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Journal of Virology, August 2000, p. 6935-6945, Vol. 74, No. 15
0022-538X/00/$04.00+0
Short- and Long-Term Clinical Outcomes in Rhesus Monkeys
Inoculated with a Highly Pathogenic Chimeric Simian/Human
Immunodeficiency Virus
Yasuyuki
Endo,1
Tatsuhiko
Igarashi,1
Yoshiaki
Nishimura,1
Charles
Buckler,1
Alicia
Buckler-White,1
Ronald
Plishka,1
Dimiter S.
Dimitrov,2 and
Malcolm
A.
Martin1,*
Laboratory of Molecular Microbiology, National Institute of
Allergy and Infectious Diseases, National Institutes of Health,
Bethesda, Maryland 20892-0460,1 and
Laboratory of Experimental and Computational Biology,
National Cancer Institute, National Institutes of Health, Frederick,
Maryland 217022
Received 29 February 2000/Accepted 9 May 2000
A highly pathogenic simian/human immunodeficiency virus (SHIV),
SHIVDH12R, isolated from a rhesus macaque that had been
treated with anti-human CD8 monoclonal antibody at the time of primary infection with the nonpathogenic, molecularly cloned
SHIVDH12, induced marked and rapid CD4+ T cell
loss in all rhesus macaques intravenously inoculated with 1.0 50%
tissue culture infective dose (TCID50) to 4.1 × 105 TCID50s of virus. Animals inoculated with
650 TCID50s of SHIVDH12R or more experienced
irreversible CD4+ T lymphocyte depletion and developed
clinical disease requiring euthanasia between weeks 12 and 23 postinfection. In contrast, the CD4+ T-cell numbers in four
of five monkeys receiving 25 TCID50s of SHIVDH12R or less stabilized at low levels, and these
surviving animals produced antibodies capable of neutralizing
SHIVDH12R. In the fifth monkey, no recovery from the
CD4+ T cell decline occurred, and the animal had to be
euthanized. Viral RNA levels, subsequent to the initial peak of
infection but not at peak viremia, correlated with the virus inoculum
size and the eventual clinical course. Both initial infection rate constants, k, and decay constants, d, were
determined, but only the latter were statistically correlated to
clinical outcome. The attenuating effects of reduced inoculum size were
also observed when virus was inoculated by the mucosal route. Because
the uncloned SHIVDH12R stock possessed the genetic
properties of a lentivirus quasispecies, we were able to assess the
evolution of the input virus swarm in animals surviving the acute
infection by monitoring the emergence of neutralization escape viral variants.
*
Corresponding author. Mailing address: Laboratory of
Molecular Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Bldg. 4, Rm. 315, 4 Ctr. Dr., MSC 0460, Bethesda, MD
20892-0460. Phone: (301) 496-4012. Fax: (301) 402-0226. E-mail: mmartin{at}niaid.nih.gov.
Journal of Virology, August 2000, p. 6935-6945, Vol. 74, No. 15
0022-538X/00/$04.00+0
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