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J Virol, May 1998, p. 3980-3990, Vol. 72, No. 5
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Natural Isolates of Simian Virus 40 from
Immunocompromised Monkeys Display Extensive Genetic Heterogeneity: New
Implications for Polyomavirus Disease
John A.
Lednicky,1
Amy S.
Arrington,1
A. Renee
Stewart,1
Xian Min
Dai,1
Connie
Wong,1
Sanjeeda
Jafar,1
Michael
Murphey-Corb,2,
and
Janet S.
Butel1,*
Division of Molecular Virology, Baylor
College of Medicine, Houston, Texas 77030,1 and
Tulane Regional Primate Research Center, Covington, Louisiana
704332
Received 6 November 1997/Accepted 10 February 1998
Simian virus 40 (SV40) DNAs in brain tissue and peripheral blood
mononuclear cells (PBMCs) of eight simian immunodeficiency virus-infected rhesus monkeys with SV40 brain disease were analyzed. We
report the detection, cloning, and identification of five new SV40
strains following a quadruple testing-verification strategy. SV40
genomes with archetypal regulatory regions (containing a duplication
within the G/C-rich regulatory region segment and a single 72-bp
enhancer element) were recovered from seven animal brains, two tissues
of which also contained viral genomes with nonarchetypal regulatory
regions (containing a duplication within the G/C-rich regulatory region
segment as well as a variable duplication within the enhancer region).
In contrast, PBMC DNAs from five of six animals had viral genomes with
both regulatory region types. It appeared, based on T-antigen
variable-region sequences, that nonarchetypal virus variants arose de
novo within each animal. The eighth animal exclusively yielded a new
type of SV40 strain (SV40-K661), containing a protoarchetypal
regulatory region (lacking a duplication within the G/C-rich segment of
the regulatory region and containing one 72-bp element in the enhancer
region), from both brain tissue and PBMCs. The presence of SV40 in
PBMCs suggests that hematogenous spread of viral infection may occur.
An archetypal version of a virus similar to SV40 reference strain 776 (a kidney isolate) was recovered from one brain, substantiating the
idea that SV40 is neurotropic as well as kidney-tropic. Indirect
evidence suggests that maternal-infant transmission of SV40 may have
occurred in one animal. These findings provide new insights for human
polyomavirus disease.
*
Corresponding author. Mailing address: Division of
Molecular Virology, Baylor College of Medicine, One Baylor Plaza,
Houston, TX 77030. Phone: (713) 798-3003. Fax: (713) 798-5019. E-mail: jbutel{at}bcm.tmc.edu.

Present address: Department of Molecular Genetics and Biochemistry,
University of Pittsburgh School of Medicine, Pittsburgh,
PA 15261.
J Virol, May 1998, p. 3980-3990, Vol. 72, No. 5
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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