Infectious Disease

To anyone who remains unconvinced of the pervasive influence of genes on human health, consider also the connection to infectious microbial parasites. A multitude of infectious viruses, bacteria, and yeasts provoke colds, influenzas, and many other annoying and sometimes life-threatening human diseases. Protozoans that produce malaria, sleeping sickness, Chagas' disease, leishmaniases, and other diseases infect more that 10 percent of the world's population and account for tens of millions of deaths every year. Throughout human history, epidemics such as smallpox have touched the lives of countless millions of people. The virus responsible for smallpox recently was eradicated,22 and the polio virus too may soon meet its demise, but numerous other microbes remain to cause such age-old scourges as measles, cholera, pneumonia, hepatitis, and tuberculosis.

Infectious microbes contain their own genes that impact human and microbial affairs, and science has unveiled many of the modes of their actions. As noted by Lewis Thomas twenty years ago, "Without the long, painstaking research on the tubercle bacillus, we would still be thinking that tuberculosis was due to night air, and we would still be trying to cure it by sunlight."23 One mounting problem in the quest to combat infectious diseases is that microbes often evolve resistance to vaccines, drugs, or other therapies directed against them. Tuberculosis bacteria, for example, have become increasingly resistant to standard antibiotics, as have the microbes responsible for malaria, cholera, pneumonia, blood infections, and a host of other infectious diseases.

On the human side of the equation, people vary greatly in their genetic susceptibility to infection. One dramatic example is provided by human resistance to the AIDS virus. Doctors long have been intrigued by the fact that some individuals repeatedly exposed to HIV nonetheless remain free from the disease. There is now an explanation for this phenomenon.24 On the cell surfaces of HIV-

susceptible individuals, a glycoprotein molecule called "CC-chemokine receptor 5" mediates cellular entry of the virus. In HIV-resistant individuals, a truncated form of the glycoprotein (due to a deletion mutation in the CCR-5 gene) blocks HIV entry. The frequency of this mutant allele in the Caucasian population is about 10 percent, and natural resistance to infection is strongest in homozygous individuals.

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