Principles of Darwinian Medicine

Principle: “Virulence is a trait of the pathogen that can increase as well as decrease” (Nesse and Williams 1998).

People who had been vaccinated or “had been vaccinated within 3 weeks of admission [to the hospital]” were more likely to survive a Smallpox infection than those who had never been vaccinated (Albert et al. 2002). Vaccinated people could and did still get sick with Smallpox and show symptoms, however the disease was much less severe than in a patient who had not been vaccinated. Therefore in a population of vaccinated people, the Smallpox disease was less virulent, likely because it was more easily wiped out by the body’s immune system. (Albert et al. 2002)

           

Principle: “Symptoms of infection can benefit the pathogen, the host, both or neither” (Nesse and Williams 1998).

The high fever that occurs before the emergence of the rash and again before scabbing is the body trying to kill the virus. However, this symptom can kill the host as well, which obviously would not be beneficial. The sores that develop on the tongue and in the mouth and later break open are mainly beneficial to the virus. Once the sores break open, fresh virus may spread throughout the host or be passed on to a new host, carried on the breath and in the saliva of the infected host. The rash that forms during a Smallpox infection is the body’s way of trying to push the virus out through the skin. This is meant to benefit the human host, though it is painful and the pus from the pustules can actually transfer the virus to a new host, which would benefit the virus. (Smallpox Disease Overview 2004)

Principle: “Each disease needs a proximate explanation… as well as an evolutionary explanation of why members of the species are vulnerable to it” (Nesse and Williams 1998).

The proximate explanation of why humans catch Smallpox is that when exposed to an infected person, the virus will jump to a new host to replicate.

The evolutionary explanation of why humans are vulnerable to smallpox is probably related to the rise of agriculture and domesticated animals. Variola virus evolved from a rodent-borne Orthopoxvirus. This virus was carried by rodents that were attracted to the abundant food sources that could be found once humans began farming. At some point the virus jumped to humans and the domesticated animals they kept in close contact with. The Variola virus then specialized to humans, while others (such as cowpox) remained zoonotic, capable of jumping between species. (Pearce-Duvet 2006)

Principle: “Specific clinical recommendations must be based on clinical studies; clinical interventions based only on theory are not scientifically grounded and may cause harm” (Nesse and Williams 1998).

Firth et al. used scientific experimentation to determine the speed of replication and evolution for the Smallpox virus (VARV). Since VARV has double-stranded DNA, the previous assumption was that it replicates slower than viruses with single-stranded DNA and therefore would be easier to prevent, treat, or eradicate before a new strain evolved. What Firth et al. actually discovered is that VARV evolves at a much higher rate than was previously assumed. This kind of data is important to understand before doctors attempt to control a disease, because moving with the assumption that the disease evolves slowly when the opposite is true could have disastrous results. (Firth et al. 2010)