Epidemic cycling in human infectious diseases is common; however, its underlying mechanisms have been poorly understood. Much effort has been made to search for external mechanisms. Multiple strains of an infectious agent were usually observed and coinfections were frequent; further, empirical evidence indicates the simultaneous transmission of coinfections. To explore intrinsic mechanisms for epidemic cycling, in this study we consider a multistrain Susceptible-Infected-Recovered-Susceptible epidemic model by including coinfections and simultaneous transmission. We show that coinfections and their simultaneous transmission widen the parameter range for coexistence and coinfections become popular when strains enhance each other and the immunity wanes quickly. However, the total prevalence is nearly independent of these characteristics and approximated by that of one-strain model. With sufficient simultaneous transmission and antigenic diversity, cyclical epidemics can be generated even when strains interfere with each other by reducing infectivity. This indicates that strain interactions within coinfections and cross-immunity during subsequent infection provide a possible intrinsic mechanism for epidemic cycling.