We introduce random directed acyclic graph and use it to model the information diffusion network. Subsequently, we analyze the cascade generation model (CGM) introduced by [19]. Until now only empirical studies of this model were done. In this paper, we present the first theoretical proof that the sizes of cascades generated by the CGM follow the power-law distribution, which is consistent with multiple empirical analysis of the large social networks. We compared the assumptions of our model with the Twitter social network and tested the goodness of approximation.
The classical example of the modified spreading process incorporates the effect of a @cite_2 . never spread the information even if they were exposed to it multiple times. Nevertheless, can actively convert other spreaders or susceptible nodes into . That complicated logic may lead to the elimination of the epidemic threshold Epidemic threshold determines whether the global epidemic occurs or the disease simply dies out. and has been actively developed @cite_22 .
@cite_22 @cite_2
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Information spreading in a population can be modeled as an epidemic. Campaigners (e.g., election campaign managers, companies marketing products or movies) are interested in spreading a message by a given deadline, using limited resources. In this paper, we formulate the above situation as an optimal control problem and the solution (using Pontryagin's Maximum Principle) prescribes an optimal resource allocation over the time of the campaign. We consider two different scenarios-in the first, the campaigner can adjust a direct control (over time) which allows her to recruit individuals from the population (at some cost) to act as spreaders for the Susceptible-Infected-Susceptible (SIS) epidemic model. In the second case, we allow the campaigner to adjust the effective spreading rate by incentivizing the infected in the Susceptible-Infected-Recovered (SIR) model, in addition to the direct recruitment. We consider time varying information spreading rate in our formulation to model the changing interest level of individuals in the campaign, as the deadline is reached. In both the cases, we show the existence of a solution and its uniqueness for sufficiently small campaign deadlines. For the fixed spreading rate, we show the effectiveness of the optimal control strategy against the constant control strategy, a heuristic control strategy and no control. We show the sensitivity of the optimal control to the spreading rate profile when it is time varying. (1) One of the most striking features in the study of epidemics is the difficulty of finding a causal factor which appears to be adequate to account for the magnitude of the frequent epidemics of disease which visit almost every population. It was with a view to obtaining more insight regarding the effects of the various factors which govern the spread of contagious epidemics that the present investigation was undertaken. Reference may here be made to the work of Ross and Hudson (1915-17) in which the same problem is attacked. The problem is here carried to a further stage, and it is considered from a point of view which is in one sense more general. The problem may be summarised as follows: One (or more) infected person is introduced into a community of individuals, more or less susceptible to the disease in question. The disease spreads from the affected to the unaffected by contact infection. Each infected person runs through the course of his sickness, and finally is removed from the number of those who are sick, by recovery or by death. The chances of recovery or death vary from day to day during the course of his illness. The chances that the affected may convey infection to the unaffected are likewise dependent upon the stage of the sickness. As the epidemic spreads, the number of unaffected members of the community becomes reduced. Since the course of an epidemic is short compared with the life of an individual, the population may be considered as remaining constant, except in as far as it is modified by deaths due to the epidemic disease itself. In the course of time the epidemic may come to an end. One of the most important probems in epidemiology is to ascertain whether this termination occurs only when no susceptible individuals are left, or whether the interplay of the various factors of infectivity, recovery and mortality, may result in termination, whilst many susceptible individuals are still present in the unaffected population. It is difficult to treat this problem in its most general aspect. In the present communication discussion will be limited to the case in which all members of the community are initially equally susceptible to the disease, and it will be further assumed that complete immunity is conferred by a single infection. Abstract Susceptible ( S ) – exposed ( E ) – infectious ( I ) – quarantined ( Q ) – recovered ( R ) model for the transmission of malicious objects in computer network is formulated. Thresholds, equilibria, and their stability are also found with cyber mass action incidence. Threshold R cq determines the outcome of the disease. If R cq ⩽ 1, the infected fraction of the nodes disappear so the disease die out, while if R cq > 1, the infected fraction persists and the feasible region is an asymptotic stability region for the endemic equilibrium state. Numerical methods are employed to solve and simulate the system of equations developed. The effect of quarantine on recovered nodes is analyzed. We have also analyzed the behavior of the susceptible, exposed, infected, quarantine, and recovered nodes in the computer network. Given a network of who-contacts-whom or who-links-to-whom, will a contagious virus product meme spread and ‘take over’ (cause an epidemic) or die out quickly? What will change if nodes have partial, temporary or permanent immunity? The epidemic threshold is the minimum level of virulence to prevent a viral contagion from dying out quickly and determining it is a fundamental question in epidemiology and related areas. Most earlier work focuses either on special types of graphs or on specific epidemiological cascade models. We are the first to show the G2-threshold (twice generalized) theorem, which nicely de-couples the effect of the topology and the virus model. Our result unifies and includes as special case older results and shows that the threshold depends on the first eigenvalue of the connectivity matrix, (a) for any graph and (b) for all propagation models in standard literature (more than 25, including H.I.V.). Our discovery has broad implications for the vulnerability of real, complex networks and numerous applications, including viral marketing, blog dynamics, influence propagation, easy answers to ‘what-if’ questions, and simplified design and evaluation of immunization policies. We also demonstrate our result using extensive simulations on real networks, including on one of the biggest available social-contact graphs containing more than 31 million interactions among more than 1 million people representing the city of Portland, Oregon, USA.