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Why Ebola virus flares up in West Africa, by scientists

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(FILES) This file photo taken on March 26, 2015 shows Sierra Leone health officials checking passengers transiting at the border crossing with Liberia in Jendema before authorities in Sierra Leone started enforcing on March 27 a three-day lockdown to curb the spread of Ebola, with the entire population ordered to stay at home. The latest flare-up of Ebola in Sierra Leone has ended, leaving no confirmed cases of the virus in West Africa, the UN said on March 17, 2016, hailing a "milestone" in the fight against the outbreak. "The World Health Organization joins the government of Sierra Leone in marking the end of the recent flare-up of Ebola virus disease in the country," a statement said. / AFP / ZOOM DOSSO

(FILES) This file photo taken on March 26, 2015 shows Sierra Leone health officials checking passengers transiting at the border crossing with Liberia in Jendema before authorities in Sierra Leone started enforcing on March 27 a three-day lockdown to curb the spread of Ebola, with the entire population ordered to stay at home.<br />The latest flare-up of Ebola in Sierra Leone has ended, leaving no confirmed cases of the virus in West Africa, the UN said on March 17, 2016, hailing a “milestone” in the fight against the outbreak. “The World Health Organization joins the government of Sierra Leone in marking the end of the recent flare-up of Ebola virus disease in the country,” a statement said. / AFP / ZOOM DOSSO

Aerial spraying of mosquitoes linked to autism risk in kids
Two new, but independent, studies published in Nature have provided clues about the repeated Ebola Virus Disease (EVD) flare-ups in West Africa and how aerial spraying to combat mosquitos is linked to increased risk of autism in children.

According to one of the researches, also published online in the journal Science Advances, Ebola virus samples taken from patients in Liberia in June 2015 are strikingly similar in their genetic makeup to other Ebola virus sequences from Western Africa.

The study sheds light on several aspects of the “flare-ups” that have occurred in Liberia since the country was initially declared free of Ebola virus disease.

As described in the paper, genomic analysis and the epidemiological investigation indicate that the June 2015 flare-up was a re-emergence of a Liberian transmission chain originating from a persistently infected source. This was also the case with a March 2015 Liberian flare-up. Neither event was caused by re-introduction of the virus from an animal reservoir or from a neighbouring country with active person-to-person transmission, according to the research team. While the March flare-up was traced to sexual contact, no definitive link has been found for the June event.

Also, another research published in Nature and to be presented at the Pediatric Academic Societies 2016 Meeting suggests that the use of airplanes to spray anti-mosquito pesticides may increase the risk of autism spectrum disorder and developmental delays among children.

The researchers who will present the abstract, “Aerial Pesticide Exposure Increases the Risk of Developmental Delay and Autism Spectrum Disorder,” identified a swampy region in central New York, United States (US), where health officials use airplanes to spray pyrethroid pesticides each summer. The pesticides target mosquitos that carry the eastern equine encephalitis virus, which can cause swelling of the brain and spinal cord.

They found that children living in ZIP codes in which aerial pesticide spraying has taken place each summer since 2003 were approximately 25 percent more likely to have an autism diagnosis or documented developmental delay compared to those in ZIP codes with other methods of pesticide distribution, such as manually spreading granules or using hoses or controlled droplet applicators.

Meanwhile, the Ebola study co-first author Dr. Jason T. Ladner, of the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID), said: “When the June cluster of cases was first detected, the initial expectation of investigators was that it likely originated from a re-introduction of the virus from Sierra Leone or Guinea, where human-to-human transmission was active.
“This explanation was favored because the typical route of Ebola virus transmission is through infectious body fluids from individuals in the acute phase of the disease, when they are most symptomatic.”

However, genomic sequencing, combined with epidemiological investigation, indicated that the cases did not represent a re-introduction from a neighbouring country.

“Although this finding did not necessarily play a major role in the control of this particular cluster, it certainly emphasized the risk for additional flare-ups, even within areas where active spread of the virus has been stopped,” Ladner said. “This understanding has led to heightened vigilance, which has allowed for rapid response to the additional flare-ups that have occurred.”

Ebola virus causes severe haemorrhagic fever in humans and nonhuman primates with high mortality rates and continues to emerge in new geographic locations, including Western Africa, the site of the largest recorded outbreak to date. More than 28,000 confirmed, probable and suspected cases have been reported in Guinea, Liberia and Sierra Leone, with more than 11,000 reported deaths, according to the World Health Organisation.

In the paper, the research team, which includes scientists from the U.S. Centres for Disease Control and Prevention, the Liberian Ministry of Health, and USAMRIID, points out the risk of Ebola virus disease flare-ups even after an outbreak is declared to be over. Since the June 2015 flare-up, at least four more documented flare-ups have occurred (two in Liberia, one in Sierra Leone and one in Guinea), according to the authors.

Co-senior author, Dr. Gustavo Palacios, of USAMRIID said: “From an epidemiological standpoint, this research demonstrated the value of full genome sequencing during an outbreak.

“The viral genomes from the June flare-up were compared to what had been sequenced already, which allowed us to determine that the virus was indeed Liberian in origin. This helped confirm what the epidemiological teams were finding in their investigation and focused efforts on looking for potential sources of persistent infection within and around the affected community.”

According to Palacios, the study was made possible by the in-country laboratory capability established by USAMRIID in 2015 in collaboration with the Liberian Institute for Biomedical Research (LIBR) and the Liberian Ministry of Health. This state-of-the-art, high-throughput sequencing facility allows the team to conduct near real-time genomic sequencing.

The viral genomes also helped to tell another story, USAMRIID co-first author Michael R. Wiley said. He noted that a reduced rate of evolution was associated with the June 2015 flare-up – meaning that the genetic signature of the virus had not changed significantly over time. When the team looked at the March 2015 cluster, which had been associated with sexual transmission, they found the same signature – a reduced rate of evolution.



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