This material is based upon work supported by the National Science Foundation through the Robert Noyce Teacher Scholarship Program under Grant No. DUE 1340110. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author(s) and do not necessarily reflect the views of the National Science Foundation. The STAR program is facilitated by the Cal Poly Center for Excellence in Science and Mathematics Education (CESaME) on behalf of the California State University (CSU). REFERENCES Understanding the very nature of infectious diseases allows for the prevention of new outbreaks as well as the development of drugs and vaccines. Three fourths of newly identified human pathogens are viruses, highlighting a need to better understand these rapidly changing pathogens. At the heart of these are mostly RNA viruses, the fastest when it comes to evolution [5]. RNA viruses replicate and may recombine quickly, due mostly to their error-prone RNA-dependent RNA polymerase (RdRp) which produces mutations in each replication cycle [1]. The RdRp also leads to frame shifts due to the secondary structure of the RNA as well as template swapping, starting on the genome of one strain and “jumping” to the genome of another co-infecting strain [4]. The lack of proofreading mechanisms that many other organisms rely on to prevent lethal mutations allows RNA viruses to balance on the edge of extinction in order to fully maximize their variability [1]. All of this leads up to the production of a highly variable and responsive population that scientists have dubbed “quasispecies” [6]. These large RNA virus populations hold many different variations of their genome, maintained by the very nature of their reproduction and the ability for the collective gene pool of the population to shift to accommodate host environment. It’s this very reason that of all the emerging infectious diseases identified since 1940 (about 400), more than 60% have been zoonotic [3]. In other words, in the past 75 years over 240 diseases have been able to swap hosts. Fig. 1: Human Rectal Tumor cells (HRT18) were grown in wells to produce monolayers (seen in the right image). Fig. 2: Cells were infected with virus at MOI 0.001. Above image shows cytopathic effect (CPE) caused by the virus. Fig. 3: RNA was extracted from the supernatant (using a Trizol extraction method) and converted to cDNA (using Invitrogen’s SuperScript III kit)
分享
引用
