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Decoding HIV-1 Next Move Through Matrix Protein p17 Quasi-Species.

Serena Messali1,2, Anna Bertelli2, Marta Giovanetti3,4

  • 1Section of Microbiology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.

Microbiologyopen
|April 3, 2026
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Summary
This summary is machine-generated.

HIV-1 matrix protein p17 variants (vp17s) with specific insertions promote lymphoma in people living with HIV (PLWHIV). The prevalence of these vp17s is increasing globally, even at the quasi-species level.

Keywords:
AIDS‐related lymphomasHIV‐1 matrix protein p17HIV‐1 mutantsclonogenic p17 variantsviral quasi‐speciesvirus evolution

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Area of Science:

  • Virology
  • Immunology
  • Oncology

Background:

  • Acquired immune deficiency syndrome (AIDS)-related lymphomas are a growing cause of death in people living with HIV (PLWHIV).
  • HIV-1 proteins, particularly matrix protein p17 (refp17), contribute to lymphoma development by affecting immune cell function.
  • Specific p17 variants (vp17s) with C-terminal insertions induce B-cell growth and are more prevalent in PLWHIV with lymphoma.

Purpose of the Study:

  • To investigate the prevalence and evolution of vp17 quasi-species in PLWHIV.
  • To understand the role of vp17 variants in the pathogenesis of AIDS-related lymphomas.
  • To identify evolutionary drivers of p17 adaptation in the human host.

Main Methods:

  • Utilized next-generation sequencing to analyze vp17 quasi-species frequency over time in PLWHIV.
  • Developed a regression model to predict the fixation probability of specific vp17 insertions.
  • Compared vp17 prevalence in PLWHIV with and without lymphoma.

Main Results:

  • The incidence of vp17s increases over time and at the quasi-species level in PLWHIV.
  • vp17s are significantly more prevalent in PLWHIV diagnosed with lymphoma.
  • The regression model identified specific C-terminal insertions with a higher probability of evolutionary fixation.

Conclusions:

  • HIV-1 mutants expressing clonogenic vp17s are spreading globally, contributing to lymphoma development.
  • The C-terminal region of p17 is crucial for its adaptation to the human host, influencing viral evolution.
  • Understanding vp17 quasi-species dynamics is vital for managing AIDS-related lymphomas in PLWHIV.