Pathophysiology of Ebola virus

ABSTRACT 

Ebola virus, a member of the Filoviridae virus family, is still an untamed, highly lethal viral pathogen that represents a nightmare for much of central Africa, which is the site of the majority of EBOV outbreaks (Geisbert et al.2010). Unfortunately there has not been a large push in the search for a vaccine as this virus, as deadly as it is, has not impacted a large portion of the world’s population with only 2,300 reported cases of hemmorraghic fever caused by filoviruses. On a more positive note there are many candidate vaccines that have displayed very effective results on non-human primates, as they have protected these patients from the viral effects of EBOV. Many of these potential cures may become a future vaccine to help save the lives of those who have fallen victim to the deadly illness. Leading the way in the race for a cure is the recent work done by Geisbert et al. (2010), who has obtained nearly flawless results through the use of siRNAs to target and inhibit the lethal effects of EBOV. With the persistence and drive of the researchers that continue to be hard at work in search for a vaccine, we may someday soon be able to eliminate the fear of future epidemic EBOV outbreaks, and save many innocent lives from being taken by the deadly virus. This review will focus the pathophysiology of Ebola virus disease and its prevention and control strategies. 

TABLE OF CONTENTS

CHAPTER ONE 

1.0 Introduction         1

CHAPTER TWO 

2.1 Ebola virus disease       3 

2.2 Transmission       5

2.3 Epidemiology                 7

CHAPTER THREE

3.1 Pathophysiology of Ebola virus       8

 3.1.1Immune System Evasion      12

3.1.2Immune Response to Ebola Virus Infections      13

3.2 Signs and Symptoms of Ebola Virus Disease          17

3.3 Persistent Virus in People Recovering From Ebola Virus Disease                    17

3.4 Prevention and Control      18

3.4.1 Controlling Infection in Health-Care Settings      19

3.5 Treatment and Vaccines        20

CHAPTER FOUR

4.1 Conclusion                  22

REFERENCE