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Nucleotide substitutions in the long terminal repeat are not required for development of neurovirulence by simian

E B Stephens1, M Sahni, K Leung

  • 1Department of Microbiology, Molecular Genetics and Immunology, Marion Merrell Dow Laboratory of Viral Pathogenesis, University of Kansas Medical Center, Kansas City 66160-7240, USA. estephen@kumc.edu

The Journal of General Virology
|May 29, 1998
PubMed

Insights

This study investigated simian immunodeficiency virus (SIV) long terminal repeat (LTR) substitutions and neurovirulence. Results indicate LTR sequences are virtually identical in neurovirulent and non-neurovirulent SIV, suggesting LTRs do not affect tissue tropism.

Area of Science:

  • Virology
  • Molecular Biology
  • Neuroscience

Background:

  • The simian immunodeficiency virus (SIV) long terminal repeat (LTR) is a key regulatory region.
  • Understanding SIV LTR's role in neurovirulence is crucial for studying lentiviral pathogenesis.
  • Previous studies have not definitively linked LTR nucleotide substitutions to SIV-induced encephalitis.

Purpose of the Study:

  • To investigate whether consensus nucleotide substitutions in the SIVmac LTR region impact neurovirulence.
  • To compare LTR sequences from neurovirulent and non-neurovirulent SIVmac strains.
  • To determine if LTR sequence variations correlate with SIV-induced encephalitis in macaques.

Main Methods:

  • Analysis of brain and lymph node tissues from macaques inoculated with SIVmac.
  • Amplification, cloning, and sequencing of the 5' LTR regions from viral isolates.
  • Comparison of LTR sequences between neurovirulent (SIVmacR71/17E, SIVmac7F-Lu) and non-neurovirulent (SIVmac239) strains.

Main Results:

  • Neurovirulent SIVmacR71/17E had three LTR consensus substitutions, while SIVmac7F-Lu had none compared to SIVmac239.
  • A single common T to C substitution at position 829 in the LTR-gag region was observed in all viruses, including SIVmac239.
  • LTR sequences from brain and lymph nodes were identical within infected animals and showed minimal variation between neurovirulent and non-neurovirulent viruses.

Conclusions:

  • The LTR region shows virtual identity between neurovirulent and non-neurovirulent SIVmac strains.
  • The analyzed LTR nucleotide substitutions, including the T to C change at position 829, do not appear to influence SIV tissue tropism or neurovirulence.
  • These findings suggest that factors other than LTR sequence variation are primarily responsible for SIV-induced encephalitis.

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