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HIV-1-induced AIDS in monkeys.

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Adapting human immunodeficiency virus type 1 (HIV-1) in macaques enabled it to overcome host restrictions and cause AIDS. Early immune modulation drastically altered disease progression, highlighting factors in AIDS pathogenesis.

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Area of Science:

  • Virology
  • Immunology
  • Primate Models

Background:

  • Primate lentiviruses have narrow host tropism, limiting zoonoses but hindering AIDS animal model development.
  • Understanding HIV-1 cross-species transmission barriers is crucial for developing effective interventions and models.

Purpose of the Study:

  • To investigate factors limiting cross-species human immunodeficiency virus type 1 (HIV-1) transmission.
  • To adapt HIV-1 in a macaque model to overcome host restriction factors and study AIDS pathogenesis.

Main Methods:

  • Passaging a modified HIV-1 in pigtailed macaques with transient CD8(+) cell depletion during acute infection.
  • Monitoring viral adaptation, replication levels, and host immune responses over four passages.

Main Results:

  • HIV-1 adapted to antagonize macaque tetherin, a key restriction factor.
  • Adapted HIV-1 replicated at higher levels, causing significant CD4(+) T cell depletion and AIDS-defining conditions.
  • Transient CD8(+) cell depletion during acute infection led to rapid AIDS progression, unlike untreated controls exhibiting an elite controller phenotype.

Conclusions:

  • An adapted HIV-1 strain can induce AIDS in macaques, demonstrating the potential for zoonosis.
  • Early immunological perturbations, such as CD8(+) cell depletion, profoundly influence HIV-1 disease progression and outcome.