A recent Penn State experiment studied the effects of weak immune systems on the virulence and aggressiveness of a malaria parasite in mice. The study involved disabling a key immune molecule, CD4 receptors, with an antibody and then infecting these mice and a control group with an uncompromised immune system with the malaria parasite Plasmodium chabaudi. It lasted 21 weeks and each week, the parasite was taken from one mice and transferred to another previously uninfected mouse. They froze the samples biweekly to analyze aggressiveness and virulence.

The surprising results indicated the parasite infecting a weak immune system becomes more aggressive and virulent than in the control mice. This is surprising for two main reasons. Firstly, the parasite need a host or else they die. This creates the need for a unique balance of the parasite that it needs to be aggressive enough to replicate and feed off of their host, yet weak enough that they do not kill their host and source of life. Yet finding indicate that in immune-compromised mice that had their CD4 receptors disabled by antibodies, the pathogen actually became more aggressive and virulent than in the control mice that had these immune molecules intact.

The second reason this study is important is because weak immune systems should not cause the parasite to evolve in order to survive or infect other hosts. It holds true that if a strong immune system can kill a majority of a parasite, the ones that are left to reproduce then must be stronger or more evolved to survive. Now it is believed that in a weak immune system, the parasite is free to replicate to very high densities, causing competition among the resources. This leads to the more mature and virulent cells surviving and replicating in the host and thus the conclusion that compromised immune systems can increase virulence as much as and more than strong immune systems.

Rachel McGee