Human immunodeficiency virus type 1 derivative with 7% simian immunodeficiency virus genetic content is able to

Tatsuhiko Igarashi1, Ranjini Iyengar, Russel A Byrum

  • 1Laboratory of Molecular Microbiology, NIAID, NIH, Bldg. 4, Room 315, 4 Center Drive, MSC 0460, Bethesda, MD 20892-0460, USA.

Journal of Virology
|August 3, 2007
PubMed

Insights

This study investigated a novel human immunodeficiency virus type 1 (HIV-1) derivative in macaques. The virus showed replication but did not induce disease, indicating a need for further adaptation for in vivo infectivity.

Area of Science:

  • Virology
  • Immunology
  • Primate models

Background:

  • A novel human immunodeficiency virus type 1 (HIV-1) derivative, HIV(NL-DT5R), was created using simian immunodeficiency virus (SIV) genetic material.
  • This derivative was previously shown to infect macaque peripheral blood mononuclear cells in vitro.

Purpose of the Study:

  • To evaluate the in vivo replicative capacity and disease-inducing potential of the HIV(NL-DT5R) derivative.
  • To determine if the chimeric virus could establish a persistent infection and cause pathogenesis in a relevant animal model.

Main Methods:

  • Pig-tailed macaques were inoculated with the HIV(NL-DT5R) derivative.
  • Plasma viremia, humoral immune responses, and CD4(+) T-lymphocyte counts were monitored.
  • Clinical signs of disease were assessed.

Main Results:

  • All inoculated macaques developed plasma viremia after HIV(NL-DT5R) infection.
  • Humoral immune responses against HIV-1 structural proteins were detected in all animals.
  • No significant CD4(+) T-lymphocyte depletion or clinical disease was observed.

Conclusions:

  • The HIV(NL-DT5R) derivative can replicate and elicit an immune response in vivo in pig-tailed macaques.
  • The current construct does not induce significant pathogenesis or CD4(+) T-lymphocyte depletion.
  • Further adaptation of the virus is necessary to enhance its in vivo infectivity and disease-inducing potential.