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Related Experiment Videos

Mouse-human heterokaryons support efficient human immunodeficiency virus type 1 assembly.

R Mariani1, B A Rasala, G Rutter

  • 1Infectious Disease Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.

Journal of Virology
|March 10, 2001
PubMed
Summary

Murine cells cannot efficiently replicate human immunodeficiency virus type 1 (HIV-1) due to an assembly block. Introducing human cofactors partially restores replication, suggesting a missing factor in mouse cells for efficient HIV-1 assembly and release.

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Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Murine cells exhibit multiple blocks to human immunodeficiency virus type 1 (HIV-1) replication, including entry, proviral expression, and virion assembly.
  • Previous studies have shown that introducing human CD4, CCR5, or CXCR4 can overcome the entry block, and human cyclin T1 can enhance proviral expression in murine cells.
  • Despite overcoming entry and expression blocks, a significant block to HIV-1 virion assembly and spread persists in murine cells.

Purpose of the Study:

  • To investigate the permissiveness of various rodent cell lines, engineered to express human CD4, CCR5, and cyclin T1, for HIV-1 replication.
  • To elucidate the specific block to HIV-1 assembly and release in murine cells.
  • To identify potential cofactors required for efficient HIV-1 assembly and release in murine cells.

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Main Methods:

  • Established and analyzed a panel of rodent cell lines (including CHO, Rat2, EL4, L1-2, and Mus dunni fibroblasts) expressing human CD4, CCR5, and cyclin T1 for HIV-1 replication.
  • Utilized mouse-human heterokaryons to investigate the mechanisms underlying the block to HIV-1 assembly and release.
  • Assessed virion release, infectious virus production, proviral transcription, and synthesis of virion components in engineered cell lines and heterokaryons.

Main Results:

  • Rodent cell lines expressing human cofactors showed only partial permissiveness for HIV-1 replication, with significantly lower infectious virus production compared to human cells.
  • Mouse-human heterokaryons demonstrated a substantial increase (12-fold in virion release, 700-fold in infectious virus) in HIV-1 production, indicating complementation of a factor.
  • The increased virus release in heterokaryons was not attributed to enhanced proviral transcription or virion component synthesis, and reciprocal fusions suggested the absence of an assembly inhibitor in mouse cells.

Conclusions:

  • Murine cells possess a critical block to HIV-1 virion assembly and release, even when entry and expression factors are provided.
  • The fusion experiments strongly suggest that murine cells lack an essential cofactor required for efficient HIV-1 assembly and release.
  • Identifying this missing cofactor could provide new avenues for understanding HIV-1 replication and developing therapeutic strategies.