FEW accidents would be more ironic than the contamination of a vaccine by a virulent disease. Fortunately, despite rumours that contaminated vaccines assisted the rapid spread of AIDS, this has never been proved to have happened in a vaccine intended for people. Chickens are not so lucky. Christian Hertig, a biologist at the University of Bern, and his colleagues have just found a beast called reticuloendotheliosis virus (REV) lurking unpronounceably in one of the vaccines used to innoculate them against fowlpox.
Like HIV, the agent that causes AIDS, REV is a retrovirus. This means that its genes are made of RNA, DNA's less stable cousin. On arrival in a cell, therefore, a retrovirus has to create DNA versions of its genes and splice them into its host's chromosomes before that host can be tricked into making copies of the intruder.
This might seem an awkward way to proceed, but it allows a retrovirus to multiply in two different ways. The viral genes may be read directly by the host's molecular machinery and used to produce new viruses straight away, or they may be copied along with the rest of the chromosome in which they are hiding every time a cell containing them divides.
This dual life-cycle means that, besides disrupting normal cellular activities in the ways that other viruses do, a retrovirus may also disrupt the normal function of its host's chromosomes. Sometimes, this disruption damages the host's genes so that they no longer work properly; sometimes, more subtly, it switches on genes that would be better left switched off. REV, for example, can trigger the activity of cancer-promoting genes and, as a consequence, it causes a wide range of gallinaceous tumours.
The significance of Dr Hertig's discovery, besides finding the flaw in the vaccine in question, is to confirm what had been shown only once before: that retroviruses have a third means of reproduction available to them. This third way is to insert their genes into another, more conventional virus instead of a traditional animal host. That means they can hitch-hike around in ways that would not normally be open to them because of their fragility.
Nor is the benefit all in one direction. Taking a hitch-hiker on board is not without its risks for the host virus—a retroviral gene in the wrong place could disrupt its DNA just as badly as it does that of an animal host—but it can also be a way for the host virus to acquire new genes. Retroviruses often accumulate bits and pieces of genes as a side-effect of their activities. When jumping into another virus, they may bring those host genes with them.
Pox viruses do, indeed, carry a range of genes that bear a striking resemblance to those of their hosts. Dr Hertig speculates that some of these genes may have been picked up from retroviruses and that they could be important in persuading animal immune systems to leave the pox virus alone.
The two sorts of virus may also help each other in another way. One of REV's effects is to suppress its host's immune response. That should assist the transmission of viruses such as fowlpox. It comes as no surprise, therefore, that Dr Hertig's results suggest that at least one sort of fowlpox had carried REV as a passenger for decades before an “attenuated” strain of it was made for use as a vaccine. That the vaccine was affected is just bad luck; when it was first produced, retroviruses were unknown. But if it happened again—particularly in a vaccine intended for people—that really would look like carelessness.
This article appeared in the Science & technology section of the print edition under the headline "Foulpox"