Susceptibility of rat-derived cells to replication by human immunodeficiency virus type 1

J Virol. 2001 Sep;75(17):8063-73. doi: 10.1128/jvi.75.17.8063-8073.2001.

Abstract

Progress in developing a small animal model of human immunodeficiency virus type 1 (HIV-1) disease would greatly facilitate studies of transmission, pathogenesis, host immune responses, and antiviral strategies. In this study, we have explored the potential of rats as a susceptible host. In a single replication cycle, rat cell lines Rat2 and Nb2 produced infectious virus at levels 10- to 60-fold lower than those produced by human cells. Rat-derived cells supported substantial levels of early HIV-1 gene expression, which was further enhanced by overexpression of human cyclin T1. Rat cells displayed quantitative, qualitative, and cell-type-specific limitations in the late phase of the HIV-1 replication cycle including relative expression levels of HIV-1 Gag proteins, intracellular Gag processing, and viral egress. Nb2 cells were rendered permissive to HIV-1 R5 viruses by coexpression of human CD4 and CCR5, indicating that the major restriction on HIV-1 replication was at the level of cellular entry. We also found that primary rat lymphocytes, macrophages, and microglia expressed considerable levels of early HIV-1 gene products following infection with pseudotyped HIV-1. Importantly, primary rat macrophages and microglia, but not lymphocytes, also expressed substantial levels of HIV-1 p24 CA and produced infectious virions. Collectively, these results identify the rat as a promising candidate for a transgenic small animal model of HIV-1 infection and highlight pertinent cell-type-specific restrictions that are features of this species.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • CD4 Antigens / metabolism
  • Cell Line
  • Cells, Cultured
  • Cyclin T
  • Cyclins / metabolism
  • Disease Models, Animal
  • HIV Infections / virology*
  • HIV Long Terminal Repeat / physiology
  • HIV-1 / genetics
  • HIV-1 / physiology*
  • Humans
  • Macrophages / virology*
  • Membrane Glycoproteins*
  • Mice
  • Microglia / virology*
  • Rats
  • Receptors, CCR5 / metabolism
  • T-Lymphocytes / virology*
  • Viral Envelope Proteins / genetics
  • Viral Envelope Proteins / metabolism
  • Viral Proteins / genetics
  • Viral Proteins / metabolism
  • Virus Replication*

Substances

  • CCNT1 protein, human
  • CD4 Antigens
  • Ccnt1 protein, mouse
  • Ccnt1 protein, rat
  • Cyclin T
  • Cyclins
  • G protein, vesicular stomatitis virus
  • Membrane Glycoproteins
  • Receptors, CCR5
  • Viral Envelope Proteins
  • Viral Proteins