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Objectives HIV and herpes simplex virus type 2 (HSV-2) infections are sexually transmitted and propagate in sexual networks. Using mathematical modeling, we aimed to quantify effects of key network statistics on infection transmission, and extent to which HSV-2 prevalence can be a proxy of HIV prevalence. Design/methods An individual-based simulation model was constructed to describe sex partnering and infection transmission, and was parameterized with representative natural history, transmission, and sexual behavior data. Correlations were assessed on model outcomes (HIV/HSV-2 prevalences) and multiple linear regressions were conducted to estimate adjusted associations and effect sizes. Results HIV prevalence was one-third or less of HSV-2 prevalence. HIV and HSV-2 prevalences were associated with a Spearman's rank correlation coefficient of 0.64 (95% confidence interval: 0.58-0.69). Collinearities among network statistics were detected, most notably between concurrency versus mean and variance of number of partners. Controlling for confounding, unmarried mean/variance of number of partners (or alternatively concurrency) were the strongest predictors of HIV prevalence. Meanwhile, unmarried/married mean/variance of number of partners (or alternatively concurrency), and clustering coefficient were the strongest predictors of HSV-2 prevalence. HSV-2 prevalence was a strong predictor of HIV prevalence by proxying effects of network statistics. Conclusion Network statistics produced similar and differential effects on HIV/HSV-2 transmission, and explained most of the variation in HIV and HSV-2 prevalences. HIV prevalence reflected primarily mean and variance of number of partners, but HSV-2 prevalence was affected by a range of network statistics. HSV-2 prevalence (as a proxy) can forecast a population's HIV epidemic potential, thereby informing interventions.

Objective: MSM are at increased risk for infection with HIV-1 and hepatitis C virus (HCV). Is HIV/HCV coinfection confined to specific HIV transmission networks? Design and methods: A HIV phylogenetic tree was constructed for 5038 HIV-1 subtype B polymerase (pol) sequences obtained from MSM in the AIDS therapy evaluation in the Netherlands cohort. We investigated the existence of HIV clusters with increased HCV prevalence, the HIV phylogenetic density (i.e. the number of potential HIV transmission partners) of HIV/HCV-coinfected MSM compared with HIV-infected MSM without HCV, and the overlap in HIV and HCV phylogenies using HCV nonstructural protein 5B sequences from 183 HIV-infected MSM with acute HCV infection. Results: Five hundred and sixty-three of 5038 (11.2%) HIV-infected MSM tested HCV positive. Phylogenetic analysis revealed 93 large HIV clusters (>= 10 MSM), 370 small HIV clusters (2-9 MSM), and 867 singletons with a median HCV prevalence of 11.5, 11.6, and 9.3%, respectively. We identified six large HIV clusters with elevated HCV prevalence (range 23.5-46.2%). Median HIV phylogenetic densities for MSM with HCV (3, interquartile range 1-7) and without HCV (3, interquartile range 1-8) were similar. HCV phylogeny showed 12 MSM-specific HCV clusters (clustersize: 2-39 HCV sequences); 12.7% of HCV infections were part of the same HIV and HCV cluster. Conclusion: We observed few HIV clusters with elevated HCV prevalence, no increase in the HIV phylogenetic density of HIV/HCV-coinfected MSM compared to HIV-infected MSM without HCV, and limited overlap between HIV and HCV phylogenies among HIV/HCV-coinfected MSM. Our data do not support the existence of MSM-specific sexual networks that fuel both the HIV and HCV epidemic. Copyright (C) 2017 Wolters Kluwer Health, Inc. All rights reserved

Whereas sexual relationships among low-risk individuals account for the majority of HIV infections in sub-Saharan Africa limited knowledge exists about the structure and characteristics of sexual networks among the general population in sub-Saharan Africa. The objectives were to investigate the population-level structure of sexual networks connecting the young adult population of several villages on Likoma Island (Malawi) and analyse the structural position of HIV-positive individuals within the sexual network. The design and methods used were a cross-sectional sociocentric survey of sexual partnerships and biomarkers of prevalent HIV infections. The study documents the existence of a large and robust sexual network linking a substantial fraction of the islands young adult population: half of all sexually active respondents were connected in a giant network component and more than a quarter were linked through multiple independent chains of sexual relationships. This high network connectivity emerges within short time frames. The prevalence of HIV also varied significantly across the network with sparser regions having a higher HIV prevalence than densely connected components. Several risk factors related to sexual mixing patterns help explain differentials in HIV prevalence across network locations. Contrary to claims that sexual networks in rural sub-Saharan Africa are too sparse to sustain generalized HIV epidemics the structure of the networks observed in Likoma appears compatible with a broad diffusion of HIV among lower-risk groups. The non-homogeneous distribution of HIV infection within the network suggests that network characteristics are an important determinant of the dynamics of HIV spread within a population. (authors)

Objectives: To determine the relationship of HIV infection in pregnant women to sexual network size and other risk factors. Design: Case–control study of women attending the public maternity hospital in Lima Peru. Methods: We interviewed 75 HIV-seropositive women 41 of their most recent male partners and two control groups totaling 137 uninfected pregnant women and 70 of their most recent male partners. Each woman’s sexual network size was estimated through second and third-generation partnerships over the past year 5 years and lifetime. Results: Few HIV-seropositive women reported behavioral risk factors for HIV infection but 79% of male partners were HIV seropositive. Risk factors in male partners included sex with a female sex worker (FSW) or with another man (MSM). The mean 5-year sexual network sizes through the second generation (8.4 persons for HIV seropositive women and 2.5 and 1.9 for women in the two control groups) predicted HIV in the women independently of her own number of partners. These differences were largely attributable to the number of partners reported by male partners. Using data from concurrent studies of FSW and MSM estimates of 5-year sexual network sizes through the third-generation excluding contacts with FSW which were protected by consistent condom use were 672 persons for HIV-seropositive women and 160 and 224 for women in the two control groups. Conclusions: HIV infection risk among pregnant women in Lima depends largely on their male partners’ risk behaviors. Even monogamous women had very large sexual networks. (authors)

More than ten years ago the concept of “concurrency” entered the epidemiological stage in the attempt to explain the differences of spread of HIV in different populations [1-4]. In recent years, following several publications and commentaries based on review of previous studies the concurrency hypothesis has been put forward more strongly to explain the rapid or slow heterosexual spread of HIV in countries around the world [5, 6]. However, the empirical basis proving that concurrency actually is the driving force behind the continuing high prevalence of HIV in sub-Saharan Africa has been lacking. While some studies investigated the impact of concurrent partnerships on the prevalence of HIV in various sub-Saharan Africa populations [7-9], they were not able to identify concurrency as a strong explanatory factor. Also, epidemiological observations like the decrease of HIV prevalence in Uganda following the advocacy of the “zero grazing” strategy for HIV prevention [10, 11] is not conclusive evidence for the impact of concurrent partnerships on HIV transmission, because of the possibility of ecological inference fallacy. Now Reniers and Watkins demonstrate in an ecological study of HIV prevalence in 34 sub-Saharan Africa countries that concurrency in the traditional form of polygyny can even be negatively correlated with HIV prevalence [12]. The authors used data from Demographic and Health Surveys (DHS) and HIV/AIDS Indicator Surveys from 19 African countries to investigate the prevalence of polygyny and HIV on country and subnational level. They show that those countries with higher levels of polygynous unions have a lower prevalence of HIV. This is true when using both male based as well as female based data. Reniers and Watkins discuss various reasons why their results seemingly contradict the concurrency hypothesis. Obviously, concurrency measured in terms of number of wives of married men is only one form of concurrency and other forms could be present simultaneously in those societies with a high HIV prevalence. Furthermore, polygyny produces a very specific type of network pattern, namely many unconnected ‘stars’ (polygynous men connected to several monogamous women), which limits the size of connected network components to the size of these ‘stars’. HIV infected women, who are in a polygynous marriage system do not directly transmit further than their husband, if at all. Finally, the authors put forward the hypothesis of the “coital dilution effect” meaning that a man with many wives may have less frequent sexual intercourse with an infected spouse the more wives he has, thereby reducing the probability of getting infected by his infected wife. Although this study is ecological and more research is needed to elucidate any causal association between polygynous unions and the transmission of HIV, the study marks a turning point in the thinking about concurrency and HIV in sub-Saharan Africa. Firstly, it clearly shows the need to view concurrent partnerships in their social and cultural context. It matters what the motivation is for establishing concurrent partnerships, how they are distributed among men and women, and in how far they are anchored in the culture of a society. The persistence of polygyny is linked to more traditional societies with other mechanisms in place that limit the transmission of HIV. For example, in societies with polygyny, more social control tends to prevent sex before marriage and early female age at first marriage is common. Polygyny also tends to be associated with longer durations of postpartum sexual abstinence between spouses and thus might protect young women from getting infected [13, 14]. For concurrent partnerships in Western societies Gorbach et al. [15] have shown that the definition of what constitutes a concurrent partnership can be further discriminated, leading to many forms of concurrency with more or less overlapping partnerships. Depending on their type, these partnerships are likely to contribute more or less to the onward transmission of HIV. A similar differentiation of types of concurrent partnerships that takes into account the motivation for their formation is needed for the sub-Saharan Africa situation. Secondly, the results of Reniers and Watkins highlight the fact that we should not interpret concurrency as an uncorrelated characteristic of a sexual network. Concurrency, as investigated in Morris & Kretzschmar [3] is a simple caricature of a complex network structure, namely the average level of concurrent partnerships in a population with a given number of partnerships. Concurrency defined in this way is shown to increase the rate of epidemic growth of HIV. However, if besides concurrency, other local or global network characteristics change when concurrency levels are reduced the effects of concurrency reduction might be modified [16]. It is known that the variance of number of partnerships within a population affects the basic reproduction number in models with only instantaneous partnerships that are stratified by sexual activity [17]. Factors, such as the variance in the number of partners or the assortativeness of partner selection with respect to number of partners therefore affect HIV transmission dynamics, and, if altered, effects on prevalence cannot be attributed solely to changing levels of concurrency. As yet it is far from well understood what the appropriate measures are to quantify non-local network structure in order to best capture HIV transmission. Also the question of the appropriate time scale on which to measure network structure needs further thought. Even in the most sophisticated empirical network studies to date such as the Likoma network study [18] it was not possible to distinguish unequivocally between concurrent partnerships and multiple monogamous partnerships accumulated over a certain time period. In view of these difficulties, we conclude that to date the proportion of HIV transmission that is due to concurrency in contemporary sub-Saharan Africa is unknown. What further research is necessary? Clearly there is a need to standardize definitions of concurrency and collect more data. Commendable efforts are already underway by UNAIDS and partners [19], but complementary studies measuring different aspects of the dynamics of concurrency and its association with STI/HIV risk are urgently needed. The continued use of robustly parameterized and validated mathematical models will be required to help interpret these data, and to help elucidate what effects can be attributed to concurrency and which to other, closely correlated risk factors, and therefore what the likely intended and unintended consequences of interventions targeting concurrency may be. This will not be straight forward and the findings are not likely to be unequivocal as suggested by the study in this issue of AIDS. What does this all mean for prevention messages that are needed for curbing the further transmission of HIV now? Based on the straight forward interpretation of the ‘concurrency hypothesis’, messages such as “not more than one partner at a time” have been suggested [20]. However, such a message might not make sense in societies with polygynous marriage systems or otherwise culturally embedded forms of concurrency that are linked with other protective behaviours. Clearly, prevention messages must take the cultural context into account, possibly even on the regional level [21]. Further, until it is better known what the unintended consequences might be of behavior change messages that seek to reduce concurrency, perhaps messages should be limited to generating awareness that the risk of becoming infected with HIV does not only depend on one’s own behavior, but also on the behavior of one’s partners and beyond. It should also be clear that this “beyond” is not visible for most individuals; nobody really knows what network location he or she occupies. But the awareness that behavior of a collective impacts on individual risk is the message that we have to bring across together with some concrete ideas about how to limit one’s risk in the face of that collective behavior.

Objective: To examine how concurrent partnerships amplify the rate of HIV spread, using methods that can be supported by feasible data collection. Methods: A fully stochastic simulation is used to represent a population of individuals, the sexual partnerships that they form and dissolve over time, and the spread of an infectious disease. Sequential monogamy is compared with various levels of concurrency, holding all other features of the infection process constant. Effective summary measures of concurrency are developed that can be estimated on the basis of simple local network data. Results: Concurrent partnerships exponentially increase the number of infected individuals and the growth rate of the epidemic during its initial phase. For example, when one-half of the partnerships in a population are concurrent, the size of the epidemic after 5 years is 10 times as large as under sequential monogamy. The primary cause of this amplification is the growth in the number of people connected in the network at any point in time: the size of the largest "component'. Concurrency increases the size of this component, and the result is that the infectious agent is no longer trapped in a monogamous partnership after transmission occurs, but can spread immediately beyond this partnership to infect others. The summary measure of concurrency developed here does a good job in predicting the size of the amplification effect, and may therefore be a useful and practical tool for evaluation and intervention at the beginning of an epidemic. Conclusion: Concurrent partnerships may be as important as multiple partners or cofactor infections in amplifying the spread of HIV. The public health implications are that data must be collected properly to measure the levels of concurrency in a population, and that messages promoting one partner at a time are as important as messages promoting fewer partners.

Obtaining large-scale sexual network data is difficult [1] and doing so in a poor country is especially difficult. We congratulate Helleringer and Kohler [2] on their pioneering study of a sexual network on Likoma Island Malawi. Their approach represents an important step toward appropriate research designs for elucidating HIV transmission dynamics in sub-Saharan Africa. Despite this achievement their results undermine their assertion that the Likoma sexual network sustains epidemic HIV transmission. In fact their findings add to the already considerable evidence against penile-vaginal intercourse as the primary driver of HIV transmission in sub-Saharan Africa [3]. In moderate prevalence Likoma Helleringer and Kohler observed an apparently paradoxical distribution of HIV prevalence. They found that persons in the core (bicomponents) of the main component of the sexual network were less likely to be HIV infected than those in peripheral positions in the main component or in small network components. This finding is at odds with prior empirical research which indicates that when significant HIV transmission occurs persons located in the core of the corresponding risk network are more likely to be infected. In one high prevalence community persons in the core of the injection and sexual network had considerably higher HIV prevalence and more frequent risk behaviors than those in peripheral or more isolated positions [4]. In that study injection and homosexual risk behaviors were positively associated with prevalent HIV infection but heterosexual risk behaviors were not. Similarly among heterosexuals in a very low prevalence setting with little ongoing HIV transmission infected persons were with one exception isolates in small components or on the periphery of the main component of the risk network [56]. In Likoma it is surprising that self-reported symptoms of sexually transmitted infections (STI) are almost evenly distributed across the sexual network and are not concentrated in the core as expected. Furthermore no sexual risk variable (condom use number of sex partners STI symptoms or age difference between sex partners) shows a meaningful association with prevalent HIV infection. Taken together these observations suggest that the measured sexual network might not underlie HIV transmission in Likoma and that other unmeasured blood and sexual exposures might be involved. To establish the primary modes of HIV transmission in sub- Saharan Africa with confidence more appropriate research designs are required. Specifically it is critical to assess blood and sexual exposures comprehensively (beyond just injections and vaginal intercourse) for incident cases and controls trace their corresponding contacts and sequence-infected persons HIV isolates [7-9]. (full-text)