Africa Resilience Initiative

Boston University scientists curbed the host response to Ebola infection by inhibiting TLR4 in macrophages. (CDC Global CC BY 2.0)

CLICK HERE - Virology - Ebolaviruses associated with differential pathogenicity induce distinct host responses in human macrophages

fiercebiotech.com - by Amirah Al Idrus - March 23, 2017

The Ebola virus causes a disease that is often fatal, in part by infecting white blood cells called macrophages and disrupting their immune response. Boston University scientists found that using drugs that block the protein TLR4 can suppress this response and potentially control infection.

Macrophages are responsible for detecting and destroying pathogens, but the Ebola virus activates them through the Toll-like receptor 4 (TLR4) pathway, causing an inappropriate immune response. The Ebola-infected macrophages end up producing excess cytokines and chemokines—proteins that promote inflammation and worsen the disease.

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CLICK HERE - International Peace Institute - The Mission to Stop Ebola: Lessons for UN Crisis Response (28 page .PDF report)

reliefweb.int - February 15, 2017
ADAM LUPEL AND MICHAEL SNYDER

Executive Summary

The Ebola epidemic of 2014–2016 was a fastmoving, multidimensional emergency that pre - sented unprecedented challenges for the multi - lateral system. In response to the outbreak, which was spreading exponentially in Guinea, Liberia, and Sierra Leone, Secretary-General Ban Ki-moon established the UN’s first-ever emergency health mission, the UN Mission for Ebola Emergency Response (UNMEER). UNMEER was mandated by the UN General Assembly in September 2014 to scale up and coordinate the activities of the UN presence on the ground working to stop the outbreak, which eventually claimed over 11,000 lives.

This report asks: Was UNMEER needed? Was it properly structured? Did it deliver? And what broader lessons can be learned from the experience of UNMEER for UN crisis response?

ANDRES MARTINEZ CASARES/REUTERS

The world’s humanitarian needs are growing. So is the aid gap.

huffingtonpost.com - by Jesselyn Cook - January 13, 2017

The global need for humanitarian aid has reached a level not seen since World War II. More than 128 million people in 33 countries are now affected by crises, including conflict and natural disaster . . . 

 . . . Despite the worsening nature of many of the world’s crises, internet traffic reveals “public fatigue” ― a decline in interest ― for the first time in three years, according to U.N. data. And, as the world’s humanitarian needs grow, the gap between funds needed and funds raised has widened.

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WIKIMEDIA, HELLERHOFF

CLICK HERE - STUDY - Detection of Viral RNA in Tissues following Plasma Clearance from an Ebola Virus Infected Patient

A case study reports evidence of viral replication lingering in the respiratory tract of an infected person, even after their blood was Ebola free.

the-scientist.com - by Bob Grant - January 5, 2017

Ebola virus may linger and continue to replicate in the lungs of patients recovering from infection, even after viral RNA is no longer detectable in their bloodstreams, according to a case study published today (January 5) in PLOS Pathogens. . . .

 . . . Ippolito and his colleagues monitored the Ebola-infected patient, who was moved from West Africa to a hospital in Italy in 2015, over the course of their infection. They found viral RNA and other markers of viral replication in the patient’s lungs five days after such markers were no longer detectable in the blood.

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