Whether you will survive an Ebola infection or not depends on the immune response of your body, not on the level of infection
a string of new human pathogens has been added recently to the popular pantheon of demonology. The Ebola virus is one of the deadliest among these. It resembles the influenza virus in the early stages of infection in terms of its effects, and rapidly induces fever accompanied by shock, diffuse bleeding and the destruction of blood cells (haemorrhagic fever). It causes death in about 70 per cent of infections.
Investigations on this virus have been difficult because reports of outbreaks come from relatively inaccessible regions and, of course, also because of the danger posed by the virus to the researchers themselves. In any infection, there tend to be a few individuals who are infected but do not die. A probable way to search for a cure is to try and find out not so much what causes death as what allows such people to survive. S Baize and colleagues from the Centre for International Medical Research in Gabon, Africa, have adopted this method ( Nature Medicine , Vol 5, No 4).
Baize and colleagues worked with samples taken from both survivors and non-survivors after two epidemics that broke out in Gabon in 1996. The first interesting observation was that both sets of people had similar viral loads in their systems. The implication is that the difference between them lay in the defence mechanisms of their bodies, rather than in their susceptibility to infection.
When examined in detail, many differences were found in the nature of the immune responses put up by the two sets of patients. In the early stages of the infection, those who were to die had higher levels of a protein known as gamma interferon, which suggests that the level of gamma interferon may be a useful clue for predicting the future of an affected individual. On the other hand, those who were to survive developed more effective immune responses early during the infection, including a higher level of circulating antibodies to viral proteins. This means that getting through an Ebola virus infection may have to do primarily with putting up a successful immune response.
To be sure, all this information is only of interest to researchers and scientists because at present, there is no way of translating it into improved therapy. But the observations have been described as among the most comprehensive analyses of the immune response to Ebola virus infection in humans, and provide interesting parallels to what happens in guinea pigs that are vaccinated with products of Ebola virus genes.
The vaccine provides some degree of immunity in these animals. And going by the present results, probably does so by controlling the growth of the virus at a fairly early stage of the infection. So far, there is no successful vaccine that works against Ebola in humans, though other anti-viral vaccines are in use. The effectiveness of a vaccine ultimately depends on a combination of innate and acquired factors. Exactly what these factors are in the case of Ebola, as well as other viruses that cause haemorrhagic fever, remains to be determined.
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