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Devangshu Datta: Lessons from the Ebola crisis

In May, a traditional healer in the small town of Koindu, Sierra Leone, died. Koindu is just across the border from Gueckedou, Guinea, where there had been an outbreak of a mystery fever in December 2013. The healer was treating patients in Guinea. Her herbal cures failed and she contracted the disease herself and died.

Her funeral was well-attended. A few weeks later, 14 of those who attended the funeral were dead, of the same illness. Some had helped to wash and dress the body for burial. Those 14 in turn, infected many more.

The fever is the Ebola virus disease (EVD). The funeral of “Patient Zero”, as the healer is referred to, unleashed an epidemic in Sierra Leone. Tragically, five members of the research team, which gene-sequenced 78 early victims and pinpointed the funeral as a source, have themselves died of EVD.

Ebola has claimed about 2,500 known mortalities since May, with cases logged in Guinea, Liberia, Nigeria and Sierra Leone. That toll includes 150-odd medical, paramedical and sanitation staff.

There is no cure. The treatment consists of support, isolation, replacement of blood and rehydration. The Ebola-Zaire strain at the centre of this epidemic has the highest mortality rates of up to 90 per cent.

EVD has at least five strains, with mortality rates of 50-90 per cent. There is terror in West Africa. Travellers out of that region are being screened and in some places, detained under observation, until the polymerase chain reaction test for EVD is negative.

The symptoms start with fever and flu-like symptoms. This is followed by internal and external bleeding. The virus is transmitted by body fluids. It gains entry through breaks in the skin, the eye-fluid, and the moist tissues of nose and mouth.

The virus carries a lone glyco-protein on its surface, which binds to the host’s cells. This glyco-protein is cloaked in benign carbohydrates, which helps it bypass immune systems. After tricking the immune system, EVD copies itself, and attacks the blood network.

Like all viruses, Ebola mutates. The Sierra Leone victims of May 2014 had 55 small mutations compared to the Guinea victims of December 2013. There are over 300 mutations compared to the last big outbreak of 1995. EVD also infects other primates. It has hit gorilla populations hard. EVD can stay infectious in dead hosts, leading to speculation that it mutated and jumped species, when a human consumed infected meat.

The World Health Organisation (WHO) has declared it an emergency. WHO estimates that the death toll could rise above 20,000 before this is controlled, in the next six to nine months. An epidemic would be reckoned over only if no new cases are registered for twice the incubation period – that is, 42 days.

Ebola was identified in 1976, when it was first seen in South Sudan and the Congo. Earlier outbreaks have all occurred in areas with low population density, cutting down public health risks. In 1976 and 1995, it proved self-limiting.

This time around, the disease has hit denser population centres, making it much harder to tackle. West Africa lacks infrastructure, equipment and protective gear to deliver isolation and to protect medics, paramedics and sanitation personnel.

WHO has relaxed its normal stringent controls against the use of experimental drugs. Researchers around the world are trying multiple methods of attacking the virus. One possible route is to use antibodies sourced from the blood of survivors. Any survivor has robust immunity to that strain, and some immunity to other strains. The use of “convalescent plasma” carries obvious dangers. But there are a large pool of survivors and plasma production could be rapidly scaled up for administration to the infected.

Vaccine developments use the recombinant approach. A different, similar virus (supposedly safe) is injected to stimulate the body into producing antibodies, which will fight EVD, Two potential vaccines are in clinical trials. The US Food and Drug Administration (FDA) officials say that initial safety data will be available in November 2014 and the vaccines could be fast-tracked for immediate use by those at high-risk.

One is an experimental blood serum, ZMapp, developed by an American pharma company, Mapp Biopharmaceutical. ZMapp uses three antibodies in a mixture to block or neutralise the virus, by binding to or coating different sites on the covering of the virus. Studies in monkeys showed strong survivals for up to five days after infection.

ZMapp had only been previously tested in primates. It was used on two American patients – aid workers evacuated from Liberia and treated in an American hospital. They survived. However, ZMapp is in short supply and in statistical terms, this is not much of a sample. The FDA is putting resources behind ZMapp but only a few hundred doses will be available by end-2014

Another drug is TKM-100802, from pharma research company TekmIra. TKM uses Small interfering Ribonucleic acid (siRNA) to target two essential viral genes to stop the virus replicating. It’s been effective in guinea pigs and monkeys. The FDA has cleared it for emergency use. Two other anti-virals with potential are AVI 7537 from pharma company Sarepta, and BCX4430 from BioCryst.

An intriguing option is Favipivavir, an anti-influenza drug, widely used in Japan. This has shown some positive results when used in very high dosages on EVD infected mice. The practical advantage is that it’s immediately available in quantity.

Some lessons have been learnt. WHO has reviewed its drug-use ethics. Policy-makers, starting with the FDA, have reviewed and accelerated drug-trial processes. The sense in the research and public health establishment is that a cure or cures will be found, however daunting the logistics of rolling that out at scale may be.

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