As the race
towards vaccines increase to prevent certain viruses such as HIV, malaria and
west nile virus, the risk must be taken into account as much as the benefit. In
the 1950s, large populations of rabbits in Australia were wiped out due to a
leakage of a virus similar to smallpox, myxoma virus (MYXV). The rabbits would
develop symptoms of myxomatosis, where the eyes, ears, and genitals swell and
seal shut with discharge. An Australian microbiologist, Frank Fenner decided to
look at the correlation between virus emergence/ virulence and host resilience.
Fenner
found that natural selection favored less lethal strains of the virus because
the rabbits could reproduce and spread the disease to offspring before they
died. Fenner also found that the rabbits started to develop resistance to the
virus, thus the virus still needed to be harsh enough not to be benign.
The virus
continued to develop through the years, and the most virulent form of the virus
was found to immunosuppress the rabbits. In this case, the effect of the virus
on the outside looked completely different than before. The newly infected
rabbits did not show on the symptoms of myxomatosis and instead died of toxic
or septic shock by lack of a cellular inflammatory response. This new virulence
was natural selection on the virus allowing it to compensate for the increased
resistance in the rabbits.
Increased
viral virulence due to increased host resistance is seen in viruses other than MYXV
such as rabitt hemorrhage disease virus (RHDV), West Nile, and the bacterial pathogen
Mycoplasma gallisepticum.
As humans
try to develop vaccines in order to help treat and prevent virus/ bacteria
causing diseases, consideration needs to be taken into how the virus might
reciprocate those effects. How could the viruses become more resistant, what
mechanisms could they possibly take to increase the virulence, and how we can
prevent mass destruction to the human population due to viruses becoming more
virulent to our preventative measures and our resilience.
Read, Andrew F. (2017, Oct. 3). Do Pathogens Gain Virulence as Hosts Become More Resistant? The
Scientist.
www.the-scientist.com/?articles.view/articleNo/50411/title/Do-Pathogens-Gain-Virulence-as-Hosts-Become-More-Resistant-/
This is a great take on an extremely relevant problem! A great solution that I've recently read about is treatment with CRISPR. Using the CRISPR technique, scientists can design a sequence to anneal to either a virulence gene or a resistance gene. One way to disable the gene is to cut it out entirely, as CRISPR was originally designed to do, however scientists have now started to disable the DNA cutting enzyme and instead of removing the gene, alter the expression. Components such as acetyl or methyl groups can be added to stop transcription of the gene product. This is super cool because this can be used on viruses as well as bacteria, and as the virus or bacteria evolves to combat our treatments, we can continue sequencing these changes and alter the CRISPR complex to attach to the more recently developed gene. It is similar to what you are talking about with anticipating the virus's next move in order to prevent that next resistance trait from developing, however, the CRISPR technique would be much more specific and accurate.
ReplyDeleteThis topic is not one that is widely known, so it's nice to see it get some attention. Most talk of resistance is about bacterial resistance to antibiotics, and none of the classes I've taken have covered viral adaptation to vaccines, at least not in very much detail. This seems very plausible due to the nature of natural selection, but my question is, is it as big of a threat as bacterial resistance to antibiotics? Since viruses don't reproduce on their own, I would expect them to have a much lower rate of mutation than bacteria, especially since they can't absorb plasmids. Regardless of whether or not this is as significant of a threat, it is not hard to believe that viral adaptation to vaccines is important to keep an eye on as time goes on.
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