Sea stars don’t have the adaptive immune system that we have (no MHC) so how did they challenge the control sea stars that were injected with heat-killed viruses?

    Histology use stains that only interact with certain cell membranes, such as targeting gram-positive bacteria. Staining did not show any bacteria in sea stars. Sand-filtered water still allowed passage of pathogen, so must be a virus.

    Studied metagenomics. (Metagenomics is the study of genetic material recovered directly from environmental samples. The broad field may also be referred to as environmental genomics, ecogenomics or community genomics.) Tissue samples from 28 specimen from multiple parts of the body were taken, homogenized, DNA of viruses were isolated, then sequenced and found that most was parvovirus-like sequences. Because there was most of this, they assumed it was densovirus (Parvoviridae) causing SSWD (sea star wasting disease).

    PCR – start with all DNA, cut out small piece, primers (tagged with fluorescents) amplify that piece until it’s big enough to see what’s going on.

    qPCR – primer tagged with fluorescents measured how fast the genetic sequence is amplifying (number). Faster-growing samples would have more SSaDV loads. (allows statistical analysis)

    Figure 6A. There are higher viral loads in symptomatic than in asymptomatic seastars, however, asymptomatic still has high loads, and they found no seastars with none of the SSaDV. Why is this? Are there carriers? A protective heterozygous type? A threshold of viral load that kills the seastar?

    Not a new virus because they found it in museum samples of asteroids. Why is the virus becoming prevalent now? Climate change - changes in temp, stress, and disease linked.

    Figure 3. Open reading frame one and open reading frame two are the arrow areas with the shaded areas are protein. And open reading frame is a stretch of DNA that CAN code for a protein. There are start and stop codons that separate the DNA into each section that code for a protein.


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