types (Table 1). Microglia/
Macrophuge: The lectin Ricinus communis agglutinin-I (RCA-I) is a marker for
macrophages and microglia (9, lo). Previous studies showing RCA-I staining
of multinucleated cells in AIDS (9) have recently been confirmed (10). A
monoclonal antibody to macrophages (HAM-56) was also used. Other markers for lymphoid cells (anti-leukocyte common antigen [ LCA]), mesenchymal
cells (vimentin), endothelial cells (lectin Ulex europueus agglutinin I [UEA-I]),
and astrocytes (polyclonal and monoclonal antibodies to glial fibrillary acidic
protein [GFAP]) were used.

Double-Labeling lmmunohistochemistry
Sequential immunostaining was used for double labeling. If the first immunostaining was performed with the avidin-peroxidase system, the sections
were colorized with AEC. After rinsing these sections in PBS, the sections
were further incubated with the second primary antibody or lectin and then
the reactions were developed with avidin 0-galactosidase system with X-gal.

660

K . K U R E E T AL.

TABLE 1 Summary of Imniunohistochemical Markers

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Dilution
antibodies
anri-HIV sp41
anli-HZV
anti-HSV
Human herpes zoster
i onvalescent serum'
(:ell Markers
R(;A-I
HAhI-56
1.(:.4
UEA-I
GFAP (monoclonal)
(;1;,4I' (polyclonal)

1
1
1

1
1

1
1

1
1

Duration

Temperature

Source

500
50
20

18 h
2h
2h

4OC

Genetic Systems, Seattle, WA
Chemicon, El Segundo, CA
Dako, Santa Barbara, CA
Dr. Marc Rosenhlum,
Memorial Cancer Center. N Y

80
200
40
200
100
250

2h
2h
2h
2h
2h
2h

40 "C

RT
RT

RT
RT
RT
RT
RT

Vector, Burlingame, C A
Enzo, New York, N Y
Dako
Vector
Dako
Dr. J . E. Goldman,
Columbia University, NY

A1)breviarions: R T = room tcmperature; HIV = human immunodeficiency virus; HZV = herpes
mswr virus. HSV = heqies simplex virus; RCA-I = Ricinus communis agglutinin I ; LCA =
.intilriihocytt corninon antigrn. LTEA-I = ULex europaeus agglutinin I ; GF.4P = anti-glial fibrillary acidic
[wotrin.

' S e e Morgello et al. (reference 8).

Controls

HIP' markers: Because anti-gp41 is an IgGl, another mouse monoclonal
antibody of the same subclass, but reactive with Alzheimer neurofibrillar tangles (ALZ.NFT.64) (11) was chosen as a control. Other controls included
HIV-infected and uninfected human T lymphoblastic cell lines (H9). The H 9
cells were smeared on glass slides, air dried, and fixed in 10% buffered formaldehyde Brain sections from an adult with subacute AIDS encephalitis were
also used as a tissue control and processed concurrently. Staining was not
detected by ALZ.NFT.64 or by any antibody on HIV-uninfected H 9 cells.
Consistent positive staining was obtained with anti-gp4l in HIV-infected H 9
cells and in sections from adult AIDS case. Cell markers: Negative controls
using antibodies of the same immunoglobulin subclasses were run in parallel.
The control for RCA-I and UEA-I was staining in the absence of the lectin.
No positivity was seen in these controls.
RESULTS

Gross Findings
The general autopsy was remarkable for Mycobacterium auium intracellulare
(MAI) infection of multiple organs (lymph nodes, spleen, liver, small intes-

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CEREBRAL VASCULOPATHY IN PEDIATRIC AIDS

661

tine, and bone marrow), dilated congestive cardiomyopathy, and mild interstitial pneumonia. There was no evidence of arteriopathy in the coronary arteries, aorta, and arteries of the systemic organs.
The brain weighed 1040 g. The dura and leptomeninges were unremarkable. There were no herniations. Arteries at the base of the brain, including
both anterior cerebral arteries, both middle cerebral arteries, and both posterior communicating arteries showed irregular nodular ectasia and tortuosity
(Fig. lc). The arterial walls had yellow-gray to chalky white irregular thickening with focal intraluminal thrombi. The basilar artery and its major
branches, except for both superior cerebellar and both posterior cerebral arteries, were spared. Small penetrating arteries originating directly from the
circle of Willis (supplying the hypothalamus and pituitary) as well as the
anterior choroidal arteries and recurrent arteries of Heubner were unaffected.
The lenticulostriate arteries were not dilated; however, the middle cerebral
arteries at their point of origin were nodular and dilated. The right middle
cerebral artery was totally occluded by an organizing thrombus at its proximal
portion. Some of the larger branches of the right middle cerebral artery were
also occluded. The transition from the dilated segments of the affected arteries
to the normal caliber segments was abrupt. The arteries assumed a normal
caliber in the brain parenchyma. The cerebral veins were not affected, nor
were arteries over the cerebral or cerebellar convexities.
Sequential sections through the cerebral hemispheres revealed multiple
areas of bland or hemorrhagic infarction of different ages (Fig. Id). The largest softenings were in the medial left cerebral hemisphere in the distribution of
the left anterior cerebral artery, the right temporal pole in the distribution of a
temporal branch of the middle cerebral artery, medial portion of right occipital lobe, and both basal ganglia. The thalamus and hippocampus showed focal
grayish discoloration. The midbrain, pons, medulla, and cerebellum were
grossly unremarkable.

Microscopic Findings
The cerebral arteries from the anterior circle of Willis showed marked
mural thickening (Fig. 2a) with occasional foci of dystrophic calcification (Fig.
2b). The thickening was composed of intimal fibroblastic proliferation with
deposition of relatively acellular myxoid material that was positive for sulfated
glycosaminoglycans using Alcian blue, p H 5.2 (Fig. 2c and d). The tunica
media was thinned. The internal elastic lamina was focally thickened or fragmented, but in most places was absent and was the site of aneurysmal dilatation. Calcification was sometimes located along the fragmented elastic lamina.
The arterial wall lacked significant inflammation; however, focal intimal
mononuclear cells were associated with organizing thrombi, and sparse

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K. KURE ET AL.

FIGURE 2. (a) Cross section of artery from the anterior circle of Willis. Note marked thickening of the
wall with an organizing thrombus. X 8 . (b) Calcification (arrowz) of the arterial wall along the fragmented
clastic lamina. X 7 . (c) Also note deposition of rnyxoid substance in the intima. Alcian blue, X 10. (d)
Higher magnification of the arterial wall shows marked intimal (i) fibromyxomatous thickening. Elastic van
Gieson, X 40.(e) Sparse chronic inflammatory cells with a multinucleated cell (arrow) in the intima. X 80.
(i)
Electron microscopy of the multinucleated cells. Note a long nuclear process interposed between the
nuclei (a7rou1; “nuclear bridse”). X 5000.

chronic inflammatory cells were noted in the adventitia. Transmural granulomatous inflammation and fibrinoid necrosis were absent. Only a few multinucleated cells were noted in one focus in the intima (Fig. 2e). Some arteries
were completely occluded by organizing thrombi. There were a few acid-fast
bacilli (AFB), mostly intracellular, in one of the organizing thrombi, and a
few macrophages containing AFB were also seen in the perivascular space of
the cerebral cortex in a single focus in an area of subacute infarction. Intraparenchymal and leptomeningeal arteries were unremarkable.

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Sections from the brain and spinal cord showed subacute AIDS encephalomyelitis. This was characterized by microglial proliferation with occasional
microglial nodules; perivascular and parenchymal infiltration of macrophages
and mononuclear cells; multinucleated giant cells; calcification of the basal
ganglia; and staining pallor of myelin in the deep white matter. As seen
grossly, there were multiple areas of liquefactive necrosis with gliosis, numerous macrophages, and focal fresh hemorrhages. The middle cerebellar peduncle and central region of the pontine base showed old infarctions. The right
internal capsule, cerebral peduncle, pyramidal tract of the basis pontis and
pyramid showed active Wallerian degeneration. The spinal cord had several
microglial nodules in the gray matter and Wallerian degeneration in the right
lateral and left anterior corticospinal tract. The nerve roots were unremarkable.
Electron Microscopy

Electron microscopic study of the affected arterial wall showed scattered
multinucleated cells and macrophages. Both cell types displayed similar cytologic features, including an irregular nucleus with clumped chromatin and
abundant cytoplasmic organelles and numerous vesicles of 100- 140 nanometers in diameter, sometimes associated with eccentric electron-dense cores resembling HIV virus. Pleomorphic lysosomal bodies and lipid granules were
also present, indicating these cells to be macrophages. O n rare occasions,
elongated tapering nucleoplasm was interposed between adjacent nuclei (“nuclear bridge”) of the multinucleated cells (Fig. 29. Macrophage cytoplasmic
processes were intercalated between the fragmented elastic lamina. In other
areas, the elastic lamina was thinner than usual. Herpes viral-like particles
and bacilli were not present in the artery.
lmmunohistochemistry

Immunohistochemical staining of the affected arteries of the circle of Willis demonstrated numerous gp41-positive cells in the superficial intima, but
also in underlying myxoid tissue (Fig. 3a). The gp41-positive cells consisted of
oval, round, or multinucleated cells. The oval or round gp4l-positive cells
were present predominantly along the intimal surface, but focally deeper in
the wall. Almost all of the round and oval gp41-positive cells were doublestained with HAM-56 (Fig. 3c), but a small number of the round cells in the
intimal aspect were colabeled with LCA. Multinculeated cells were also
double-stained with anti-gp41 and HAM-56 (Fig. 3d). Vimentin labeled not
only gp41-positive round or oval cells, but also spindle cells in the deeper
layers. However, spindle cells were not colabeled with anti-gp4l. UEA-I

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FIGURE 3 . ( u ) The affected vessels of the circle of Willis with anti-gp41 immunohistochemistry. Note
p ~ s ~ i i vcrlls
?
along the superficial intimal aspect and in the underlying fibroblastic areas. Focal brown
pigincnts are hemosiderin. ( L : lumen) P-galactosidase-X-gal system (blue). X 90. (a, inset) Gp41-positive
,,\.a1 cell x 360. (b) HAM-56 irnmunostaining of the artery with peroxidase-AEC system (red). Note
\imiIar distribution of positive cells to the gp41 immunostaining as in (a). ( L : lumen) X360. (c and d)
1)~iuble-immunostaining
of the artery with anti-gp41 (blue) and HAM-56 (red). Note the double-stained
rouncl and oval cells (c, X 180) and the double-labeled multinucleated cell (arrow) surrounded by scattered,
d(iubIr-staineJ mononuclear rells (d, X 360). X-gal and AEC.

CEREBRAL VASCULOPATHY IN PEDIATRIC AIDS

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showed endothelial staining, but no double-labeling with anti-gp4l. Results of
HZV and HSV immunohistochemistry (‘performed in two separate laboratories) on the arteries of the circle of Willis were negative.
In the cerebrum, gp41-positive cells were located predominantly in the
white matter and included perivascular mono- and caltinucleated cells. A
minority of intraparenchymal gp41-positive cells were dollhle-stained with
LCA. Small gp4l-positive round or rod-shaped cells were not colabeled with
LCA. Gp41-positive process-bearing cells were negative for GFAP; however,
RCA-I and HAM-56 were double-stained in some of these cells.

DISCUSSION
This type of aneurysmal arteriopathy of the circle of Willis, associated
with immunohistochemical demonstration of HIV related antigens in the affected arteries, has not been previously reported. Although other arteriopathies, such as “granulomatous angiitis,” have been reported (12) in patients with AIDS, the pathological findings are different from this case.
Arteriopathies somewhat resembling the present case have rarely been reported in patients with AIDS (5, 13, 14). Joshi et al. (5) described an arteriopathy affecting small and medium-sized arteries in various organs and
pointed to similarities with Kawasaki’s disease, but an arteriopathy involving
the large cerebral arteries like our case was not seen in their study. Multinucleated cells have also been described in cerebral arteriopathy in a patient with
AIDS (13). Cho et al. (14) reported in abstract a cerebral arteriopathy in both
children and adults with AIDS. Some of their cases had involvementLofthe
circle of Willis and were associated with cerebral infarcts, similar to the
present case; although affected vessels were usually the meningocerebral arteries. HIV immunohistochemistry has not been performed in any previous
studies of vascular disease in AIDS.
Immunostaining demonstrated gp4 1-positive cells within the involved artery, both in the organizing thrombi and the thickened intima. The gp41positive cells were colabeled with HAM-56 and rarely with LCA. The distribution of gp41-positive cells suggested that the cells in the superficial intima
might have been derived from hematogenous cells involved in ongoing thrombosis. Dual staining of gp41-positive cells with HAM-56 or LCA also supports
a hematogenous origin (macrophages, lymphocytes, or monocytes). Although
some of the vimentin positive cells, mostly round cells, were also labeled with
anti-gp41, they appeared to be macrophages, rather than mesenchymal elements, since they were also colabeled with HAM-56. Lastly, absence of immunostaining of the gp41-labeled cells with UEA-I makes HIV infection of endothelia unlikely.
Although a focus of acid fast bacilli was present in the intima of one of the

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K. KURE ET AL.

arteries, and mycobacteria may produce a cerebral angiitis, no other such foci
were present, and an aneurysmal arteriopathy such as this case has never been
described in MA1 infection to our knowledge. Furthermore, granulomatous
inflammation was absent, and MA1 was only clinically apparent in the last
hospitalization 1 month before the patient died. I n most previous reports of
MA1 involvement in the CNS in AIDS, MA1 has been an incidental finding
in lesions because of other factors. It would, thus, seem unlikely to be directly
involved in the arteriopathy in this case. Varicella zoster is also known to
produce cerebral arteritis (a), most commonly following infection of the ophthalmic division of the trigeminal nerve, but it has not been described following an uncomplicated varicella infection. Zoster mediated angiitis most commonly affects superficial leptomeningeal arteries producing concentric
fibromuscular intimal proliferation with characteristic Cowdry A type inclusions and occasional multinucleated giant cells. The present case showed no
viral inclusions or immunohistochemical evidence of HZV in the affected arteries. An unusual form of herpes zoster-mediated angiitis has been described
limited to basilar arteries of the brain in AIDS (Marc Rosenblum, personal
communication). Immunohistochemically, this HZV-mediated basilar arteritis demonstrates HZV antigen in smooth muscle of the affected arterial wall.
Similar immunostaining in our case was negative (Marc Rosenblum, personal
communication). Electron microscopic studies failed to show evidence of herpes virus or mycobacterial infection. O n the other hand, HIV was demonstrated in cells in the walls of the affected arteries, and multinucleated cells
with “nuclear bridges,” similar to previous reports of multinucleated cells in
subacute AIDS encephalitis (15), were documented in the intima with electron microscopy. Although one might speculate that HIV infection produced
the arteriopathy in the present case, there may be other explanations for HIV
antigens in the vessel wall. H I V may have infected arteries that were already
injured by other pathogens or exposure to elastases released from inflammatory cells in response to repeated bacterial infections (5). Finally, HIV may
have been carried in blood cells involved in thrombosis and/or thrombus organization.
Cerebral pathology in our case was characterized by bilateral multiple
cerebral infarcts of various histologic ages resulting from thrombosis of the
branches of the circle of Willis and by subacute AIDS encephalomyelitis.
Immunohistochemical staining with anti-gp4l revealed characteristic findings
of AIDS subacute encephalitis, namely, labeling of mono- and multinucleated
cells predominantly in perivascular spaces and deep white matter. Doubleinimunostaining with GFAP, RCA-I, and HAM-56 suggested that some of the
gp4 1-positive, process-bearing cells were microglia but not astrocytes. Similar
gp41-positive, process-bearing cells have been described in subacute AIDS
encephalitis in adults, and they also can be colabeled by either RCA-I or

CEREBRAL VASCULOPATHY IN PEDIATRIC AIDS

667

HAM-56 (16). The present case of cerebral aneurysmal arteriopathy, in addition to other reported features in pediatric AIDS, such as arterial calcification
in the basal ganglia, HIV-positive endothelia of the parenchymal arteries, and
other forms of systemic vasculopathies (17), is further support for the hypothesis that HIV infection may produce cerebral vasculopathies.

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15. Mizusawa H, Hirano A , Llena F. Nuclear bridges within multinucleated giant cells in subacute encephalitis of acquired immune deficiency syndrome (AIDS). Acta Neuropathol 1988:76:166-9.
16. Kure K, Lyman WD, Weidenheim KM, Dickson DW. Subacute AIDS encephalitis: Identification of
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Received February 2 7, 1989
Accepted June 19, 1989