deadly – BioQuakes

There is a reason why it is not advisable to eat wild mushrooms; Amanita phalloides, nicknamed death cap mushrooms, closely resemble edible mushroom variants—but are deadly if ingested. If a person chances upon one and happens to eat it, regardless of whether it is cooked, there is a high likelihood that they die.

A. phalloides are the most toxic of any mushroom species and are responsible for the majority of fatal mushroom poisonings. Notable victims of death cap mushroom poisoning include Roman Emperor Claudius, Pope Clement VII, and Holy Roman Emperor Charles VI. A. phalloides poisoning has always been difficult to diagnose and even more difficult to treat, as symptoms emerge after a long delay and there has been no known antidote to A. phalloides toxin—that is, until researchers utilized CRISPR-Cas9.

Death cap mushrooms contain the amatoxin alpha-amanitin. The amatoxins are a group of toxins that share the trait of inhibiting the enzyme RNA polymerase II. In our AP Biology class, we discussed DNA polymerases and their vital function in DNA replication. Similarly, RNA polymerases are a vital component of RNA transcription and synthesis. RNA polymerase II synthesizes mRNA, the template for protein synthesis. Upon the inhibition of RNA polymerase II, cell metabolism comes to a halt and apoptosis (cell self-destruction) ensues.

Alpha-amanitin is possibly the most deadly of the amatoxins. The particular human genes that are triggered by alpha-amanitin were previously unknown, but CRISPR recently revealed these genes, one of which produces the protein STT3B. STT3B is a required component of alpha-amanitin toxicity, therefore an inhibitor of STT3B would negate the effects of alpha-amanitin.

Researchers found just that—an inhibitor of STT3B, indocyanine green. Once the effectiveness of indocyanine green was confirmed in vitro, scientists experimented with a mouse model of alpha-amanitine poisoning and found that indocyanine green had a profound effect if given one to four hours after ingestion of the toxin. However, if eight to 12 hours had elapsed before the indocyanine green was introduced, its effectiveness was greatly reduced, possibly because irreversible organ damage had already occurred in the subject. This fact poses concern, as alpha-amanitine poisoning symptoms take at least six hours to occur after A. phalloides ingestion.

While more investigation needs to be undertaken before indocyanine green can be proposed as a treatment for death cap mushroom poisoning, these latest discoveries represent a significant advancement in our understanding of the process. Any thoughts regarding CRISPR or this topic as a whole are encouraged.

There’s no doubt you’ve heard of HIV, or Human Immunodeficiency Virus. The HIV virus, if left untreated can lead to AIDS, or Acquired Immunodeficiency Syndrome, which leads to progressive immune system failure (http://en.wikipedia.org/wiki/HIV#Discovery). HIV didn’t become a problem in the United States until the 1980s, but was around long before then. Alfred Roca, an assistant Professor at the University of Illinois believes HIV was around for much longer than we believe.

The Origins

HIV was thought to be originated from SIV, or Simian Immunodeficiency Virus, that infected Chimpanzees in Central Africa. About ninety percent of humans infected with HIV are infected with a strain called HIV-1 Type M, which was believed to have crossed the species barrier anywhere between 1884 and 1924. However, believes that HIV crossed the species barrier many times before 1884, but was most prevalent in rural areas, so it remained undetected.

Why it was a mystery

If HIV was around long before we initially thought, why did it remain undetected. According to Roca, “the persistence of HIV in humans requires population densities typically of larger cities that appeared in West Central Africa during the colonial period.” HIV didn’t spread amongst humans pre-1884 because the population was not dense enough. In addition, diseases spread much faster. Many people would have died early from diseases such as smallpox, and those with compromised immune systems would have been hit first, thus the disease couldn’t spread.

Map of the prevalence of HIV in the world, according to the 2008 UNAIDS Preport

Roca also believes that different strains of HIV could affect people with different genes. Using data from The Human Genome Project, Roca was able to analyze the DNA of the Biaka people, who live in the forests where the chimpanzees responsible for our current HIV pandemic reside and 4 other African populations which live outside the chimpanzees’ range. Research done in the 1980s concluded there are 26 genomic locations that help resist HIV.

The results of the research were astounding. Roca and his team identified four genes that code for proteins that affect the ability of the HIV to affect the host or the progression of the disease. Several of these genes were common among the Biaka people. Though the results aren’t definitive, they show that natural selection does play a part in the transfer of HIV to human populations, which is why the disease didn’t thrive earlier.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: deadly

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