Here is a technique to produce a vaccine that I thought was rather clever. It was reported in last week's New Scientist. I don't know if it this technique has a definite name, so this node title is a provisional description.

A vaccine is something that resembles the target germ closely enough that antibodies created in response to the vaccine will also respond to the real live germ if it's ever encountered. It can be a fragment of the germ, or broken-up dead bodies of the germs killed to prevent their infecting the host, or live germs genetically modified to lack the nasty effects of the disease. This is applicable whether the germ (which seems almost an old-fashioned term - do we say 'disease agent' or something these days?) is a virus, a bacterium, or a fungus.

In this case it's the Herpes Simplex Virus, which has two main forms HSV-1 and HSV-2, causing cold sores and genital herpes. There has been progress but no success in creating vaccines against HSV in the conventional ways described above. The shape and complexity of the virus apparently mean there is no easily accessible molecule on its surface that is a clear sign detectable by antibodies.

The problem with using live but attenuated (harmless) versions of the virus is that herpes hangs around in the body for years. Some fortuitous combination of stress, mutation, or exchange of genes with virulent organisms could turn the latent herpes back into a harmful infection. You don't want the vaccine to hang around after it's done its job of priming the immune system to create antibodies.

The clever trick is to take one of its reproductive genes, in this case one called gH that codes for a bit of the protein coat, and transplant it into human cells. These are then cultured in vitro. The HSV happily reproduces because when it infects the human cells they produce this essential protein. A virus is, after all, a highly efficient scavenger of other cells' genetic repositories. It doesn't care if the ability is no longer resident in its own genes.

So after a while you have a great big Petri dish full of genetically modified HSV, which is missing both the nasty disease-causing effect and the ability to produce its own protein coat. When given to normal human cells in a human being, it infects them, triggers antibodies, tries to reproduce, and dies for lack of gH.

An abstract of an article entitled 'Recent Progress in Herpes Simplex Virus Immunobiology and Vaccine Research' is available at the following address, where they describe (what I presume are) the above forms as 'mutant strains that undergo incomplete lytic replication':