Three Rotavirus Outbreaks in the Postvaccine Era - California, 2017.

Before the introduction of rotavirus vaccine in 2006, rotavirus was the most common cause of severe diarrhea among U.S. children (1). Currently, two rotavirus vaccines are licensed for use in the United States, both of which have demonstrated good field effectiveness (78%-89%) against moderate to severe rotavirus illness (2), and the use of these vaccines has substantially reduced the prevalence of rotavirus in the United States (3). However, the most recent national vaccine coverage estimates indicate lower full rotavirus vaccine-series completion (73%) compared with receipt of at least 3 doses of vaccines containing diphtheria, tetanus, and pertussis antigens (95%), given on a similar schedule to rotavirus vaccines (4). In the postvaccine era in the United States, rotavirus activity persists in a biennial pattern (3). This report describes three rotavirus outbreaks that occurred in California in 2017. One death was reported; however, the majority of cases were associated with mild to moderate illness, and illness occurred across the age spectrum as well as among vaccinated children. Rotavirus vaccines are designed to mimic the protective effects of natural infection and are most effective against severe rotavirus illness (2). Even in populations with high vaccination coverage, some rotavirus infections and mild to moderate illnesses will occur. Rotavirus vaccination should continue to be emphasized as the best means of reducing disease prevalence in the United States.

Uncovering buffered pleiotropy: a genome-scale screen for mel-28 genetic interactors in Caenorhabditis elegans.

mel-28 (maternal-effect-lethal-28) encodes a conserved protein required for nuclear envelope function and chromosome segregation in Caenorhabditis elegans. Because mel-28 is a strict maternal-effect lethal gene, its function is required in the early embryo but appears to be dispensable for larval development. We wanted to test the idea that mel-28 has postembryonic roles that are buffered by the contributions of other genes. To find genes that act coordinately with mel-28, we did an RNA interference-based genetic interaction screen using mel-28 and wild-type larvae. We screened 18,364 clones and identified 65 genes that cause sterility in mel-28 but not wild-type worms. Some of these genes encode components of the nuclear pore. In addition we identified genes involved in dynein and dynactin function, vesicle transport, and cell-matrix attachments. By screening mel-28 larvae we have bypassed the requirement for mel-28 in the embryo, uncovering pleiotropic functions for mel-28 later in development that are normally provided by other genes. This work contributes toward revealing the gene networks that underlie cellular processes and reveals roles for a maternal-effect lethal gene later in development.