Products of Compartmental Models in Epidemiology.

We show that many structured epidemic models may be described using a straightforward product structure in this paper. Such products, derived from products of directed graphs, may represent useful refinements including geographic and demographic structure, age structure, gender, risk groups, or immunity status. Extension to multistrain dynamics, that is, pathogen heterogeneity, is also shown to be feasible in this framework. Systematic use of such products may aid in model development and exploration, can yield insight, and could form the basis of a systematic approach to numerical structural sensitivity analysis

On a Two-Sex Model for Gonorrhea Transmission Dynamics Incorporating Treatment and Condom Use

In  this study we  developed a two sex model for gonorrhea transmission dynamics incorporating treatment and condom use as control measures using a system of ordinary differential equations. We further derive an epidemic threshold as the effective reproduction number,  using the next generation method. We established both the disease-free equilibrium and endemic equilibrium states using the linearization method and the manifold theory respectively. From the analysis of the model and results, it was shown that, the disease free equilibrium state is locally and asymptotically stable if  The implication is that gonorrhea can be eliminated fro the population if the effective reproduction number, is less than unity. The endemic equilibrium state is locally and asymptotically stable for  and this implies that gonorrhea disease can spread and there could disease persistence. Key words: Gonorrhea disease, effective reproduction number, equilibrium state, centre manifold theory

Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa

<p>Abstract</p> <p>Background</p> <p>The cause of the high HIV prevalence in sub-Saharan Africa is incompletely understood, with heterosexual penile-vaginal transmission proposed as the main mechanism. Heterosexual HIV transmission has been estimated to have a very low probability; but effects of cofactors that vary in space and time may substantially alter this pattern.</p> <p>Methods</p> <p>To test the effect of individual variation in the HIV infectiousness generated by co-infection, we developed and analyzed a mathematical sexual network model that simulates the behavioral components of a population from Malawi, as well as the dynamics of HIV and the co-infection effect caused by other infectious diseases, including herpes simplex virus type-2, gonorrhea, syphilis and malaria.</p> <p>Results</p> <p>The analysis shows that without the amplification effect caused by co-infection, no epidemic is generated, and HIV prevalence decreases to extinction. But the model indicates that an epidemic can be generated by the amplification effect on HIV transmission caused by co-infection.</p> <p>Conclusion</p> <p>The simulated sexual network demonstrated that a single value for HIV infectivity fails to describe the dynamics of the epidemic. Regardless of the low probability of heterosexual transmission per sexual contact, the inclusion of individual variation generated by transient but repeated increases in HIV viral load associated with co-infections may provide a biological basis for the accelerated spread of HIV in sub-Saharan Africa. Moreover, our work raises the possibility that the natural history of HIV in sub-Saharan Africa cannot be fully understood if individual variation in infectiousness is neglected.</p

THE ROLE OF CO-INFECTION IN THE SPREAD OF HIV IN SUB-SAHARAN AFRICA

The cause of the high HIV prevalence in sub-Saharan Africa is incompletely understood, with heterosexual penile-vaginal transmission proposed as the main mechanism. Heterosexual HIV transmission has a very low probability; further, a single estimation of heterosexual probability of HIV transmission fails to reproduce the variation associated with important biological cofactors. In particular, studies of HIV incidence suggest that co-infection with other infectious diseases influence the HIV transmission, and therefore might substantially vary the pattern of the spread of the infection. To assess the effect of co-infection on the spread of HIV, I developed and analyzed several mathematical and statistical models based on published data. The results show that despite the low probability of heterosexual transmission per sexual contact, the inclusion of individual variation generated by transient but repeated increases in HIV viral load associated with co-infections may provide a biological basis for the accelerated spread of HIV in sub-Saharan Africa, and raises the possibility that that the natural history of HIV in sub-Saharan Africa cannot be fully understood if individual variation in infectiousness is neglected. Co-infection might be a key explanatory variable for the rapid spread of HIV infection in sub-Saharan Africa; in fact, co-infection may be a necessary factor, rather than merely being a contributing factor, in the successful spread and survival of HIV in populations where heterosexual vaginal-penile contact is the main mechanism of transmission. Consequently, broad population based control strategies to decrease infectivity and reduce the incidence of other sexual and parasitic infectious diseases might be effective strategies in diminishing the spread of HIV in sub-Saharan Africa

Implementation of and Early Outcomes From Anal Cancer Screening at a Community-Engaged Health Care Facility Providing Care to Nigerian Men Who Have Sex With Men.

PurposeAnal cancer risk is substantially higher among HIV-infected men who have sex with men (MSM) as compared with other reproductive-age adults, but screening is rare across sub-Saharan Africa. We report the use of high-resolution anoscopy (HRA) as a first-line screening tool and the resulting early outcomes among MSM in Abuja, Nigeria.MethodsFrom August 2016 to August 2017, 424 MSM enrolled in an anal cancer screening substudy of TRUST/RV368, a combined HIV prevention and treatment cohort. HRA-directed biopsies were diagnosed by histology, and ablative treatment was offered for high-grade squamous intraepithelial lesions (HSIL). HRA proficiency was assessed by evaluating the detection of squamous intraepithelial lesions (SIL) over time and the proportion biopsied. Prevalence estimates of low-grade squamous intraepithelial lesions and HSIL with 95% CIs were calculated. Multinomial logistic regression was used to identify those at the highest risk of SIL.ResultsMedian age was 25 years (interquartile range [IQR], 22-29), median time since sexual debut was 8 years (IQR, 4-12), and 59% (95% CI, 54.2% to 63.6%) were HIV infected. Rate of detection of any SIL stabilized after 200 screenings, and less than 20% had two or more biopsies. Preliminary prevalence estimates of low-grade squamous intraepithelial lesions and HSIL were 50.0% (95% CI, 44.7% to 55.3%) and 6.3% (95% CI, 4.0% to 9.3%). HIV infection, at least 8 years since anal coital debut, concurrency, and external warts were independently statistically associated with SIL.ConclusionProficiency with HRA increased with experience over time. However, HSIL detection rates were low, potentially affected by obstructed views from internal warts and low biopsy rates, highlighting the need for ongoing evaluation and mentoring to validate this finding. HRA is a feasible first-line screening tool at an MSM-friendly health care facility. Years since anal coital debut and external warts could prioritize screening

Sex Transm Dis

BackgroundSexually transmitted infections (STIs) are associated with an increased risk of HIV acquisition and transmission. We estimated the proportion of HIV incidence among men who have sex with men attributable to infection with the two most common bacterial STIs, Neisseria gonorrhoeae (NG) and Chlamydia trachomatis (CT).MethodsWe used a stochastic, agent-based model of a sexual network of MSM with co-circulating HIV, NG, and CT infections. Relative risk (RR) multipliers, specific to anatomic site of infection, modified the risk of HIV transmission and acquisition based on STI status. We estimated the effect of NG and CT on HIV incidence overall and on HIV acquisition and HIV transmission separately. Each scenario was simulated for ten years. The population attributable fraction (PAF) was determined for each combination of RRs by comparing the incidence in the final year of a scenario to a scenario in which the RRs associated with NG and CT were set to 1.0.ResultsOverall, 10.4% (IQR: 7.9,12.4) of HIV infections were attributable to NG/CT infection. Then in sensitivity analyses, the PAF for HIV transmission ranged from 3.1% (IQR: 0.5, 5.2) to 20.4% (IQR: 17.8, 22.5) and the PAF for HIV acquisition ranged from 2.0% (IQR: 120.7, 4.3) to 13.8% (IQR: 11.7, 16.0).ConclusionsDespite challenges in estimating the causal impact of NG/CT on HIV risk, modeling is an alternative approach to quantifying plausible ranges of effects given uncertainty in the biological co-factors. Our estimates represent idealized public health interventions in which STI could be maximally prevented, setting targets for real-world STI interventions that seek to reduce HIV incidence.R01 AI138783/AI/NIAID NIH HHS/United StatesP30 AI050409/AI/NIAID NIH HHS/United StatesR01 HD068395/HD/NICHD NIH HHS/United StatesCC999999/ImCDC/Intramural CDC HHS/United StatesU38 PS004646/PS/NCHHSTP CDC HHS/United StatesR21 HD075662/HD/NICHD NIH HHS/United StatesR21 MH112449/MH/NIMH NIH HHS/United StatesR24 HD042828/HD/NICHD NIH HHS/United States2020-06-01T00:00:00Z31095100PMC65304907736vault:3226

Genital Herpes Has Played a More Important Role than Any Other Sexually Transmitted Infection in Driving HIV Prevalence in Africa

Extensive evidence from observational studies suggests a role for genital herpes in the HIV epidemic. A number of herpes vaccines are under development and several trials of the efficacy of HSV-2 treatment with acyclovir in reducing HIV acquisition, transmission, and disease progression have just reported their results or will report their results in the next year. The potential impact of these interventions requires a quantitative assessment of the magnitude of the synergy between HIV and HSV-2 at the population level.A deterministic compartmental model of HIV and HSV-2 dynamics and interactions was constructed. The nature of the epidemiologic synergy was explored qualitatively and quantitatively and compared to other sexually transmitted infections (STIs). The results suggest a more substantial role for HSV-2 in fueling HIV spread in sub-Saharan Africa than other STIs. We estimate that in settings of high HSV-2 prevalence, such as Kisumu, Kenya, more than a quarter of incident HIV infections may have been attributed directly to HSV-2. HSV-2 has also contributed considerably to the onward transmission of HIV by increasing the pool of HIV positive persons in the population and may explain one-third of the differential HIV prevalence among the cities of the Four City study. Conversely, we estimate that HIV had only a small net impact on HSV-2 prevalence.HSV-2 role as a biological cofactor in HIV acquisition and transmission may have contributed substantially to HIV particularly by facilitating HIV spread among the low-risk population with stable long-term sexual partnerships. This finding suggests that prevention of HSV-2 infection through a prophylactic vaccine may be an effective intervention both in nascent epidemics with high HIV incidence in the high risk groups, and in established epidemics where a large portion of HIV transmission occurs in stable partnerships