The Pharmaceutical Journal
Vol 273 No 7307 p47
10 July 2004

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Strategies for TB and HIV vaccines need rethinking

Strategies used in the development of vaccines against tuberculosis and HIV need to be rethought, according to the authors of two recently published articles.

In the first, researchers from the University of Washington examined the way in which Mycobacterium tuberculosis infects host cells. More specifically, they looked at the mechanisms used by mycobacteria to re-emerge at times of poor health and at how new strains of the bacteria are able to reinfect the same person despite vigorous host immune responses.

The researchers explain that immunity to tuberculosis is concentrated in complex immune structures called granulomas. These structures comprise various immune cells and are thought to act by containing the bacteria. Theories behind reinfection have included an assumption that new bacteria are able to evade established granulomas.

With this in mind, the tenet of vaccine strategies so far has been to improve the immunogenicity or persistence of vaccine strains. However, the researchers show, using animal models of TB infection, that newly infecting bacteria rapidly enter and survive in these granuloma. So, rather than bacteria avoiding the granuloma, reinfection can occur because the original immune response is not mounted effectively. “Consequently, a thorough re-evaluation of strategies for the development of an improved tuberculosis vaccine is warranted,” they conclude (Nature Immunology published online on 27 June).

The authors of the second article, from the International AIDS Vaccine Initiative in New York, say that the challenge of developing a vaccine effective enough to stem the spread of HIV-1 is daunting. They suggest that research should concentrate on improving vaccine vectors and new vaccine strategies. They point to various aspects about the virus that are poorly understood — its structural vulnerability to neutralising antibody, its multiple cellular immune interactions, early events during the establishment of persistent infection and the association between human immune responses and the genetics of HIV. “Addressing these issues will require a degree of collaborative scientific activity and commitment well beyond the current global effort.” (Science 2004;304:1913.)