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Ebola Virus Infection Treatment & Management

  • Author: John W King, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
Updated: Jun 03, 2016

Approach Considerations

General medical support is critical and should include replacement of coagulation factors and heparin if disseminated intravascular coagulation develops. Such care must be administered with strict attention to barrier isolation. All body fluids (blood, saliva, urine, and stool) contain infectious virions and should be handled with great care.

Currently, no specific therapy is available that has demonstrated efficacy in the treatment of Ebola hemorrhagic fever. Surgical intervention generally follows a mistaken diagnosis in which Ebola-associated abdominal signs are mistaken for a surgical abdominal emergency. Such a mistake may be fatal for the patient and for any surgical team members who become contaminated with the patient’s blood.

There are no commercially available Ebola vaccines. However, a recombinant human monoclonal antibody directed against the envelope GP of Ebola has been demonstrated to possess neutralizing activity. This Ebola neutralizing antibody may be useful in vaccine development or as a passive prophylactic agent. Work on a vaccine continues.


Supportive Care

Supportive therapy with attention to intravascular volume, electrolytes, nutrition, and comfort care is of benefit to the patient. Intravascular volume repletion is one of the most important supportive measures.

Survivors can produce infectious virions for prolonged periods. Therefore, strict barrier isolation in a private room away from traffic patterns must be maintained throughout the illness. Patient’s urine, stool, sputum, and blood, along with any objects that have come in contact with the patient or the patient’s body fluids (such as laboratory equipment), should be disinfected with a 0.5% sodium hypochlorite solution. Patients who have died of Ebola virus disease should be buried promptly and with as little contact as possible.


Pharmacologic Therapy

Nucleoside analogue inhibitors of the cell-encoded enzyme S-adenosylhomocysteine hydrolase (SAH) have been shown to inhibit Zaire Ebolavirus replication in adult BALB/c mice infected with mouse-adapted Ebola virus.[21] Inhibition of SAH indirectly inhibits transmethylation reactions required for viral replication. Treatment response was dose-dependent. When doses of 0.7 mg/kg or more every 8 hours were begun on day 0 or 1 of infection, mortality was completely prevented. Even when the drug was given on day 2, 90% survived.

Smith et al found that in rhesus macaques infected with a lethal dose of Ebola virus, treatment with interferon beta early after exposure led to a significant increase in survival time, though it did not reduce mortality significantly.[22] These findings suggest that early postexposure interferon-beta therapy may be a promising adjunct in the treatment of Ebola virus infection.

Passive immunity has been attempted by using equine-derived hyperimmune globulins and human-derived convalescent immune globulin preparations. In Ebolavirus -infected cynomolgus macaques, use of human recombinant interferon alfa-2b in conjunction with hyperimmune equine immunoglobulin G (IgG) delayed but did not prevent death.

Equine IgG containing high-titer neutralizing antibodies to Ebola virus protected guinea pigs and baboons but was not effective in protecting infected rhesus monkeys.

During the 1995 outbreak in Kikwit, DRC, human convalescent plasma was used to treat 8 patients with proven Ebola disease, and only 1 patient died. Subsequent studies could not demonstrate survival benefit conferred by convalescent plasma products. The survival of these patients suggests that passive immunity may be of benefit in some patients.

Four laboratory workers in Russia who had possible Ebola exposure were treated with a combination of a goat-derived anti-Ebola immunoglobulin plus recombinant human interferon alfa-2. One of these patients had a high-risk exposure and developed clinical evidence of Ebola virus infection. All 4 patients recovered.

A recombinant human monoclonal antibody directed against the envelope glycoprotein (GP) of Ebola virus has been demonstrated to possess neutralizing activity. This Ebola virus−neutralizing antibody may be useful in vaccine development or as a passive prophylactic agent.

DNA vaccines expressing either envelope GP or nucleocapsid protein (NP) genes of Ebola virus have been demonstrated to induce protection in adult mice exposed to the virus. These vaccines were administered by coating gold beads with DNA expressing the genes for either GP or NP, and they were delivered by skin particle bombardment using a PowderJect-XR gene gun. Both vaccines induced measurable antibody responses detected by enzyme-linked immunosorbent assay (ELISA) and induced cytotoxic T-cell immunity.

Other experimental therapies that use available drugs, though not approved by the US Food and Drug Administration (FDA) for treatment of Ebola virus infection, may be considered. Agents that may reduce mortality without directly effecting viral replication include activated protein C[1] and a recombinant nematode anticoagulant protein (NAP) that inhibits activated factor VII-tissue factor complex.[2] NAP resulted in attenuation of the coagulopathy associated with decreased fibrinolysis and fibrin deposition with a resultant decrease in the severity of the systemic inflammatory response syndrome.

In a rhesus macaque model of Ebola hemorrhagic fever, which carries a mortality approaching 100%, Geisbert et al administered recombinant nematode anticoagulant protein, a potent inhibitor of TF-initiated coagulation.[2] One third of the monkeys given the nematode anticoagulant protein survived a lethal dose of Ebola virus, whereas 16 of the 17 (94%) control animals died. This approach targeted the hemorrhagic disease component of the infection rather than the virus itself.

In April 2016, the FDA granted orphan designation to aphidicolin for the treatment of Ebola virus infection. Aphidicolin is an inhibitor of B-family DNA polymerases, which inhibit the cell cycle at the G1/S border. If the cell is exposed to aphidicolin during S-phase, DNA replication is interrupted.[23]

In a benchtop experiment analyzing the influence of cell cycle arrest on Ebola virus infection, cells in G1/S phase were exposed to aphidicolin, a potent cell cycle inhibitor. A dose-dependent decrease in Ebola-infected cells was noted. Cells exposed to aphidicolin were allowed to resume cell cycle and then exposed to Ebola virus, which showed a time-dependent increase in infected cells.[24]

Small interfering RNA

One approach to blocking Ebola virus replication involves the use of antisense nucleotides that are complementary to sequences in the RNA polymerase complex. Shortly after a lethal challenge of Zaire Ebola virus was given, the administration of small interfering RNAs (siRNAs) packaged in stable nucleic acid-lipid particles targeting the RNA polymerase L protein protected guinea pigs[25] and macaques[26] .

More recently, third-generation synthetic antisense oligonucleotides called phosphorodiamidate morpholino oligomers (PMOs) have been shown to sterically hinder mRNA processing. Positively charged Ebola virus–specific PMOs that target VP24 and VP35 mRNA sequences (AVI-6002, a combination of AVI-7537 and AVI-7539) protect rhesus monkeys after lethal viral challenge.[27, 28] In addition, a recently completed phase I study of AVI-6002 in human volunteers showed that the drug was safe and well-tolerated.[29]

Monoclonal antibodies

Postexposure prophylaxis

Preliminary studies in cynomolgus macaques given a cocktail of 3 different murine monoclonal antibodies (mAbs; ZMab) directed against Ebola virus envelope glycoprotein epitopes demonstrated postexposure prophylactic activity 1-2 days after an Ebola virus challenge.[30] That result was matched by a mixture of 3 chimerized anti–Ebola virus mAbs (MB-003) having human constant regions produced in genetically modified tobacco plants. When given as postexposure prophylaxis 2 days after viral challenge, MB-003 was active both in mice and rhesus macaques.[31, 32]


The focus of mAb research is now shifting toward treatment of established infection. In that regard, 43% of rhesus macaques treated with MB-003 after onset of Ebola virus infection survived versus none of the untreated controls.[33] Established infection was defined as fever and positive Ebola virus reverse-transcription polymerase chain reaction (RT-PCR) result. Similarly, ZMab yielded a 50% survival rate in cynomolgus macaques when given starting on day 4 after viral challenge.[34]

Recently, an optimized combination of humanized mAbs produced in genetically modified tobacco plants and having specificity for 3 different Ebola virus glycoprotein epitopes rescued 100% of rhesus macaques even when given at advanced stages of disease 5 days after viral challenge (ZMapp; Mapp Biopharmaceutical, Inc., San Diego, CA, USA; and Defyrus, Inc., Toronto, Canada).[35, 36] In addition, two patients with Ebola virus disease in the United States who recently received ZMapp through emergency investigational new drug approval (US FDA) experienced declines in viral load and survived.[37] Subsequently, another 3 of 4 individuals treated with ZMapp survived.[38] These results suggest that ZMapp may prove useful for the treatment of established infection in humans.


Diet and Activity

Nutrition is complicated by the patient’s nausea, vomiting, and diarrhea.

Recovery often requires months, and delays may be expected before full resumption of normal activities. Weight gain and return of strength are slow. Ebola virus continues to be present for many weeks after resolution of the clinical illness. Semen from men recovering from Ebola infection has been shown to contain infectious virus, and Ebola has been transmitted by sexual intercourse involving recovering men and their sex partners. Any individuals who were exposed to infected patients should be watched closely for signs of early Ebola virus disease.



Prevention in healthcare personnel

Recent (2014) guidance from the CDC recommends that healthcare personnel who care for patients infected with Ebola virus (ie, physicians, nurses, other clinicians) wear personal protective equipment (PPE) that does not expose any skin. This includes a surgical hood that covers the head and neck and a single-use full face shield (rather than goggles), in addition to either a N95 respirator or powered air-purifying respirator instead of a mask.

The CDC now recommends that clinicians train rigorously at donning and doffing PPE in a stepwise manner and demonstrate competency. A trained monitor should oversee each time a clinician puts on and takes off this gear.

During patient care, the PPE should not be adjusted, and the worker’s gloved hands should be disinfected frequently using an alcohol-based hand rub (ABHR), especially after body fluids are handled.[39]


Work continues on a vaccine for Ebola virus infection in primates. Sullivan et al reported on the combination of naked DNA vaccine capable of encoding Ebola proteins followed by a booster vaccination with a recombinant adenoviral vector expressing Ebola GP(Z).[40]

In this study, cynomolgus macaques were injected with 3 doses of the DNA vaccine, 1 dose every 4 weeks.[40] Twelve weeks later, the macaques were vaccinated with the recombinant adenoviral vector. After another 12 weeks, unvaccinated macaques and vaccinated macaques were injected with a lethal dose of Ebola virus. All of the unvaccinated macaques died, whereas none of the vaccinated macaques died.

This work indicates that primates can be vaccinated against Ebola virus and can develop both a cell-mediated response (thought to be a result of the DNA vaccine) and a humoral antibody response (thought to be a result of the recombinant adenoviral vaccine).

Other efforts to design vaccines that work in primates used strategies that were successful in mice and guinea pigs. Geisbert et al studied a series of vaccines containing RNA replicon particles from an attenuated strain of Venezuelan equine encephalitis virus that expressed Ebola virus GP and NP, a recombinant vaccinia virus that expressed Ebola virus GP, liposomes containing lipid A and inactivated Ebola virus, and a concentrated, inactivated whole-virion Ebola preparation.[41]

Although these vaccines protected rodents against an Ebola virus challenge, they did not protect cynomolgus macaques or rhesus macaques against exposure to the virus.

Ebola is transmissible from person to person via direct contact with an infected patient’s blood or other body fluids. Airborne transmission of Reston ebolavirus is known to have occurred among primates; thus, although most cases in humans occur after direct contact with a patient or their blood or body fluids, transmission of Ebola virus via the airborne route cannot be dismissed.

Infection control inside and outside of medical facilities relies on barrier protection using double gloves, fluid-impermeable gowns, face shields with eye protection, and coverings for legs and shoes.



Whenever the diagnosis of Ebola or any other viral hemorrhagic fever is considered, the Centers for Disease Control and Prevention (CDC), along with local and state health officials, should be contacted. A consultation with an infectious diseases physician should be promptly obtained, and strict barrier isolation should be instituted.

No attempt should be made to culture the virus, except when culture can be performed in a maximum-containment biosafety level 4 laboratory with laboratory personnel wearing positive-pressure suits equipped with high-efficiency particulate air filters and an umbilical-fed air supply.

Contributor Information and Disclosures

John W King, MD Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, Association of Subspecialty Professors, American Society for Microbiology, Infectious Diseases Society of America, Sigma Xi

Disclosure: Nothing to disclose.


Hashmi Rafeek, MBBS Fellow in Infectious Diseases, Louisiana State University School of Medicine in Shreveport

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.


Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Amir A Khan, MD Fellow in Infectious Diseases, Louisiana State University School of Medicine in Shreveport

Amir A Khan, MD is a member of the following medical societies: American College of Physicians and American Medical Association

Disclosure: Nothing to disclose.

Rushdah Malik, MD Fellow, Department of Infectious Diseases, Louisiana State University Health Science Center

Rushdah Malik, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Ebola virus. Courtesy of the US Centers for Disease Control and Prevention.
Table 1. History of Sudan Ebola Virus Outbreaks
Year Location Reported Cases, No. Deaths, No. (%)
1976 Sudan 284 151 (53)
1976 England* 1 0 (0)
1979 Sudan 34 22 (65)
2000-2001 Uganda 425 224 (53)
2004 Sudan 17 7 (41)
2011 Sudan 1 1 (100)
Total   762 405 (53)
Data from Centers for Disease Control and Prevention and World Health Organization.

* Occurred after laboratory accident.

Table 2. History of Zaire Ebola Virus Outbreaks
Year Location Reported Cases, No. Deaths, No. (%)
1976 Zaire 318 280 (88)
1977 Zaire 1 1 (100)
1994 Gabon 52 31 (60)
1995 DRC 315 250 (81)
Jan 1996 to Apr 1996 Gabon 37 21 (57)
Jul 1996 to Jan 1997 Gabon 60 45 (74)
1996 South Africa (acquired in Gabon) 1 1 (100)
Oct 2001 to Mar 2002 Gabon 65 53 (82)
Oct 2001 to Mar 2002 DRC 59 44 (75)
Dec 2002 to Apr 2003 DRC 143 128 (89)
Nov 2003 to Dec 2004 DRC 35 29 (83)
2007 DRC 264 187 (71)
Dec 2008 to Feb 2009 DRC 32 15 (47)
July 2012 Uganda 24 17 (71)
Nov 2012 DRC 77 36 (46)
Dec 2012 Uganda 7 4 (57)
2014 (as of October 17, 2014) Guinea, Liberia, Sierra Leone, Nigeria, United States, Senegal, Spain (as of October 17, 2014) 8997 (as of October 17, 2014) 4493 (50) (as of October 17, 2014)
Total   10487 5634 (53.7)
Data from Centers for Disease Control and Prevention and World Health Organization.
Table 3. History of Tai Forest (Ivory Coast, Côte-d’Ivoire) Ebola Virus Outbreaks (No Deaths Reported)
Year Location Reported Cases, No.
1994 Côte-d’Ivoire 1
Total   1
Data from Centers for Disease Control and Prevention and World Health Organization.
Table 4. History of Reston Ebola Virus Outbreaks (No Deaths Reported)
Year Location Proven * Cases Reported, No.
1989 Virginia, Texas, Pennsylvania 0
1990 Virginia and Texas 4
1989-1990 Philippines 3
1992 Italy 0
1990 Alice, TX 0
1996 Philippines 0
Nov 2008 Philippines 6
Total   13
Data from Centers for Disease Control and Prevention and World Health Organization.

* Humans with serologic evidence of infection but without clinical disease.

Associated with pig farming.[15, 16]

Table 5. History of Bundibugyo Ebola Virus Outbreak
Year Location Reported Cases, No. Deaths, No. (%)
Dec 2007 to Jan 2008 Uganda 149 37 (25)
Jun to Nov 2012 Democratic Republic of the Congo 36 13 (36.1)
Total   185 50 (27)
Data from Centers for Disease Control and Prevention and World Health Organization.
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