One of the dreaded features of an Human Immunodeficiency Virus (HIV) infection can be the possible rebound of the virus after undergoing an otherwise successful antiretroviral (ART) regimen. Understanding the viral replication and dramatic growth that sometimes appears subsequent to ART treatment is the subject of a new study by scientists from Los Alamos National Laboratory and the National Institutes of Health’s National Institute of Allergy and Infectious Diseases.
The virologists have defined the principles governing whether HIV-1 spread among cells fails or becomes established by coupling stochastic modelling with laboratory experiments. HIV-1 is the most common and pathogenic strain of the virus (one of the challenges for the treatment of the human immunodeficiency virus is its high genetic variability).
The formerly suppressed cells are rare, according to study co-author Alan Perelson of Los Alamos’s Theoretical Division; however, occasionally cells rebound with exponential growth, in situations where the virus manages to exceed a particular, critical population size.
The researchers note that if a single infected cell produces virus, this virus just might infect a nearby cell, which might eventually result in a sustained chain reaction of infection spread. Alternatively, viral extinction may occur at any early step. The process is highly random (stochastic), posing challenges for experimental capture and analysis.
The mathematics behind the new analysis were performed at Los Alamos, in the Theoretical Biology and Biophysics group, seeking to define the crucial transition from latency to exponential spread and to document the probability of establishing exponential viral growth.
The research paper was published in the journal Cell Host & Microbe on November 21, 2019, and it is titled “Principles Governing Establishment versus Collapse of HIV-1 Cellular Spread.”
