Ebolaviruses: Infectious substances Pathogen Safety Data Sheet

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For more information on Ebolavirus, see the following:

Section I: Infectious agent


Agent type




Bundibugyo ebolavirus, Reston ebolavirus, Sudan ebolavirus, Taï Forest ebolavirus, Zaire ebolavirus, Bombali ebolavirus

Synonym or cross reference
Also known as African haemorrhagic fever, Ebola haemorrhagic fever (EHF, Ebola HF, Ebola), Filovirus, Ebola virus (EBOV), Zaire virus (EBOV), Sudan virus (SUDV), Ivory Coast ebolavirus (ICEBOV), Taï Forest virus (TAFV), Ebola-Reston (REBOV, EBO-R, Reston virus, (RESTV), Bundibugyo virus (BDBV), Bombali virus (BOMV) and Ebola virus disease (EVD).Footnote 1Footnote 2Footnote 3Footnote 4Footnote 5


Brief description

Ebola virus was discovered in 1976 and is a member of the Filoviridae family. Six ebolavirus species have been identified: Zaire ebolavirus, which was first identified in 1976 and is the most virulent; Sudan ebolavirus; Taï Forest ebolavirus (formerly Ivory Coast ebolavirus); Reston ebolavirus, originating from the Philippines; Bundibugyo ebolavirus, discovered in 2008; and Bombali ebolavirus, which is the most recently discovered in 2018 and its ability to cause disease is currently unknown Footnote 1Footnote 2Footnote 3Footnote 5Footnote 6Footnote 7Footnote 8. Ebolaviruses are an elongated filamentous virus, which can vary between 800 - 1000 nm in length, and can reach up to 14,000 nm long (due to concatemerization) with a uniform diameter of 80 nm. Footnote 2Footnote 6Footnote 9Footnote 10 It contains a helical nucleocapsid (with a central axis), 20 - 30 nm in diameter, and is enveloped by a helical capsid, 40 - 50 nm in diameter, with 5 nm cross-striations.Footnote 2Footnote 5Footnote 9Footnote 10Footnote 11 The pleomorphic viral fragment may take on several distinct shapes (e.g., in the shape of a "6", a "U", or a circle) and are contained within a lipid membrane.Footnote 2Footnote 6 Each virion contains a single-strand of non-segmented, negative-sense viral genomic RNA of approximately 19kb in length.Footnote 6Footnote 12Footnote 13 The virion surface is coated with glycoproteins of 10 nm in length, which are anchored to the membrane.Footnote 13


Ebolaviruses exhibit a broad cell tropism, with several cell types supporting viral replication, including: monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, and adrenal cortical cells.Footnote 14 The viral life cycle is initiated upon virus entry in the cell by micropinocytosis which utilizes the interaction of the GP envelope protein with cell surface determinants. Footnote 15 The viral genome is released in the host cell cytoplasm where virus replication begins. The L protein, which contains the RNA-dependent RNA polymerase (RdRp) domain, as well as NP, VP35, and VP30, are required for replication. Virion assembly follows with the formation of nucleocapsids that are released from the host cell plasma membrane via budding. Ebolaviruses are able to evade the immune system, making them highly infectious. VP24 and VP35 ebolavirus structural proteins play a role in immune evasion by supressing the type I interferon response. Footnote 16 sGP is released at high levels during illness and acts as a decoy to inhibit the protective humoral response by binding to ebolavirus-neutralizing antibodies.

Section II: Hazard identification

Pathogenicity and toxicity

Ebolavirus virions enter host cells through endocytosis and replication occurs in the cytoplasm. Upon infection, the virus affects the host blood coagulative and immune defense system and leads to severe immunosuppression. Footnote 11Footnote 17 Early signs of infection are non-specific and flu-like, and may include sudden onset of fever, asthenia, diarrhoea, headache, myalgia, arthralgia, vomiting, and abdominal pains. Footnote 18Footnote 19 Less common early symptoms include conjunctival injection, sore throat, rashes, and bleeding. Shock, cerebral oedema, coagulation disorders, and secondary bacterial infection may co-occur later in infection.Footnote 9 Haemorrhagic symptoms may begin 4 - 5 days after onset, including hemorrhagic conjunctivitis, pharyngitis, bleeding gums, oral/lip ulceration, hematemesis, melena, hematuria, epistaxis, and vaginal bleeding.Footnote 20 Hepatocellular damage, marrow suppression (such as thrombocytopenia and leucopenia), serum transaminase elevation, and proteinuria may also occur. Persons that are terminally ill typically present with obtundation, anuria, shock, tachypnea, normothermia to hypothermia, arthralgia, and ocular diseases.Footnote 21 Haemorrhagic diathesis is often accompanied by hepatic damage and renal failure, central nervous system involvement, and terminal shock with multi-organ failure.Footnote 1Footnote 2 Contact with the virus may also result in symptoms such as severe acute viral illness, malaise, and maculopapular rash. Pregnant women will usually abort their foetuses and experience copious bleeding. Footnote 2Footnote 22 Fatality rates range between 50 - 100%, with most dying of hypovolemic shock and multisystem organ failure.Footnote 23 The length of illness depends on the severity of disease, but recovery typically occurs after four weeks.Footnote 16

Pathogenicity between the ebolaviruses does not differ greatly in that they have all been associated with hemorrhagic fever outbreaks in humans (excluding Reston virus) and non-human primates. Ebola virus and Sudan virus are especially known for their virulence with up to a 90% fatality rate,Footnote 24 with reduced virulence noted in the Taï Forest virus and the more recently discovered Bundibugyo virus, which caused a single outbreak in Uganda. Footnote 7Footnote 8 Bundibugyo virus was also responsible for an outbreak in Isiro, Democratic Republic of Congo, in 2012. Reston virus was isolated from cynomolgus monkeys from the Philippines in 1989 and is less pathogenic in non-human primates. Reston virus appears to be non-pathogenic in humans, with reported health effects limited to serological evidence of exposure as identified in 4 animal handlers working with infected non-human primates.Footnote 25 Seven SUDV outbreaks were reported between 1976 and 2012, comprising 778 cases.Footnote 26

The largest outbreak of Ebola virus disease began in Guinea in December 2013.Footnote 19 This outbreak was marked by gastrointestinal clinical presentation, although the most common symptoms for Ebola virus disease are fever with anorexia, asthenia, and maculopapular rash 5 to 7 days after disease onset.Footnote 19 The case fatality rate during this outbreak is estimated to be around 50%.Footnote 19

Predisposing factors

Risk factors for Sudan virus include interaction with acutely ill patients or deceased patients that were infected with ebolavirus. Footnote 27Footnote 28Footnote 29 Nosocomial transmission amongst patients and staff is a major source of epidemic spread.Footnote 27Footnote 29 A serosurvey of healthcare workers suggests that seropositivity may be associated with positions that offer less occupational training and access to personal protective equipment (PPE).Footnote 30 Comparative serological studies of gold mining communities in Western Uganda and non-mining communities in Central Uganda identified mining, male gender, going inside mines, cleaning corpses, and contact with suspected filovirus cases as risk factors for filovirus seropositivity.Footnote 31 Miners have an increased risk of filovirus exposure likely to due the increased risk of exposure to bats, a putative reservoir host.


Communicable through contact with infected blood, body fluids or organs. Ebolaviruses have been isolated from semen 61 to 82 days after the onset of illness, and transmission through semen is thought to be possible.Footnote 1Footnote 2Footnote 32Footnote 33

In an outbreak, it is hypothesized that the first patient becomes infected as a result of contact with an infected animal.Footnote 33 Person-to-person transmission occurs via close personal contact with an infected individual or their body fluids during the late stages of infection or after death. Footnote 1Footnote 2Footnote 34Footnote 35 Principle routes of infection include injection, mucous membranes, and abraded or injured skin.Footnote 19 Nosocomial infections can occur through direct contact with infected body fluids, for example due to the reuse of unsterilized syringes, needles, or other medical equipment contaminated with these fluids.Footnote 1Footnote 2 Humans may be infected by handling sick or dead non-human primates and are also at risk when handling the bodies of deceased humans in preparation for funerals.Footnote 2Footnote 11Footnote 36 The index case in the outbreak that originated in Guinea in December 2013 is believed to have resulted from consuming infected bush meat.Footnote 19

In laboratory settings, non-human primates exposed to aerosolized Ebola virus from pigs have become infected; however, airborne transmission has not been demonstrated between non-human primates. Footnote 1Footnote 11Footnote 21Footnote 37Footnote 38 Viral shedding has been observed in nasopharyngeal secretions and rectal swabs of pigs following experimental inoculation.Footnote 39Footnote 40 Intranasal infection studies in guinea pigs suggests that transmission through direct contact with infectious materials, including those transported in aerosols over short distances, is more infectious compared to systemic infection.Footnote 41


Occurs mainly in areas surrounding rain forests in equatorial AfricaFootnote 11 with the exception of Reston virus, which is documented to have originated in the Philippines.Footnote 8 No predispositions to infection have been identified among infected persons.

The largest recorded Ebola virus outbreak to date began in December 2013, with initial cases reported in Guinea and then additional cases identified in the surrounding regions (Liberia, Sierra Leone, Nigeria). A new strain of the Ebola virus was identified as the causative agent of the outbreakFootnote 19Footnote 22Footnote 34Footnote 42 and has resulted in more than 10,000 deaths and more than 20,000 suspected, probable, and confirmed cases.Footnote 43

A Bundibugyo virus outbreak began in the Bikoro region, Equateur Province, in the Democratic Republic of the Congo in May 2018 with confirmed cases reaching 38 by the middle of June 2018.Footnote 44Footnote 45

Seven Sudan virus outbreaks were reported in South Sudan and Uganda between 1976 and 2012, comprising 778 cases.Footnote 26 A recent Sudan virus outbreak was declared in Uganda as of 20 September 2022. Footnote 46 According to the Uganda Ministry of Health, as of 23 October 2022, there are 75 cumulative confirmed cases.

Host range

Natural host(s)

Humans, various monkey species, chimpanzees, gorillas, baboons, and duikers are natural animal hosts for ebolavirus.Footnote 1Footnote 2Footnote 6Footnote 34Footnote 39Footnote 40Footnote 47Footnote 48Footnote 49Footnote 50Footnote 51Footnote 52Footnote 53 Serological evidence of immunity markers to ebolavirus in serum collected from domesticated dogs suggests asymptomatic infection is plausible, likely following exposure to infected humans or animal carrion.Footnote 54Footnote 55 The Ebolavirus genome was discovered in two species of rodents and one species of shrew living in forest border areas, raising the possibility that these animals may be intermediary hosts.Footnote 56

Other host(s)

Experimental studies of the virus have been done using mouse, pig, guinea pig, and hamster models, suggesting wild-type ebolavirus has limited pathogenicity in these models. Footnote 57Footnote 58

Infectious dose

Although aerosol transmission of ebolaviruses is not considered to be a primary mode of infection, viral hemorrhagic fevers have an experimentally determined infectious dose of 1 - 10 organisms by aerosol in non-human primates.Footnote 59 The specific infectious dose for ebolaviruses is unknown; however, rhesus monkeys exposed by the aerosol route in an artificial setting experience clinical disease with inhaled doses of 2.6 log10 PFUs of ebolavirus particles with diameters ranging from 0.8 to 1.2 µm.Footnote 60

Incubation period

Range of 2-21 days, but normally 4-10 days. Footnote 1Footnote 19Footnote 21Footnote 23

Section III: Dissemination


The natural reservoir of ebolaviruses is unknown, but specific species of bat are considered a possible natural reservoir based on the presence of serum antibodies and viral RNA. Footnote 2Footnote 19Footnote 61Footnote 62Footnote 63Footnote 64Footnote 65 Serological evidence of infection with ebolaviruses (antibody detection to ebolaviruses, including Ebola and/or Reston virus) has been reported in fruit bats collected from woodland and forested areas near Ghana and Gabon, with reduced frequency of isolation from bats collected in mainland China and Bangladesh.Footnote 62Footnote 63Footnote 64Footnote 65 Antibodies to the virus have been found in the serum of domestic guinea pigs and wild rodents, with no relation to human transmission.Footnote 56Footnote 66

Zoonosis/Reverse zoonosis

Zoonosis between animals and humans is suspected.Footnote 2Footnote 19Footnote 34Footnote 64



Section IV: Stability and viability

Drug susceptibility

In Canada, approved vaccines or therapeutics are only available for the prevention or post-exposure prophylaxis of the Ebola virus. The ERVEBO (rVSV-ZEBOV) vaccine is the primary preventative measure,Footnote 67 while post-exposure measures include the monoclonal antibody (mAb)-based therapeutics ansuvimab (Ebanga) and atoltivimab+maftivimab+odesivimab (Inmazeb).Footnote 68 The symptoms of the disease may be treated by providing intravenous fluids and balancing electrolytes, maintaining oxygen status and blood pressure, replacement of lost blood and clotting factors, and treating other infections if they occur. Footnote 69

Recombinant vesicular stomatitis virus (VSV) based vaccines have demonstrated efficacy in nonhuman primate models as both single preventative vaccines and as post-exposure treatments.Footnote 70 VSV-EBOV is an experimental vaccine developed in Canada that contains an Ebola virus glycoprotein instead of a VSV glycoprotein. The vaccine has undergone clinical trials in Canada and the United States.

Candidate vaccines for Sudan virus are in development. These are several types being trialed including a DNA vaccine, heterologous vector vaccines, and replication-defective recombinant vector vaccine.Footnote 67Footnote 71Footnote 72Footnote 73Footnote 74Footnote 75 All vaccines encode for glycoproteins (GP) of various ebolaviruses, primarily EBOV and SUDV.

Monoclonal antibodies have also shown great promise as an effective treatment for Ebola virus disease. ZMapp, a cocktail of 3 highly purified monoclonal antibodies, has shown 100% protection of nonhuman primates when treatment is initiated up to 5 days post-exposure.Footnote 76 ZMapp has not yet been tested for safety and efficacy in a human clinical trial, although trials for monoclonal antibodies are underway.Footnote 77

Drug resistance

There are no known antiviral treatments available for human infections.

Susceptibility to disinfectants

Ebolaviruses are susceptible to 3% acetic acid, 1% glutaraldehyde, alcohol-based products, calcium hypochlorite (bleach powder), and dilutions of 5.25% household bleach (i.e., 0.525% to 0.0525% sodium hypochlorite for ≥ 10 min).Footnote 78Footnote 79Footnote 80Footnote 81 The WHO recommendations for cleaning up spills of blood or body fluids suggest flooding the area with a 1:10 dilution of 5.25% household bleach (i.e., 1 part household bleach diluted in 9 parts water, or 0.525% sodium hypochlorite) for 10 minutes for surfaces that can tolerate stronger bleach solutions (e.g., cement, metal).Footnote 81 For surfaces that may corrode or discolour, careful cleaning is recommended to remove visible stains followed by contact with a 1:100 dilution of 5.25% household bleach (i.e., 1 part household bleach diluted in 99 parts water, or 0.0525% sodium hypochlorite) for more than 10 minutes.

Laboratory tests have demonstrated that the use of 70% ethanol for 1 minute is effective at inactivating Mayinga and Kikwit strains of the Ebola virus, whereas 2.5 minutes is required to inactivate the Makona variant. Use of 0.5% and 1% sodium hypochlorite solutions (i.e., 50 mL household bleach into 450 mL or 200mL water, respectively) for 5 minutes is effective at inactivating all three variants.Footnote 82Footnote 83 A 0.5% chlorine solution is also recommended by the WHO to disinfect surfaces contaminated with ebolavirus.Footnote 82

Physical inactivation

Ebolaviruses are moderately thermolabile and can be inactivated by heating for 30 minutes to 60 minutes at 60°C, boiling for 5 minutes, or gamma irradiation (1.2 x106 rads to 1.27 x106 rads) combined with 1% glutaraldehyde.Footnote 11Footnote 78Footnote 80 Ebola virus has also been determined to be moderately sensitive to UVC radiation.Footnote 84 Ebola virus Makona strain virions in spike serum samples can be inactivated after incubation for 1 hour with 0.5% Tween-20 at 56°C, which is considered a more practical application in the field.Footnote 85 A high viral load in whole-blood thin-smear samples can be inactivated using a 15 minute 100% methanol fixation step.Footnote 86

Virus inactivation is recommended for samples intended for clinical laboratory testing. Guanidine thiocyanate-based lysis buffers commonly used during nucleic acid extraction processes (e.g., for downstream PCR applications) may be effective for the inactivation of enveloped RNA viruses.Footnote 87Footnote 88Footnote 89 The inactivation method should be selected based on its viral inactivation efficacy, as well as its interference with the subsequent test results (e.g., electrolytes, glucose, enzymes, protein, etc.). Please see the Biosafety Guidelines for Laboratories Handling Specimens from patients Under Investigation for Ebola Virus Disease for more information.

Survival outside host

Filoviruses have been reported capable to survive for weeks in blood and can also survive on contaminated surfaces, particularly at low temperatures (4°C).Footnote 90Footnote 91 Under West African climate conditions of 28°C and 90% relative humidity, ebolavirus can persist in dried human or non-human primate blood for 7 to 10 days.Footnote 83 One study could not recover any Ebola virus from experimentally contaminated surfaces (plastic, metal or glass) at room temperature.Footnote 91 In another study, Ebolaviruses dried onto glass, polymeric silicone rubber, or painted aluminum alloy was able to survive in the dark for several hours under ambient conditions (between 20°C and 25°C and 30–40% relative humidity; amount of virus reduced to 37% after 15.4 hours), but was less stable than some other viral hemorrhagic fevers, such as Lassa virus.Footnote 84Footnote 92 When dried in tissue culture media onto glass and stored at 4 °C, Ebola virus survived for over 50 days.Footnote 91 Ebola virus Makona strain suspended in organic soil has been shown to persist on steel and plastic surfaces for up to 192 hours compared to less than 24 hours on cotton. Ebola virus suspended in serum can persist in the environment for up to 46 days.Footnote 82 This information is based on experimental findings only and not based on observations in nature. This information is intended to be used to support local risk assessments in a laboratory setting.

In average West African climatic conditions of 27°C and 80% relative humidity, Ebola virus Makona strain can remain viable on gloves (<1 hour), cotton and goggles (<24 hours), and other PPE such as respirators, suits and hoods (<72 hours).Footnote 93

A study on transmission of Ebola virus from fomites in an isolation ward concludes that the risk of transmission is low when recommended infection control guidelines for viral hemorrhagic fevers are followed.Footnote 94 These infection control protocols included decontamination of floors with 0.5% bleach daily and decontamination of visibly contaminated surfaces with 0.05% bleach as necessary.

Section V: First aid/medical


Definitive diagnosis can be reached rapidly in an appropriately equipped laboratory using a multitude of approaches, including RT-PCR to detect viral RNA, ELISA based techniques to detect antiviral antibodies or viral antigens, immunoelectron microscopy to detect ebolavirus particles in tissues and cells, and indirect immunofluorescence to detect antiviral antibodies.Footnote 1Footnote 2Footnote 20Footnote 59 It is useful to note that Marburgvirus is morphologically indistinguishable from ebolaviruses, and laboratory surveillance of ebolaviruses is extremely hazardous. Footnote 1Footnote 2Footnote 20Footnote 95 Please see the Biosafety Guidelines for Laboratories Handling Specimens from patients Under Investigation for Ebola Virus Disease for more information.

Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook (CBH).

First aid/treatment

Favipiravir can rescue animals following a lethal dose of Ebola virus, antiviral activity against Ebola virus is considered relatively weak and there is no efficacy data available.Footnote 96 In Canada, post-exposure measures are currently only available for Ebola virus, namely ansuvimab (Ebanga) and atoltivimab+maftivimab+odesivimab (Inmazeb) which are monoclonal antibody (mAb)-based therapeutics.Footnote 67 In general, due to the lack of effective pharmaceutical treatment available, treatment is supportive and may include providing intravenous fluids and balancing electrolytes, maintaining oxygen status and blood pressure, replacement of lost blood and clotting factors, and treating other infections if they occur for maintenance of organ function, and combating haemorrhage and shock.Footnote 34Footnote 69Footnote 97 Monoclonal antibodies are also under investigation for treatment for Ebola virus disease, but have not been approved for use.Footnote 96 A Phase 1 clinical trial evaluating the safety and tolerability of a single monoclonal antibody (mAb114) developed from an Ebola virus survivor is underway.Footnote 77 Convalescent blood products from survivors of Ebola virus disease have been administered to patients in Africa, but the benefits of such a treatment remain unclear.Footnote 96

Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which is developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the CBH.


In Canada, the ERVEBO (rVSV-ZEBOV) vaccine has been approved for the Ebola virus.Footnote 98

Other potential vaccine candidates moving towards clinical trials include human adenovirus serotype 26 or 35 platforms with a Modified vaccinia Ankara (MVA) boost. Vaccine efficacy has been studied in Guinea pigs mucosally-infected with Ebola virus, as this is a more common infection route compared to intramuscular infection in non-human primate models. Guinea pigs infected intranasally showed 100% survival with prior administration of adjuvanted Ad5-ZGP.Footnote 98

Note: More information on the medical surveillance program can be found in the CBH, and by consulting the Canadian Immunization Guide.


Post-exposure measures are currently available for Ebola virus in the form of monoclonal antibody (mAb)-based therapeutics: ansuvimab (Ebanga) and atoltivimab+maftivimab+odesivimab (Inmazeb)Footnote 67. Management of the ebolaviruses is also based on isolation and barrier-nursing with symptomatic and supportive treatments.Footnote 9 The vaccine rVSV-ZEBOV has been used as post-exposure prophylaxis in humans; however, findings suggest that immunity is insufficiently rapid to reliably prevent Ebola virus disease in human beings when administered following exposure.Footnote 98

Note: More information on prophylaxis as part of the medical surveillance program can be found in the CBH.

Section VI: Laboratory hazards

Laboratory-acquired infections

One reported near-fatal case following a finger prick in an English laboratory (1976).Footnote 95 A Swiss zoologist contracted Ebola virus after performing an autopsy on a chimpanzee in 1994.Footnote 2Footnote 99 An incident occurred in Germany in 2009 when a laboratory scientist pricked herself with a needle that had just been used on a mouse infected with Ebola virus; however, human infection was not confirmed. Additional incidents were recorded in the US in 2004 and a fatal case in Russia in 2004.Footnote 9

Note: Please consult the Canadian Biosafety Standard (CBS) and CBH for additional details on requirements for reporting exposure incidents. A Canadian biosafety guideline describing notification and reporting procedures is also available.


Blood, vomit, serum, urine, respiratory and throat secretions, semen, and organs or their homogenates from human or animal hosts.Footnote 1Footnote 2Footnote 92 Human or animal hosts, including non-human primates, may represent a further source of infection.Footnote 95

Primary hazards

Accidental parenteral inoculation, respiratory exposure to infectious aerosols/droplets, and/or direct contact with skin or mucous membranes are the primary hazards associated with exposure to ebolaviruses.Footnote 95

Special hazards

Work with, or exposure to, infected non-human primates, rodents, or their carcasses represents a risk of human infection.Footnote 95

Section VII: Exposure controls/personal protection

Risk group classification

All members of the genus Ebolavirus are considered to be a RG4 Human Pathogen and RG4 Animal Pathogen. Ebolaviruses are also Security Sensitive Biological Agents (SSBA).Footnote 100

Containment requirements

Containment Level 4 facilities, equipment, and operational practices outlined in the CBS for work involving infectious or potentially infectious materials, animals, or cultures.

The Biosafety Guidelines for Laboratories Handling Specimens from Patients Under Investigation for Ebola Virus Disease are to be followed.

Note that there are additional security requirements, such as obtaining a Human Pathogens and Toxins Act Security Clearance, for work involving SSBAs.

Additional Information:

For clinical diagnostic laboratories handling patient specimens that may contain Ebola, the following resources may be consulted:

  • Human Diagnostic Activities Biosafety Guideline
  • Local Risk Assessment Biosafety Guideline

Protective clothing

The applicable Containment Level 4 requirements for personal protective equipment and clothing outlined in the CBS to be followed.

The use of a positive-pressure suit or use of a Class III biological safety cabinet (BSC) line is required for all work with RG4 pathogens.

Note: A local risk assessment will identify the appropriate hand, foot, head, body, eye/face, and respiratory protection, and the personal protective equipment requirements for the containment zone must be documented.

Other precautions

All activities involving open vessels of infectious material are to be performed in a certified biological safety cabinet (BSC) or other appropriate primary containment device. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are unloaded in a biological safety cabinet. The integrity of positive pressure suits must be routinely checked for leaks. The use of needles, syringes, and other sharp objects is to be strictly limited. Open wounds, cuts, scratches, and grazes are to be covered with waterproof dressings Additional precautions must be considered with work involving animals or large scale activities.

Section VIII: Handling and storage


In laboratories handling specimens from patients under investigation for Ebola disease: Allow aerosols to settle. Wearing protective clothing, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up.Footnote 101

The spill area to be evacuated and secured. Aerosols must be allowed to settle for a minimum of 30 minutes. Spills of potentially contaminated material to be covered with absorbent paper-based material (e.g., paper towels), liberally covered with an effective disinfectant (e.g., 1% sodium hypochlorite), and left to soak for an appropriate amount of time (e.g., 10 minutes) before being wiped up. Following the removal of the initial material, the disinfection process to be repeated. Individuals performing this task must wear PPE, including particulate respirators (e.g., N95 or higher). Disposable gloves, impermeable gowns and protective eye wear are to be removed immediately after completion of the process, placed in an autoclave bag, and decontaminated prior to disposal.


All materials/substances that have come in contact with the infectious agent must be completely decontaminated before they are removed from the containment zone. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the infectious material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (CBH).


The applicable Containment Level 4 requirements for storage outlined in the CBS are to be followed. Pathogens and other regulated infectious material to be stored inside the containment zone.

SSBA: Inventory of Risk Group 4 (RG4) pathogens and security sensitive biological agents (SSBAs) in long-term storage to be maintained and to include:

  • specific identification of the pathogens, toxins, and other regulated infectious material; and
  • a means to allow for the detection of a missing or stolen sample in a timely manner

Section IX: Regulatory and other information

Canadian regulatory context

Controlled activities with ebolaviruses require a Human Pathogens and Toxins Licence issued by the Public Health Agency of Canada and additional security requirements, such as obtaining a Human Pathogens and Toxins Act Security Clearance, for work involving SSBAs. Ebolaviruses are a non-indigenous animal pathogen in Canada; therefore, importation of ebolaviruses requires an import permit, issued by the Canadian Food Inspection Agency.

The following is a non-exhaustive list of applicable designations, regulations, or legislations:

November 2022

Prepared by
Centre for Biosecurity, Public Health Agency of Canada.


The scientific information, opinions, and recommendations contained in this Pathogen Safety Data Sheet have been developed based on or compiled from trusted sources available at the time of publication. Newly discovered hazards are frequent and this information may not be completely up to date. The Government of Canada accepts no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information.

Persons in Canada are responsible for complying with the relevant laws, including regulations, guidelines and standards applicable to the import, transport, and use of pathogens in Canada set by relevant regulatory authorities, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. The risk classification and related regulatory requirements referenced in this Pathogen Safety Data Sheet, such as those found in the Canadian Biosafety Standard, may be incomplete and are specific to the Canadian context. Other jurisdictions will have their own requirements.

Copyright©Public Health Agency of Canada, 2022, Canada


Footnote 1

Anonymous 2004. Plague, p. 40-44. In R. G. Darling and J. B. Woods (eds.), USAMRIID's Medical Management of Biological Casualties Handbook, 5th ed.. USAMRIID, Fort Detrick M.D.

Return to footnote 1 referrer

Footnote 2

Acha, P. N., and B. Szyfres. 2003., p. 142-145. In Pan american Health Organization (ed.), Zoonoses and Communicable Diseases Common to Man and Animals, 3rd ed., vol. I Bacterioses and Mycoses. Pan American Health Organization, Washington D.C.

Return to footnote 2 referrer

Footnote 3

International Committee on Taxonomy of Viruses (2017 Release). 2017.

Return to footnote 3 referrer

Footnote 4

Kuhn, J. H., S. Becker, H. Ebihara, T. W. Geisbert, K. M. Johnson, Y. Kawaoka, W. I. Lipkin, A. I. Negredo, S. V. Netesov, and S. T. Nichol. 2010. Proposal for a revised taxonomy of the family Filoviridae: classification, names of taxa and viruses, and virus abbreviations. Arch. Virol. 155:2083-2103.

Return to footnote 4 referrer

Footnote 5

Goldstein, T., S. J. Anthony, A. Gbakima, B. H. Bird, J. Bangura, A. Tremeau-Bravard, M. N. Belaganahalli, H. L. Wells, J. K. Dhanota, E. Liang, M. Grodus, R. K. Jangra, V. A. DeJesus, G. Lasso, B. R. Smith, A. Jambai, B. O. Kamara, S. Kamara, W. Bangura, C. Monagin, S. Shapira, C. K. Johnson, K. Saylors, E. M. Rubin, K. Chandran, W. I. Lipkin, and J. A. K. Mazet. 2018. The discovery of Bombali virus adds further support for bats as hosts of ebolaviruses. Nat. Microbiol. 3:1084-1089.

Return to footnote 5 referrer

Footnote 6

Sanchez, A. 2001. Filoviridae: Marburg and Ebola Viruses, p. 1279-1304. In D. M. Knipe and P. M. Howley (eds.), Fields virology, 4th ed., vol. 2. Lippencott-Ravenpp., Philadelphia, PA.

Return to footnote 6 referrer

Footnote 7

Takada, A., and Y. Kawaoka. 2001. The pathogenesis of Ebola hemorrhagic fever. Trends Microbiol. 9:506-511.

Return to footnote 7 referrer

Footnote 8

Towner, J. S., T. K. Sealy, M. L. Khristova, C. G. Albarino, S. Conlan, S. A. Reeder, P. L. Quan, W. I. Lipkin, R. Downing, J. W. Tappero, S. Okware, J. Lutwama, B. Bakamutumaho, J. Kayiwa, J. A. Comer, P. E. Rollin, T. G. Ksiazek, and S. T. Nichol. 2008. Newly discovered ebola virus associated with hemorrhagic fever outbreak in Uganda. PLoS Pathog. 4:e1000212.

Return to footnote 8 referrer

Footnote 9

Feldmann, H. 2010. Are we any closer to combating Ebola infections? Lancet. 375:1850-1852.

Return to footnote 9 referrer

Footnote 10

Beran, G. W. (ed.), 1994. Handbook of Zoonosis, Section B: Viral. CRC Press, LLC, Boca Raton, Florida.

Return to footnote 10 referrer

Footnote 11

Mwanatambwe, M., N. Yamada, S. Arai, M. Shimizu-Suganuma, K. Shichinohe, and G. Asano. 2001. Ebola hemorrhagic fever (EHF): mechanism of transmission and pathogenicity. J. Nippon Med. Sch. 68:370-375.

Return to footnote 11 referrer

Footnote 12

Sanchez, A., M. P. Kiley, H. D. Klenk, and H. Feldmann. 1992. Sequence analysis of the Marburg virus nucleoprotein gene: comparison to Ebola virus and other non-segmented negative-strand RNA viruses. J. Gen. Virol. 73 (Pt 2):347-357.

Return to footnote 12 referrer

Footnote 13

Feldmann, H., A. Sanchez, and T. Geisbert. 2013. Chapter 32 - Filoviridae: Marburg and Ebola viruses, p. 923-956. In D. M. Knipe and P. Howley (eds.), Fields Virology: Sixth Edition. Wolters Kluwer Health Adis (ESP).

Return to footnote 13 referrer

Footnote 14

Feldmann, H., and T. W. Geisbert. 2011. Ebola haemorrhagic fever. The Lancet. 377:849-862.

Return to footnote 14 referrer

Footnote 15

Valle, C., B. Martin, F. Debart, J. Vasseur, I. Imbert, B. Canard, B. Coutard, and E. Decroly. 2020. The C-terminal domain of the Sudan ebolavirus L protein is essential for RNA binding and methylation. J. Virol. 94:e00520-20.

Return to footnote 15 referrer

Footnote 16

Baseler, L., D. S. Chertow, K. M. Johnson, H. Feldmann, and D. M. Morens. 2017. The Pathogenesis of Ebola Virus Disease∗. Annu. Rev. Pathol. Mech. Dis. 12:387-418.

Return to footnote 16 referrer

Footnote 17

Harcourt, B. H., A. Sanchez, and M. K. Offermann. 1999. Ebola virus selectively inhibits responses to interferons, but not to interleukin-1beta, in endothelial cells. J. Virol. 73:3491-3496.

Return to footnote 17 referrer

Footnote 18

Bwaka, M. A., M. J. Bonnet, P. Calain, R. Colebunders, A. De Roo, Y. Guimard, K. R. Katwiki, K. Kibadi, M. A. Kipasa, K. J. Kuvula, B. B. Mapanda, M. Massamba, K. D. Mupapa, J. J. Muyembe-Tamfum, E. Ndaberey, C. J. Peters, P. E. Rollin, E. Van den Enden, and E. Van den Enden. 1999. Ebola hemorrhagic fever in Kikwit, Democratic Republic of the Congo: clinical observations in 103 patients. J. Infect. Dis. 179 Suppl 1:S1-7.

Return to footnote 18 referrer

Footnote 19

Goeijenbier, M., J. Van Kampen, C. Reusken, M. Koopmans, and E. Van Gorp. 2014. Ebola virus disease: a review on epidemiology, symptoms, treatment and pathogenesis. Neth. J. Med. 72:442-448.

Return to footnote 19 referrer

Footnote 20

Zilinskas, R. A. (ed.), 2000. Biololgical Warfare - Modern Offense and Defense. Lynne Rienner Publishers, Inc., Boulder, Colorado, USA.

Return to footnote 20 referrer

Footnote 21

Feigin, R. D. (ed.), 2004. Textbook of Pediatric Infectious Diseases. Elsevier, Inc., Philadelphia, USA.

Return to footnote 21 referrer

Footnote 22

Baize, S., D. Pannetier, L. Oestereich, T. Rieger, L. Koivogui, N. Magassouba, B. Soropogui, M. S. Sow, S. Keïta, and H. De Clerck. 2014. Emergence of Zaire Ebola virus disease in Guinea. N. Engl. J. Med. 371:1418-1425.

Return to footnote 22 referrer

Footnote 23

Casillas, A. M., A. M. Nyamathi, A. Sosa, C. L. Wilder, and H. Sands. 2003. A current review of Ebola virus: pathogenesis, clinical presentation, and diagnostic assessment. Biol. Res. Nurs. 4:268-275.

Return to footnote 23 referrer

Footnote 24

World Health Organization (WHO). 2018. Ebola virus disease.

Return to footnote 24 referrer

Footnote 25

Centers for Disease Control (CDC). 1990. Update: filovirus infection in animal handlers. MMWR Morb. Mortal. Wkly. Rep. 39:221.

Return to footnote 25 referrer

Footnote 26

US CDC. 2021. Ebola Virus Disease Distribution Map: Cases of Ebola Virus Disease in Africa Since 1976. https://www.cdc.gov/vhf/ebola/history/distribution-Map.html

Return to footnote 26 referrer

Footnote 27

Baron, R. C., J. B. McCormick, and O. A. Zubeir. 1983. Ebola virus disease in southern Sudan: hospital dissemination and intrafamilial spread. Bull. World Health Organ. 61:997-1003.

Return to footnote 27 referrer

Footnote 28

Shears, P., and T. J. D. O'Dempsey. 2015. Ebola virus disease in Africa: Epidemiology and nosocomial transmission. J. Hosp. Infect. 90:1-9.

Return to footnote 28 referrer

Footnote 29

WHO. 1978. Ebola haemorrhagic fever in Sudan, 1976. Bull World Health Organ. 56:247-270.

Return to footnote 29 referrer

Footnote 30

Shaffer, K. C. L., S. Hui, A. Bratcher, L. B. King, R. Mutombe, N. Kavira, J. P. Kompany, M. Tambu, K. Musene, P. Mukadi, P. Mbala, A. Gadoth, B. R. West, B. K. Ilunga, D. Kaba, J. J. Muyembe-Tanfum, N. A. Hoff, A. W. Rimoin, and E. O. Saphire. 2022. Pan-ebolavirus serology study of healthcare workers in the Mbandaka Health Region, Democratic Republic of the Congo. PLoS. Negl. Trop. Dis. 16.

Return to footnote 30 referrer

Footnote 31

Nyakarahuka, L., I. J. Schafer, S. Balinandi, S. Mulei, A. Tumusiime, J. Kyondo, B. Knust, J. Lutwama, P. Rollin, S. Nichol, and T. Shoemaker. 2020. A retrospective cohort investigation of seroprevalence of Marburg virus and ebolaviruses in two different ecological zones in Uganda. BMC Infect. Dis. 20.

Return to footnote 31 referrer

Footnote 32

Rowe, A. K., J. Bertolli, A. S. Khan, R. Mukunu, J. Muyembe-Tamfum, D. Bressler, A. Williams, C. Peters, L. Rodriguez, and H. Feldmann. 1999. Clinical, virologic, and immunologic follow-up of convalescent Ebola hemorrhagic fever patients and their household contacts, Kikwit, Democratic Republic of the Congo. J. Infect. Dis. 179:S28-S35.

Return to footnote 32 referrer

Footnote 33

Rodriguez, L., A. De Roo, Y. Guimard, S. Trappier, A. Sanchez, D. Bressler, A. Williams, A. Rowe, J. Bertolli, and A. Khan. 1999. Persistence and genetic stability of Ebola virus during the outbreak in Kikwit, Democratic Republic of the Congo, 1995. J. Infect. Dis. 179:S170-S176.

Return to footnote 33 referrer

Footnote 34

Bausch, D. G., Jeffs B.S.A.G, and P. Boumandouki. 2008. Treatment of Marburg and Ebola haemorrhagic fevers: a strategy for testing new drugs and vaccines under outbreak conditions. Antiviral Res. 78:150-161.

Return to footnote 34 referrer

Footnote 35

Arthur, R. R. 2002. Ebola in Africa--discoveries in the past decade. Euro Surveill. 7:33-36.

Return to footnote 35 referrer

Footnote 36

Hewlett, B. S., and R. P. Amolat. 2003. Cultural contexts of Ebola in Northern Uganda. Emerging Infectious Diseases. 9:1242-1248.

Return to footnote 36 referrer

Footnote 37

Reed, D. S., M. G. Lackemeyer, N. L. Garza, L. J. Sullivan, and D. K. Nichols. 2011. Aerosol exposure to Zaire ebolavirus in three nonhuman primate species: differences in disease course and clinical pathology. Microb. Infect. 13:930-936.

Return to footnote 37 referrer

Footnote 38

Twenhafel, N., M. Mattix, J. Johnson, C. Robinson, W. Pratt, K. Cashman, V. Wahl-Jensen, C. Terry, G. Olinger, and L. Hensley. 2013. Pathology of experimental aerosol Zaire ebolavirus infection in rhesus macaques. Vet. Pathol. 50:514-529.

Return to footnote 38 referrer

Footnote 39

Kobinger, G. P., A. Leung, J. Neufeld, J. S. Richardson, D. Falzarano, G. Smith, K. Tierney, A. Patel, and H. M. Weingartl. 2011. Replication, pathogenicity, shedding, and transmission of Zaire ebolavirus in pigs. J. Infect. Dis. 204:200-208.

Return to footnote 39 referrer

Footnote 40

Marsh, G. A., J. Haining, R. Robinson, A. Foord, M. Yamada, J. A. Barr, J. Payne, J. White, M. Yu, and J. Bingham. 2011. Ebola Reston virus infection of pigs: clinical significance and transmission potential. J. Infect. Dis. 204:S804-S809.

Return to footnote 40 referrer

Footnote 41

Wong, G., X. Qiu, J. S. Richardson, T. Cutts, B. Collignon, J. Gren, J. Aviles, C. Embury-Hyatt, and G. P. Kobinger. 2015. Ebola virus transmission in guinea pigs. J. Virol. 89:1314-1323.

Return to footnote 41 referrer

Footnote 42

Centers for Disease Control and Prevention (CDC). 2017. 2014-2016 Ebola Outbreak Distribution in West Africa.

Return to footnote 42 referrer

Footnote 43

Centers for Disease Control and Prevention (CDC). 2017. Number of Cases and Deaths in Guinea, Liberia, and Sierra Leone during the 2014-2016 West Africa Ebola Outbreak.

Return to footnote 43 referrer

Footnote 44

World Health Organization (WHO). June 2018. Ebola situation reports: Democratic Republic of the Congo.

Return to footnote 44 referrer

Footnote 45

Centers for Disease Control and Prevention (CDC). May 2018. 2018 Democratic Republic of the Congo, Bikoro.

Return to footnote 45 referrer

Footnote 46

WHO. 2022. Ebola Disease caused by Sudan virus- Uganda. https://www.who.int/emergencies/disease-Outbreak-news/item/2022-DON410

Return to footnote 46 referrer

Footnote 47

World Health Organization (WHO). 2007. Ebola haemorrhagic fever in the Democratic Republic of the Congo.

Return to footnote 47 referrer

Footnote 48

World Health Organization (WHO). 2007. Ebola haemorrhagic fever in Uganda - update.

Return to footnote 48 referrer

Footnote 49

Formenty, P., C. Boesch, M. Wyers, C. Steiner, F. Donati, F. Dind, F. Walker, and B. Le Guenno. 1999. Ebola virus outbreak among wild chimpanzees living in a rain forest of Cote d'Ivoire. J. Infect. Dis. 179 Suppl 1:S120-6.

Return to footnote 49 referrer

Footnote 50

Bray, M. 2003. Defense against filoviruses used as biological weapons. Antiviral Res. 57:53-60.

Return to footnote 50 referrer

Footnote 51

Leroy, E. M., P. Rouquet, P. Formenty, S. Souquière, A. Kilbourne, J. -. Froment, M. Bermejo, S. Smit, W. Karesh, R. Swanepoel, S. R. Zaki, and P. E. Rollin. 2004. Multiple Ebola Virus Transmission Events and Rapid Decline of Central African Wildlife. Science. 303:387-390.

Return to footnote 51 referrer

Footnote 52

Nfon, C. K., A. Leung, G. Smith, C. Embury-Hyatt, G. Kobinger, and H. M. Weingartl. 2013. Immunopathogenesis of severe acute respiratory disease in Zaire ebolavirus-infected pigs. PloS One. 8:e61904.

Return to footnote 52 referrer

Footnote 53

Morris, K. 2009. First pig-to-human transmission of Ebola Reston virus. 9:148.

Return to footnote 53 referrer

Footnote 54

Allela, L., O. Boury, R. Pouillot, A. Delicat, P. Yaba, B. Kumulungui, P. Rouquet, J. P. Gonzalez, and E. M. Leroy. 2005. Ebola virus antibody prevalence in dogs and human risk. Emerg. Infect. Dis. 11:385-390.

Return to footnote 54 referrer

Footnote 55

Olson, S. H., P. Reed, K. N. Cameron, B. J. Ssebide, C. K. Johnson, S. S. Morse, W. B. Karesh, J. A. Mazet, and D. O. Joly. 2012. Dead or alive: animal sampling during Ebola hemorrhagic fever outbreaks in humans. Emerging Health Threats Journal. 5:9134.

Return to footnote 55 referrer

Footnote 56

Morvan, J. M., E. Nakouné, V. Deubel, and M. Colyn. 2000. Ebola virus and forest ecosystem. Bulletin De La Societe De Pathologie Exotique. 93:172-175.

Return to footnote 56 referrer

Footnote 57

Connolly, B. M., K. E. Steele, K. J. Davis, T. W. Geisbert, W. M. Kell, N. K. Jaax, and P. B. Jahrling. 1999. Pathogenesis of experimental Ebola virus infection in guinea pigs. J. Infect. Dis. 179 Suppl 1:S203-17.

Return to footnote 57 referrer

Footnote 58

Ebihara, H., M. Zivcec, D. Gardner, D. Falzarano, R. LaCasse, R. Rosenke, D. Long, E. Haddock, E. Fischer, and Y. Kawaoka. 2012. A Syrian golden hamster model recapitulating ebola hemorrhagic fever. J. Infect. Dis. 207:306-318.

Return to footnote 58 referrer

Footnote 59

Franz, D. R., P. B. Jahrling, D. J. McClain, D. L. Hoover, W. R. Byrne, J. A. Pavlin, G. W. Christopher, T. J. Cieslak, A. M. Friedlander, and J. Eitzen E.M. 2001. Clinical recognition and management of patients exposed to biological warfare agents. Clin. Lab. Med. 21:435-473.

Return to footnote 59 referrer

Footnote 60

Johnson, E., N. Jaax, J. White, and P. Jahrling. 1995. Lethal experimental infections of rhesus monkeys by aerosolized Ebola virus. Int. J. Exp. Pathol. 76:227-236.

Return to footnote 60 referrer

Footnote 61

ABSA. Risk Group Classification for Infectious Agents. 2010.

Return to footnote 61 referrer

Footnote 62

Leroy, E. M., B. Kumulungui, X. Pourrut, P. Rouquet, A. Hassanin, P. Yaba, A. Délicat, J. T. Paweska, J. -. Gonzalez, and R. Swanepoel. 2005. Fruit bats as reservoirs of Ebola virus. Nature. 438:575-576.

Return to footnote 62 referrer

Footnote 63

Hayman, D. T., M. Yu, G. Crameri, L. F. Wang, R. Suu-Ire, J. L. Wood, and A. A. Cunningham. 2012. Ebola virus antibodies in fruit bats, Ghana, West Africa. Emerg. Infect. Dis. 18:1207-1209.

Return to footnote 63 referrer

Footnote 64

Yuan, J., Y. Zhang, J. Li, Y. Zhang, L. Wang, and Z. Shi. 2012. Serological evidence of ebolavirus infection in bats, China. Virology Journal. 9:236.

Return to footnote 64 referrer

Footnote 65

Olival, K. J., A. Islam, M. Yu, S. J. Anthony, J. H. Epstein, S. A. Khan, S. U. Khan, G. Crameri, L. F. Wang, W. I. Lipkin, S. P. Luby, and P. Daszak. 2013. Ebola virus antibodies in fruit bats, bangladesh. Emerg. Infect. Dis. 19:270-273.

Return to footnote 65 referrer

Footnote 66

Stansfield, S. K., C. L. Scribner, R. M. Kaminski, T. Cairns, J. B. McCormick, and K. M. Johnson. 1982. Antibody to Ebola virus in guinea pigs: Tandala, Zaire. J. Infect. Dis. 146:483-486.

Return to footnote 66 referrer

Footnote 67

Milligan, J. C., C. W. Davis, X. Yu, P. A. Ilinykh, K. Huang, P. J. Halfmann, R. W. Cross, V. Borisevich, K. N. Agans, J. B. Geisbert, C. Chennareddy, A. J. Goff, A. E. Piper, S. Hui, K. C. L. Shaffer, T. Buck, M. L. Heinrich, L. M. Branco, I. Crozier, M. R. Holbrook, J. H. Kuhn, Y. Kawaoka, P. J. Glass, A. Bukreyev, T. W. Geisbert, G. Worwa, R. Ahmed, and E. O. Saphire. 2022. Asymmetric and non-stoichiometric glycoprotein recognition by two distinct antibodies results in broad protection against ebolaviruses. Cell. 185:995-1007.e18.

Return to footnote 67 referrer

Footnote 68

Gilchuk, P., C. D. Murin, R. W. Cross, P. A. Ilinykh, K. Huang, N. Kuzmina, V. Borisevich, K. N. Agans, J. B. Geisbert, S. J. Zost, R. S. Nargi, R. E. Sutton, N. Suryadevara, R. G. Bombardi, R. H. Carnahan, A. Bukreyev, T. W. Geisbert, A. B. Ward, and J. E. Crowe. 2021. Pan-ebolavirus protective therapy by two multifunctional human antibodies. Cell. 184:5593-5607.e18.

Return to footnote 68 referrer

Footnote 69

Centers for Disease Control and Prevention (CDC). 2016. Ebola Virus Disease (EVD) Information for Clinicians in U.S. Healthcare Settings.

Return to footnote 69 referrer

Footnote 70

Mire, C. E., J. B. Geisbert, A. Marzi, K. N. Agans, H. Feldmann, and T. W. Geisbert. 2013. Vesicular stomatitis virus-based vaccines protect nonhuman primates against Bundibugyo ebolavirus. PLoS Neglected Tropical Diseases. 7:e2600.

Return to footnote 70 referrer

Footnote 71

. Kibuuka, H., N. M. Berkowitz, M. Millard, M. E. Enama, A. Tindikahwa, A. B. Sekiziyivu, P. Costner, S. Sitar, D. Glover, Z. Hu, G. Joshi, D. Stanley, M. Kunchai, L. A. Eller, R. T. Bailer, R. A. Koup, G. J. Nabel, J. R. Mascola, N. J. Sullivan, B. S. Graham, M. Roederer, N. L. Michael, M. L. Robb, and J. E. Ledgerwood. 2015. Safety and immunogenicity of Ebola virus and Marburg virus glycoprotein DNA vaccines assessed separately and concomitantly in healthy Ugandan adults: A phase 1b, randomised, double-blind, placebo-controlled clinical trial. Lancet. 385:1545-1554.

Return to footnote 71 referrer

Footnote 72

Sarwar, U. N., P. Costner, M. E. Enama, N. Berkowitz, Z. Hu, C. S. Hendel, S. Sitar, S. Plummer, S. Mulangu, R. T. Bailer, R. A. Koup, J. R. Mascola, G. J. Nabel, N. J. Sullivan, B. S. Graham, and J. E. Ledgerwood. 2015. Safety and immunogenicity of DNA vaccines encoding ebolavirus and marburgvirus wild-type glycoproteins in a phase i clinical trial. J. Infect. Dis. 211:549-557.

Return to footnote 72 referrer

Footnote 73

Karita, E., J. Nyombayire, R. Ingabire, A. Mazzei, T. Sharkey, J. Mukamuyango, S. Allen, A. Tichacek, R. Parker, F. Priddy, F. Sayinzoga, S. Nsanzimana, C. Robinson, M. Katwere, D. Anumendem, M. Leyssen, M. Schaefer, and K. M. Wall. 2022. Safety, reactogenicity, and immunogenicity of a 2-dose Ebola vaccine regimen of Ad26.ZEBOV followed by MVA-BN-Filo in healthy adult pregnant women: study protocol for a phase 3 open-label randomized controlled trial. Trials. 23.

Return to footnote 73 referrer

Footnote 74

74. Bockstal, V., G. Shukarev, C. McLean, N. Goldstein, S. Bart, A. Gaddah, D. Anumenden, J. N. Stoop, A. M. de Groot, M. G. Pau, J. Hendriks, S. C. De Rosa, K. W. Cohen, M. J. McElrath, B. Callendret, K. Luhn, M. Douoguih, and C. Robinson. 2022. First-in-human study to evaluate safety, tolerability, and immunogenicity of heterologous regimens using the multivalent filovirus vaccines Ad26.Filo and MVA-BN-Filo administered in different sequences and schedules: A randomized, controlled study. Plos One. 17.

Return to footnote 74 referrer

Footnote 75

Ledgerwood, J. E., A. D. DeZure, D. A. Stanley, E. E. Coates, L. Novik, M. E. Enama, N. M. Berkowitz, Z. Hu, G. Joshi, A. Ploquin, S. Sitar, I. J. Gordon, S. A. Plummer, L. A. Holman, C. S. Hendel, G. Yamshchikov, F. Roman, A. Nicosia, S. Colloca, R. Cortese, R. T. Bailer, R. M. Schwartz, M. Roederer, J. R. Mascola, R. A. Koup, N. J. Sullivan, and B. S. Graham. 2017. Chimpanzee Adenovirus Vector Ebola Vaccine. N. Engl. J. Med. 376:928-938.

Return to footnote 75 referrer

Footnote 76

Qiu, X., G. Wong, J. Audet, A. Bello, L. Fernando, J. B. Alimonti, H. Fausther-Bovendo, H. Wei, J. Aviles, and E. Hiatt. 2014. Reversion of advanced Ebola virus disease in nonhuman primates with ZMapp. Nature. 514:47.

Return to footnote 76 referrer

Footnote 77

National Institutes of Health. 2018. NIH begins testing Ebola treatment in early-stage trial.

Return to footnote 77 referrer

Footnote 78

Mitchell, S. W., and J. B. McCormick. 1984. Physicochemical inactivation of Lassa, Ebola, and Marburg viruses and effect on clinical laboratory analyses. J. Clin. Microbiol. 20:486-489.

Return to footnote 78 referrer

Footnote 79

Elliott, L. H., J. B. McCormick, and K. M. Johnson. 1982. Inactivation of Lassa, Marburg, and Ebola viruses by gamma irradiation. J. Clin. Microbiol. 16:704-708.

Return to footnote 79 referrer

Footnote 80

World Health Organization. 2014. Interim infection prevention and control guidance for care of patients with suspected or confirmed filovirus haemorrhagic fever in health-care settings, with focus on Ebola.

Return to footnote 80 referrer

Footnote 81

United States Environmental Protection Agency. (2022). List L: Disinfectants for Use Against Ebola Virus. Retrieved 12/21, 2022 from https://www.epa.gov/pesticide-registration/list-l-disinfectants-use-against-ebola-virus

Return to footnote 81 referrer

Footnote 82

Cook, B. W., T. A. Cutts, A. M. Nikiforuk, P. G. Poliquin, J. E. Strong, and S. S. Theriault. 2015. Evaluating environmental persistence and disinfection of the Ebola virus Makona variant. Viruses. 7:1975-1986.

Return to footnote 82 referrer

Footnote 83

Cook, B. W., T. A. Cutts, A. M. Nikiforuk, A. Leung, D. Kobasa, and S. S. Theriault. 2016. The disinfection characteristics of Ebola Virus outbreak variants. Scientific Reports. 6:38293.

Return to footnote 83 referrer

Footnote 84

Sagripanti, J., and C. D. Lytle. 2011. Sensitivity to ultraviolet radiation of Lassa, vaccinia, and Ebola viruses dried on surfaces. Arch. Virol. 156:489-494.

Return to footnote 84 referrer

Footnote 85

Cutts, T., A. Grolla, S. Jones, B. W. Cook, X. Qiu, and S. S. Theriault. 2016. Inactivation of Zaire Ebolavirus variant Makona in human serum samples analyzed by enzyme-linked immunosorbent assay. J. Infect. Dis. 214:S218-S221.

Return to footnote 85 referrer

Footnote 86

Cutts, T., B. Cook, G. Poliquin, J. Strong, and S. Theriault. 2016. Inactivating Zaire Ebolavirus in Whole-Blood Thin Smears Used for Malaria Diagnosis. J. Clin. Microbiol. 54:1157-1159.

Return to footnote 86 referrer

Footnote 87

Centers for Disease Control and Prevention (CDC). 2018. Guidance for the Collection, Transport and Submission of Specimens for Ebola Virus Testing.

Return to footnote 87 referrer

Footnote 88

Grolla, A., S. M. Jones, L. Fernando, J. E. Strong, U. Ströher, P. Möller, J. T. Paweska, F. Burt, P. P. Palma, and A. Sprecher. 2011. The use of a mobile laboratory unit in support of patient management and epidemiological surveillance during the 2005 Marburg Outbreak in Angola. PLoS Neglected Tropical Diseases. 5:e1183.

Return to footnote 88 referrer

Footnote 89

Blow, J. A., D. J. Dohm, D. L. Negley, and C. N. Mores. 2004. Virus inactivation by nucleic acid extraction reagents. J. Virol. Methods. 119:195-198.

Return to footnote 89 referrer

Footnote 90

Belanov, E. F., V. P. Muntianov, V. D. Kriuk, A. V. Sokolov, N. I. Bormotov, O. V. P'iankov, and A. N. Sergeev. 1996. Survival of Marburg virus infectivity on contaminated surfaces and in aerosols. Vopr. Virusol. 41:32-34.

Return to footnote 90 referrer

Footnote 91

Piercy, T. J., S. J. Smither, J. A. Steward, L. Eastaugh, and M. S. Lever. 2010. The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. J. Appl. Microbiol.

Return to footnote 91 referrer

Footnote 92

Sagripanti, J., A. M. Rom, and L. E. Holland. 2010. Persistence in darkness of virulent alphaviruses, Ebola virus, and Lassa virus deposited on solid surfaces. Arch. Virol. 155:2035-2039.

Return to footnote 92 referrer

Footnote 93

Nikiforuk, A. M., T. A. Cutts, S. S. Theriault, and B. W. Cook. 2017. Challenge of Liquid Stressed Protective Materials and Environmental Persistence of Ebola Virus. Scientific Reports. 7:4388.

Return to footnote 93 referrer

Footnote 94

Bausch, D. G., J. S. Towner, S. F. Dowell, F. Kaducu, M. Lukwiya, A. Sanchez, S. T. Nichol, T. G. Ksiazek, and P. E. Rollin. 2007. Assessment of the risk of Ebola virus transmission from bodily fluids and fomites. J. Infect. Dis. 196:S142-S147.

Return to footnote 94 referrer

Footnote 95

Centers for Disease Control and Prevention. 2009. Biosafety in Microbiological and Biomedical Laboratories. U.S. Department of Health and Human Services, USA.

Return to footnote 95 referrer

Footnote 96

Fischer, W. A., P. Vetter, D. G. Bausch, T. Burgess, R. T. Davey, R. Fowler, F. G. Hayden, P. B. Jahrling, A. C. Kalil, and D. L. Mayers. 2017. Ebola virus disease: an update on post-exposure prophylaxis. The Lancet Infectious Diseases.

Return to footnote 96 referrer

Footnote 97

Clark, D. V., P. B. Jahrling, and J. V. Lawler. 2012. Clinical management of filovirus-infected patients. Viruses. 4:1668-1686.

Return to footnote 97 referrer

Footnote 98

Wong, G., J. S. Richardson, T. Cutts, X. Qiu, and G. P. Kobinger. 2015. Intranasal immunization with an adenovirus vaccine protects guinea pigs from Ebola virus transmission by infected animals. Antiviral Res. 116:17-19.

Return to footnote 98 referrer

Footnote 99

Formenty, P., C. Hatz, B. Le Guenno, A. Stoll, P. Rogenmoser, and A. Widmer. 1999. Human infection due to Ebola virus, subtype Cote d'Ivoire: Clinical and biologic presentation. J. Infect. Dis. 179:S48-S53.

Return to footnote 99 referrer

Footnote 100

Anonymous 2009. Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009.

Return to footnote 100 referrer

Footnote 101

Public Health Agency of Canada (PHAC). 2016. Canadian Biosafety Handbook. Public Health Agency of Canada.

Return to footnote 101 referrer

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