Genetic Resistance to Infection

In certain cases, the genetic makeup of an individual is different enough to ensure protection from infection by some pathogens. One explanation for this phenomenon is that some pathogens have such great specificity for one host species that they are incapable of infecting other species. Another way of putting it is: “Humans can’t acquire distemper from cats, and cats can’t get mumps from humans.” This specificity is particularly true of viruses, which can invade only by attaching to a specific host receptor. But it does not hold true for zoonotic infectious agents that attack a broad spectrum of animals. Genetic differences in susceptibility can also exist within members of one species. Humans carrying a gene or genes for sickle-cell anemia are resistant to malaria. Genetic differences also exist in susceptibility to tuberculosis, leprosy, and certain systemic fungal infections.

The vital contribution of barriers is clearly demonstrated in people who have lost them or never had them. Patients with severe skin damage due to burns are extremely susceptible to infections; those with blockages in the salivary glands, tear ducts, intestine, and urinary tract are also at greater risk for infection. But as important as it is, the first line of defense alone cannot provide adequate protection. Because many pathogens find a way to circumvent the barriers by using their virulence factors, a whole new set of defenses – inflammation, phagocytosis, specific immune responses – is brought into play.