Despite an initial success, Israel’s quarantine-isolation COVID-19 policy has abruptly collapsed. This study’s aim is to identify the causes that led to this exponential rise in the accumulation of confirmed cases. Epidemiological investigation reports were used to reconstruct chains of transmission as well as assess the net contribution of local infections relative to imported cases, infected travelers arriving from abroad. A mathematical model was implemented in order to describe the efficiency of the quarantine-isolation policy and the inflow of imported cases. The model’s simulations included two scenarios for the actual time series of the symptomatic cases, providing insights into the conditions that lead to the abrupt change. The abrupt change followed a Jewish holiday, Purim, in which many public gatherings were held. According to the first scenario, the accumulation of confirmed cases before Purim was driven by imported cases resulting in a controlled regime, with an effective reproduction number, Re, of 0.69. In the second scenario, which followed Purim, a continuous rise of the local to imported cases ratio began, which led to an exponential growth regime characterized by an Re of 4.34. It was found that the change of regime cannot be attributed to super-spreader events, as these consisted of approximately 5% of the primary cases, which resulted in 17% of the secondary cases. A general lesson for health policymakers should be that even a short lapse in public responsiveness can lead to dire consequences.
Both monogenic diseases and viral infections can manifest in a broad spectrum of clinical phenotypes that range from asymptomatic to lethal, suggesting that other factors modulate disease severity. Here, we examine the interplay between the genetic neuronopathic Gaucher’s disease (nGD), and neuroinvasive Sindbis virus (SVNI) infection. Infection of nGD mice with SVNI had no influence on nGD severity. However, nGD mice were more resistant to SVNI infection. Significantly different inflammatory responses were seen in nGD brains when compared with SVNI brains: the inflammatory response in the nGD brains consisted of reactive astrocytes and microglia with no infiltrating macrophages, but the inflammatory response in the brains of SVNI-infected mice was characterized by infiltration of macrophages and altered activation of microglia and astrocytes. We suggest that the innate immune response activated in nGD confers resistance against viral infection of the CNS.