Neuropathogenesis of chimeric simian human immunodeficiency virus infection in rhesus macaques

S. Buch, D. Pinson, Y. Hou, I. Adany, Z. Li, S. Mukherjee, F. Jia, G. Mackay, P. Silverstein, A. Kumar, O. Narayan

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Comparative studies were performed to determine the neuropathogenesis of infection in macaques with simian human immunodeficiency virus (SHIV)89.6P and SHIV(KU). Both viruses utilize the CD4 receptor and CXCR4 co-receptor. However, in addition, SHIV89.6P uses the CCR5 co-receptor. Both agents are dual tropic for CD4+ T cells and blood-derived macrophages of rhesus macaques. Following inoculation into macaques, both caused rapid elimination of CD4+ T cells but they varied greatly in mechanisms of neuropathogenesis. Two animals infected with SHIV89.6P developed typical lentiviral encephalitis in which multinucleated giant cell formation, nodular accumulations of microglial cells, activated macrophages and astrocytes, and perivascular accumulations of mononuclear cells were present in the brain. Many of the macrophages in these lesions contained viral RNA. Three macaques infected with SHIV(KU) and killed on days 6, 11 and 18, respectively, developed a slowly progressive infection in the CNS but macrophages were not productively infected and there were no pathological changes in the brain. Two other animals infected with this virus and killed several months later showed minimal infection in the brain even though one of the two developed encephalitis of unknown etiology. The basic difference in the mechanisms of neuropathogenesis by the two viruses may be related to co-receptor usage. SHIV89.6P, in utilizing the CCR5 co-receptor, caused neuropathogenic effects that are similar to other neurovirulent primate lentiviruses. (C) Munksgaard, Copenhagen.

Original languageEnglish (US)
Pages (from-to)96-106
Number of pages11
JournalJournal of medical primatology
Volume29
Issue number3-4
StatePublished - Jan 1 2000

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Simian Immunodeficiency Virus
HIV infections
Virus Diseases
Macaca mulatta
Macaca
Macrophages
CCR5 Receptors
HIV
Human immunodeficiency virus
macrophages
receptors
Encephalitis
Viruses
encephalitis
Brain
brain
Primate Lentiviruses
Infection
viruses
CXCR4 Receptors

Keywords

  • AIDS
  • CNS
  • Macrophages

ASJC Scopus subject areas

  • Animal Science and Zoology
  • veterinary(all)

Cite this

Buch, S., Pinson, D., Hou, Y., Adany, I., Li, Z., Mukherjee, S., ... Narayan, O. (2000). Neuropathogenesis of chimeric simian human immunodeficiency virus infection in rhesus macaques. Journal of medical primatology, 29(3-4), 96-106.

Neuropathogenesis of chimeric simian human immunodeficiency virus infection in rhesus macaques. / Buch, S.; Pinson, D.; Hou, Y.; Adany, I.; Li, Z.; Mukherjee, S.; Jia, F.; Mackay, G.; Silverstein, P.; Kumar, A.; Narayan, O.

In: Journal of medical primatology, Vol. 29, No. 3-4, 01.01.2000, p. 96-106.

Research output: Contribution to journalArticle

Buch, S, Pinson, D, Hou, Y, Adany, I, Li, Z, Mukherjee, S, Jia, F, Mackay, G, Silverstein, P, Kumar, A & Narayan, O 2000, 'Neuropathogenesis of chimeric simian human immunodeficiency virus infection in rhesus macaques', Journal of medical primatology, vol. 29, no. 3-4, pp. 96-106.
Buch, S. ; Pinson, D. ; Hou, Y. ; Adany, I. ; Li, Z. ; Mukherjee, S. ; Jia, F. ; Mackay, G. ; Silverstein, P. ; Kumar, A. ; Narayan, O. / Neuropathogenesis of chimeric simian human immunodeficiency virus infection in rhesus macaques. In: Journal of medical primatology. 2000 ; Vol. 29, No. 3-4. pp. 96-106.
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