One-Two Punch: Vaccine fights herpes with antibodies, T cells

An experimental vaccine tested in animals incites a double-edged immune reaction against the virus that causes genital herpes. The finding may pave the way for tests in people. The vaccine stirred up both antibodies and immune cells against herpes simplex virus 2, suggesting it might work as both a preventive and a treatment. Herpes causes painful skin blisters and spreads easily from person to person.

Other herpes vaccines created from viral proteins (SN: 12/21/02, p. 399: Available to subscribers at Herpes vaccine progresses) and viral DNA (SN: 8/19/00, p. 116: Available to subscribers at DNA vaccine immunizes fetal lambs) have induced antibody production against the virus but delivered inconsistent benefits. The new vaccine, called dl5-29 and made by Avant Immunotherapeutics of Needham, Mass., instead consists of a live herpes virus that’s missing two critical genes. Another potential vaccine, further along in testing, is made by removing different genes.

With these genes missing, the viruses can’t replicate. When injected into mice and guinea pigs, dl5-29 survives long enough to infect cells and trigger an immune response that includes antibodies and immune cells called CD8 T cells.

In the new study, which appears in the January Journal of Virology, researchers injected some animals with dl5-29, while giving others a protein-based or DNA-based vaccine. The Avant vaccine protected against new herpes infections as well as or better than the others did, says coauthor David M. Knipe, a virologist at Harvard Medical School in Boston.

Also, in guinea pigs previously infected with genital herpes, dl5-29 limited disease recurrence significantly more effectively than the other types of vaccine did.

The scientists didn’t test the new vaccine against the other experimental live-virus herpes vaccine, Delta PK, made by AuRx of Glen Burnie, Md. Delta PK, has halted herpes recurrences for a year in nearly half of infected people given the vaccine, AuRx scientists have reported.

Immunologist Laure Aurelian of the University of Maryland School of Medicine in Baltimore says it isn’t clear whether the new vaccine represents an improvement over Delta PK, which has also outperformed virus-protein and DNA-based herpes vaccines by eliciting antibody and T cell responses.

Aurelian notes that both dl5-29 and Delta PK hike production of a CD8 T cell protein called interferon gamma. Previous evidence indicated that interferon gamma suppresses symptoms by preventing re-emergence of herpes virus, which lurks in the nervous system.

The choice of genes knocked out in the Delta PK vaccine might make it more powerful than dl5-29, Aurelian suggests. Without a gene that serves as a signal to shut off an attack on herpes, Delta PK instructs the immune system to root out the symptom-causing viruses.

Combining aspects of dl5-29 and Delta PK could produce a potent vaccine, Aurelian says, but because different companies own the patents to the processes behind these vaccines, such a move seems unlikely.

Aurelian cautions that when vaccines are made by growing viruses in cells in a lab dish, the viruses might pick up the cells’ replication genes and become infectious. Thus, Delta PK will probably be used not for preventing herpes infections but “solely by people already being treated for the disease,” says Gary J. Calton, president of AuRx.

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