A model with both casual and long-term partnerships is considered with respect to the impact of a pre-exposure prophylaxis (PrEP) on the spread of HIV. We consider the effect of the effectiveness of PrEP, the rate that susceptible individuals choose to take PrEP, and compliance with the daily dose of the pre-exposure prophylaxis. The rate of infection in long-term partnerships is computed using a linearized expected value as a means for including the nonlocal effects of long-term partnerships while maintaining computational feasibility. The reproduction numbers for models with casual partnerships, long-term partnerships, and a combination of both are analytically computed and global stability of both disease-free and endemic equilibria is shown. Sensitivity and PRCC analysis results suggest that increasing the compliance among the current PrEP users is a more effective strategy in the fight against the HIV epidemic than increased coverage with poor compliance. Furthermore, an analysis of the reproduction number shows that models with either casual or monogamous long-term partnerships can reach the desired $ R_0 < 1 $ threshold for high enough levels of compliance and uptake, however, a model with both casual and monogamous long-term partnerships will require additional interventions. Methods highlighted in this manuscript are applicable to other incurable diseases or diseases with imperfect vaccines effected by long-term partnerships.
The transmission dynamics of HIV are closely tied to the duration and overlap of sexual partnerships. We develop an autonomous population model that can account for the possibilities of an infection from either a casual sexual partner or a long-term partner who was either infected at the start of the partnership or has been newly infected since the onset of the partnership. The impact of the long-term partnerships on the rate of infection is captured by calculating the expected values of the rate of infection from these extended contacts. The model includes three stages of infectiousness: acute, chronic, and virally suppressed. We calculate HIV incidence and the fraction of new infections attributed to casual contacts and long-term partnerships allowing for variability in condom usage, the effect of achieving and maintaining viral suppression, and early intervention by beginning HAART during the acute phase of infection. We present our results using data on MSM HIV transmission from the CDC in the U.S. While the acute stage is the most infectious, the majority of the new infections will be transmitted by long-term partners in the chronic stage when condom use is infrequent as is common in long-term relationships. Time series analysis of the solution, as well as parameter sensitivity analysis, are used to determine effective intervention strategies.
more » « less- Award ID(s):
- 2000044
- NSF-PAR ID:
- 10406674
- Publisher / Repository:
- Springer Science + Business Media
- Date Published:
- Journal Name:
- Journal of Mathematical Biology
- Volume:
- 86
- Issue:
- 5
- ISSN:
- 0303-6812
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract Background Brain tissue-derived extracellular vesicles (bdEVs) act locally in the central nervous system (CNS) and may indicate molecular mechanisms in human immunodeficiency virus (HIV) CNS pathology. Using brain homogenate (BH) and bdEVs from a simian immunodeficiency virus (SIV) model of HIV disease, we identified RNA networks in SIV infection and neuroinflammation.
Methods Postmortem occipital cortex samples were obtained from uninfected controls and SIV-infected subjects (acute and chronic phases with or without CNS pathology [SIV encephalitis]). bdEVs were separated and characterized per international consensus guidelines. RNAs from bdEVs and BH were sequenced and quantitative polymerase chain reaction (qPCR)-amplified to detect levels of small RNAs (sRNAs, including microRNAs [miRNAs]) and longer RNAs including messenger RNAs (mRNAs) and circular RNAs (circRNAs).
Results Dysregulated RNAs in BH and bdEVs were identified in acute and chronic infection with pathology groups, including mRNAs, miRNAs, and circRNAs. Most dysregulated mRNAs in bdEVs reflected dysregulation in source BH. These mRNAs are disproportionately involved in inflammation and immune responses. Based on target prediction, several circRNAs that were differentially abundant in source tissue might be responsible for specific differences in sRNA levels in bdEVs during SIV infection.
Conclusions RNA profiling of bdEVs and source tissues reveals potential regulatory networks in SIV infection and SIV-related CNS pathology.
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