The apparent ability of certain viruses, such as HIV, to develop (“evolve”) immunity to drug treatment represents convincing, real-time proof of evolutionary advance, according to some biologists. 1 Recent research, however, poses a potent threat to this emerging icon of evolutionary theory. 2 Scientists have uncovered an alternative explanation for the acquired immunity, one that argues against naturalistic evolution.
The viruses in question, RNA viruses also called “retroviruses,” act like other viruses in most respects. All viruses may be described as protein capsules with genetic material (usually DNA) in their core. 3 Viruses first attach themselves to healthy cells and then inject their genetic material into those cells. The viral genetic material takes over the cells’ operation, forcing the repeated production of viral proteins and genetic material. Eventually, the accumulating viral particles cause the host cell to rupture. This burst sends out large numbers of viruses to repeat the cycle of infection.
Since the genetic material in retroviruses is RNA, it must convert into DNA inside the host cell. 4 This newly made DNA directs the manufacture and assembly of more retroviruses. But the enzyme (reverse transcriptase) in charge of copying the viral RNA to make retroviral DNA is prone to error. The high rate of copying errors means a high mutation rate for RNA viruses. 5
Mutations alter the viral proteins, thus the drug-protein interaction. Antiviral drugs targeting the original viral proteins may have little or no effect on the mutated (modified) proteins. When this happens, the drugs lose their capacity to halt the spread of an RNA virus. Natural selection receives the credit for this change. In the lingo of evolution, a mutation that benefits the virus (in this case, one that enables it to avoid the drug’s impact) has become fixed in the virus’s genetic material, and it will remain as long as the virus is exposed to the antiviral therapy.
Researchers at the Pasteur Institute uncovered a different scenario, one that does not adhere to the pattern depicted above. 6 Based on their study of 85 sets of proteins from viruses that infect mammals, plants, and bacteria, they concluded that RNA viruses change by genetic drift (random genetic variations within the viral material) rather than in response to drugs. Genetic drift proceeds at a clock-like, roughly consistent rate, regardless of exposure to drug treatment. In other words, the rate and type of protein change caused by RNA viruses remained the same whether or not the viruses encountered antiviral drugs.
Independent modeling studies designed to identify the origin of drug resistance in retroviruses affirm this conclusion. 7 If drug resistance evolves, it should stem from new viral strains (mutations) generated in the midst of drug treatment. Instead, modeling studies show that the drug-resistant strains are already present when drug therapy begins. They do not emerge after drug therapy is initiated. In other words, pre-existing strains of RNA viruses happen to be insensitive to specific antiviral drugs, and these continue to live while the drug-sensitive strains die off.
In his book Icons of Evolution, biologist Jonathan Wells cites many textbook evidences for evolution (including some that scientists have relied on most heavily) that lack or contradict experimental and observational confirmation. 8-9 The case for adaptive immunity of RNA viruses would seem to belong on that list.