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Why does age at HIV infection correlate with set point viral load? An evolutionary hypothesis
Steven M Goodreau1, Sarah E Stansfield2, John E Mittler3
1Departments of Anthropology & Epidemiology, University of Washington, Seattle, WA 98195, USA.
Epidemics
|September 26, 2022
Summary
Older age at HIV acquisition is linked to higher viral loads due to selection bottlenecks, not just immunosenescence. Behavioral factors significantly influence this age-related increase in set-point viral load (SPVL).
Area of Science:
- Virology
- Epidemiology
- Evolutionary Biology
Background:
- Set-point viral load (SPVL) in HIV correlates with acquisition age.
- Immunosenescence is an insufficient explanation for age-SPVL relationship, especially when source partner SPVL is considered.
- An alternative hypothesis suggests age-related decreasing acquisition risk creates a selection bottleneck favoring more virulent HIV strains.
Purpose of the Study:
- To investigate the relationship between age at HIV acquisition and SPVL in men who have sex with men (MSM).
- To test the hypothesis that a selection bottleneck, driven by age-related changes in acquisition risk and behavior, influences SPVL.
- To evaluate the impact of behavioral and clinical parameters on the age-SPVL correlation.
Main Methods:
- Adapted the EvoNetHIV model for MSM.
- Conducted simulation experiments varying seven behavioral/clinical parameters.
- Performed regressions to assess SPVL increase per decade of seroconversion age, with and without source SPVL.
Main Results:
- Significant age-SPVL relationships were observed when source SPVL was excluded.
- Including source SPVL attenuated these relationships significantly.
- Behavioral factors like relational duration, age homophily, coital frequency, and age at relationship formation impacted the relationship as hypothesized.
- Combined behavioral heterogeneity resulted in a 0.056 log10 copies/mL SPVL increase per decade of seroconversion age.
Conclusions:
- Higher HIV virulence in later-life infections can be attributed to selective bottlenecks and age-related behavioral heterogeneity.
- Variations in this effect across populations may stem from differing behavioral, epidemiological, and clinical conditions, rather than solely immunosenescence patterns.
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