bioRxiv ScienceSearch

Biology subjects

Goodreau, S.

Publications and source records attributed to Goodreau, S..

2 recordsLinked to original sources

Agent-based network model predicts strong benefits to youth-centered HIV treatment-as-prevention efforts

We used an agent-based network model to examine the effect of targeting different risk groups with unsuppressed HIV viral load for linkage or re-linkage to HIV-related treatment services in a heterosexual population with annual testing. Our model identifies prevention strategies that can reduce incidence to negligible levels (i.e., less than 0.1 infections per 100 person-years) 20 years after a targeted Treatment-as-Prevention (TasP) campaign. The model assumes that most (default 95%) of the population is reachable (i.e., could, in principle, be linked to effective care) and a modest (default 5% per year) probability of a treated person dropping out of care. Under random allocation or CD4-based targeting, the default version of our model predicts that the TasP campaign would need to suppress viral replication in ~80% of infected people to halt the epidemic. Under age-based strategies, by contrast, this percentage drops to 50% to 60% (for strategies targeting those <30 and <25, respectively). Age-based targeting did not need to be highly exclusive to yield significant benefits; e.g. the scenario that targeted those <25 years old saw ~80% of suppressed individuals fall outside the target group. This advantage to youth-based targeting remained in sensitivity analyses in which key age-related risk factors were eliminated one by one. As testing rates increase in response to UNAIDS 90-90-90 goals, we suggest that efforts to link all young people to effective care could be an effective long-term method for ending the HIV epidemic. Linking greater numbers of young people to effective care will be critical for developing countries in which a demographic \"youth bulge\" is starting to increase the number of young people at risk for HIV infection.

epidemiology

HIV population-level adaptation can rapidly diminish the impact of a partially effective vaccine

Development of an HIV vaccine is essential to ending the HIV/AIDS pandemic. However, vaccines can result in the emergence and spread of vaccine-resistant strains. Indeed, analyses of breakthrough infections in the HIV vaccine trial RV144 identified HIV genotypes with differential rates of transmission in vaccine and placebo recipients. We hypothesized that, for HIV vaccination programs based on partially effective vaccines similar to RV144, HIV adaptation will diminish the expected vaccine impact. Using two HIV epidemic models, we simulated large-scale vaccination programs and, critically, included HIV strain diversity with respect to the vaccine response. We show here that rapid population-level viral adaptation can lead to decreased overall vaccine efficacy and substantially fewer infections averted by vaccination, when comparing scenarios with and without viral evolution (depending on vaccination coverage, vaccine efficacy against the sensitive allele, and the initial resistant allele frequency). Translating this to the epidemic in South Africa, a scenario with 70% vaccination coverage may result in 250,000 new infections within 10 years of vaccine rollout that are due solely to HIV adaptation, all else being equal. These findings suggest that approaches to HIV vaccine development, program implementation, and epidemic modeling may require attention to viral evolutionary responses to vaccination.

evolutionary biology