The described outbreaks highlight the threat represented by pockets of susceptible populations, even in the presence of good coverage levels in the overall population [27] . These groups include hard-to-reach populations (HRP) such as the Roma/Sinti communities (estimated MMR coverage in Italy below 10%,) [11] , families who refuse vaccination for ideological or religious reasons, as reported in recent outbreaks amongst students in private religious schools and orthodox communities in Europe and Israel [28] [29] [30] , and families objecting to having their children vaccinated out of concern for vaccinerelated adverse events [31] [32] [33] . The risk for the community represented by HRP or organized groups of objectors should not be underestimated and represent a more serious treat than sporadic susceptible individuals. Susceptible population groups may reintroduce indigenous measles virus transmission even in countries confirmed as disease-free or in a population with high immunization coverage [34] facilitating the transmission of the disease to susceptible individuals still present in the region. Efforts are needed to improve methods to identify areas with low coverage and to develop specific strategies which target susceptible groups. An improvement in health services delivery may be needed to reach Roma/Sinti communities and new immigrants. At the same time, more effective communication strategies should be defined to address subjects objecting to vaccination either for religious or other reasons, involving these subjects in a wider discussion on their responsibility toward the community. The implementation of catch up campaigns targeting adolescents and young adults should also be considered, with the additional objective of protecting women of childbearing age against rubella. Systematic Identification of Novel, Essential Host Genes Affecting Bromovirus RNA Replication Positive-strand RNA virus replication involves viral proteins and cellular proteins at nearly every replication step. Brome mosaic virus (BMV) is a well-established model for dissecting virus-host interactions and is one of very few viruses whose RNA replication, gene expression and encapsidation have been reproduced in the yeast Saccharomyces cerevisiae. Previously, our laboratory identified ∼100 non-essential host genes whose loss inhibited or enhanced BMV replication at least 3-fold. However, our isolation of additional BMV-modulating host genes by classical genetics and other results underscore that genes essential for cell growth also contribute to BMV RNA replication at a frequency that may be greater than that of non-essential genes. To systematically identify novel, essential host genes affecting BMV RNA replication, we tested a collection of ∼900 yeast strains, each with a single essential gene promoter replaced by a doxycycline-repressible promoter, allowing repression of gene expression by adding doxycycline to the growth medium. Using this strain array of ∼81% of essential yeast genes, we identified 24 essential host genes whose depleted expression reproducibly inhibited or enhanced BMV RNA replication. Relevant host genes are involved in ribosome biosynthesis, cell cycle regulation and protein homeostasis, among other cellular processes. BMV 2a(Pol) levels were significantly increased in strains depleted for a heat shock protein (HSF1) or proteasome components (PRE1 and RPT6), suggesting these genes may affect BMV RNA replication by directly or indirectly modulating 2a(Pol) localization, post-translational modification or interacting partners. Investigating the diverse functions of these newly identified essential host genes should advance our understanding of BMV-host interactions and normal cellular pathways, and suggest new modes of virus control. Viruses survive with limited genetic material by interacting with and exploiting host factors at essentially every replication step [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14] . Identifying the host factors and pathways exploited in virus replication and the nature of their contributions and interactions with virus-encoded replication factors represent major challenges and opportunities for understanding and controlling viruses.