13.19: HIV illustrates the difficulty of controlling infectious viruses.

New infectious diseases—some caused by bacteria and others by viruses—emerge quite frequently. Many of these new diseases originate in other species of animals and subsequently acquire the ability to infect humans. There are enough of these new diseases to fill the monthly issues of the journal Emerging Infectious Diseases, which is published by the Centers for Disease Control and Prevention. But even in that crowd, acquired immunodeficiency syndrome (AIDS) stands out. AIDS is caused by the human immunodeficiency virus (HIV), which is derived from a strain of the simian immunodeficiency virus (SIV) that jumped from chimpanzees to humans in the early 1900s. HIV has all of the characteristics that make viral diseases hard to control—plus an additional characteristic of its own.

HIV mutates easily. HIV is a retrovirus, an RNA-containing virus that also contains a viral enzyme called reverse transcriptase that uses a strand of viral RNA as a template to synthesize a single strand of DNA. That DNA strand, in turn, is used as a template to make a complementary strand of DNA, and the resulting double-stranded DNA is integrated into the host cell’s DNA. From here, the DNA is used by the host cell’s machinery to make more viral RNA (FIGURE 13-29). Reverse transcriptase is so error-prone, however, that virtually every copy of HIV in an infected individual’s body has a different mutation.

This enormous genetic variation in the HIV particles circulating in an infected person’s body makes the infection hard to treat. Virus particles with different mutations can have different proteins on their surfaces, and these surface proteins change each time the virus replicates inside a host cell. Each new generation of HIV in the infected individual contains viruses with surface proteins that his or her immune system has never seen. Furthermore, some of the HIV mutations will confer resistance to the drugs that are being used to treat the patient, and new drugs must be used.

HIV attacks white blood cells. All of those problems would apply to any disease caused by a retrovirus, but HIV offers an additional challenge: it targets cells in the host’s immune system, especially white blood cells, and particularly those that search for and attack invading bacteria or viruses. During the incubation period, which can last for many years, HIV infects white blood cells. New ones are produced to replace those killed by the virus, however, and the infected person has virtually no symptoms. Nonetheless, HIV is present in the individual’s body fluids during the incubation period and can be transmitted to other individuals. HIV testing is used to detect infections during this stage.

Each time HIV infects another white blood cell, the reverse transcriptase makes errors in transcribing the RNA to DNA, and eventually one of the mutations allows the virus to bind to the glycoprotein on the surface of a specialized type of white blood cell—a bacteria- and virus-hunting white blood cell that is critically important in identifying disease-causing threats. A suitable mutation may occur in a couple of years, though more often it takes about 10 years or longer. But when it does happen, it signals a new stage in the HIV infection: the development of AIDS (FIGURE 13-30).

The immune system collapses. Normally, white blood cells all work together to identify and destroy cells that have been infected by a virus. When HIV begins to kill the cells that hunt for viruses and bacteria, the immune system begins to fail—it can no longer respond to HIV, or to any other infectious agent. Patients with AIDS develop multiple infections, bacterial and viral, as well as cancers, because they have lost the immune system cells that would normally have marked infected and cancerous cells for destruction.