Indian Journal of Medical Microbiology IAMM  | About us |  Subscription |  e-Alerts  | Feedback |  Login   
  Print this page Email this page   Small font sizeDefault font sizeIncrease font size
 Home | Ahead of Print | Current Issue | Archives | Search | Instructions  
Users Online: 2241 Official Publication of Indian Association of Medical Microbiologists 
 ~  Similar in PUBMED
 ~  Search Pubmed for
 ~  Search in Google Scholar for
 ~  Article in PDF (1,047 KB)
 ~  Citation Manager
 ~  Access Statistics
 ~  Reader Comments
 ~  Email Alert *
 ~  Add to My List *
* Registration required (free)  

 ~ Introduction
 ~  References
 ~  Article Figures
 ~  Article Tables

 Article Access Statistics
    PDF Downloaded771    
    Comments [Add]    

Recommend this journal


  Table of Contents  
Year : 2014  |  Volume : 32  |  Issue : 4  |  Page : 364-370

The threat of Ebola: An update

Department of Microbiology, All India Institute of Medical Sciences, Bhubaneswar 751 019, Orissa, India

Date of Submission02-Sep-2014
Date of Acceptance12-Sep-2014
Date of Web Publication4-Oct-2014

Correspondence Address:
Baijayantimala Mishra
Department of Microbiology, All India Institute of Medical Sciences, Bhubaneswar 751 019, Orissa
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0255-0857.142230

Rights and Permissions

How to cite this article:
Mishra B. The threat of Ebola: An update. Indian J Med Microbiol 2014;32:364-70

How to cite this URL:
Mishra B. The threat of Ebola: An update. Indian J Med Microbiol [serial online] 2014 [cited 2021 Jan 19];32:364-70. Available from:

 ~ Introduction Top

The world experienced the largest and most widespread Ebola virus outbreak in West Africa, 2014. The current outbreak which began in Guinea in December, 2013, and came to notice in March, 2014, has already affected five African countries. Till now, the threat of the virus for the world outside Africa was mainly for its potential as a biological weapon. The present one is the largest, longest and most widespread outbreak shaking the world for the first time with the scare of Ebola virus disease (EVD), due to the possibility of natural disease transmission from the affected African countries which was never realized before so seriously. On 28 th August 2014 the World Health Organization (WHO) warned that the number of people affected by Ebola virus could rise to 20,000 within coming 9 months. Nearly 45% of the total number of reported cases have occurred only within a span of 3 weeks with cumulative number of 3944 cases and 2097 deaths (as of 5 th September 2014) despite significant gaps in reporting. [1] On 8 th August, 2014 WHO declared the West Africa Ebola virus outbreak as a "Public Health Emergency of International concern" (PHEIC).

The current outbreak

The epicenter of the present outbreak which began in December, 2013 was the remote South-east rainforest region of Guinea. The index case, a 2-year-old boy, resident of Meliandou Village of Guéckédou, died on 6 th of December 2013. Three of his family members along with two healthcare workers who had come in contact with the index case, had also died of Ebola virus infection. [2] The infection then spread to the neighbouring villages, and finally crossed the Guinea border and entered sequentially to Liberia, Sierra Leone, Nigeria and Senegal in March, May, July and August affecting near 4000 cases and more than 2000 deaths (by 5 th September 2014; [Figure 1]). [1],[3] [Figure 2] depicts the important timeline of the current outbreak.
Figure 1: Ebola outbreak West Africa 2014 as at 5th September 2014

Click here to view
Figure 2: Timeline of West Africa Ebola virus disease outbreak 2014

Click here to view

Ebola virus (formerly Zaire ebolavirus), was found to be the causative strain of the present outbreak, for the first time, in West Africa. The phylogenetic analysis has shown the present Guinean strain is an outlier within the EBOV, suggesting that the introduction of the virus into West Africa has not occurred recently. [2] Phylogenetic comparison to genomes from previous outbreaks has revealed that the divergence from Central African strain had occurred at around a decade back in 2004, and have been circulating amongst the bat population in Guinea, suggesting there by an independent zoonotic event for the current outbreak. [3] Genetic similarities among the samples of the 2014 West Africa outbreak suggests a single event of virus transmission from the natural reservoir, followed by sustained human to human transmission. [3]

The virus

The family Filoviridae consists of two genera, Ebola virus and Marburg virus. Filoviruses have a uniform diameter of 80 nm and variable length, which may be up to 1400 nm. The viral genome is a single stranded, negative sense, non-segmented RNA molecule, that encodes seven genes; nucleoprotein (NP), virion protein (VP) 35, VP40, glycoprotein (GP), VP30, VP24, RNA-dependent RNA polymerase (L). Amongst these, NP, VP35, VP30 and RNA-dependent RNA polymerase are associated with viral replication and transactivation. VP40 is the matrix protein and involves in budding and release of viral particle, whereas VP24 is the minor matrix protein and associated with nucleocapsid formation. Both the matrix proteins, VP40 and VP24 are known to block interferon signaling. The only surface protein possessed by the filovirus is the glycoprotein, present as trimeric spikes consisting of GP 1 and GP 2 . The non-structural soluble form of glycoprotein, sGP, a unique product of EBOV GP gene, gets secreted from infected cells. [4]

Ebola virus has five species, Zaire, Sudan, Tai Forest, Reston and Bundibugyo. The sequence difference within species is rarely more than 3%. Among the Ebola virus species, maximum divergence has been reported between Tai Forest virus and Reston virus [5] , whereas the maximum divergence is 3% between the strains of current West Africa outbreak (Gueéckeédou-C05) and 1994 Gabon strain. [2]


In 1976, outbreak of haemorrhagic fever was reported in two adjacent localities in Africa, southern Sudan and northern Zaire (presently named as Democratic Republic of Congo (DRC)). The outbreak started with an index case with malaria like symptoms and spread due to use of unsterilized needles in the hospital, affected 318 cases with a case fatality rate of 88%. An unknown pathogen was isolated from patients' blood sample, which was named as Ebola virus after the name of the Ebola river in North Western DRC. [6] The two outbreaks were initially thought to be caused by two different viruses, which later found to be two species of Ebola virus, Sudan Ebola virus (SEBOV) and Zaire Ebola virus (ZEBOV). [7] The third species, Tai forest Ebola virus (previously called Ivory Coast or Coˆ te d'Ivoire) was isolated from an individual who worked in Tai forest and had conducted a necropsy on a chimpanzee that had stayed with a troop where several members had died due to Ebola haemorrhagic fever. [8] The latest human pathogenic Ebola virus is the Bundibugyo virus, found in equatorial region of Africa. [9] Another species of Ebola virus, Reston Ebola virus, is considered non-pathogenic for humans. This species was first discovered in Reston, Virginia, USA, in November, 1989 where high mortality was noticed in a shipment of Cyanomolgus monkeys that was imported from Philippines. Serological testing amongst animal handlers showed the evidence of recent infection in four, but none of them developed any manifestation of haemorrhagic fever like illness. [10] Several outbreaks due to various species of Ebola virus have been recorded in different parts of Africa.


Ebola virus disease is a classical zoonotic disease. Evidences suggest fruit bats as the reservoir for both Ebola and Marburg virus. The viral RNA and antibodies of Zaire Ebola virus have been detected in three species of fruit bats; Hypsignathus monstrosus (the hammer-headed fruit bat), Epomops franqueti (Franquet'sepauletted fruit bat) and Monycteris torquata (the little-collared bat) and therefore have been implicated as the potential spill over source for Ebola virus. [11] Detection of similar EBOV sequences from fruit bats and the infected patients in the outbreak locality also reconfirms bats as the reservoir of filoviruses. [12],[13] Spill over from bats is believed to cause outbreaks. The infection in bats is or associated with sub-clinical infection. Mammalian species including non-human primates that are susceptible to infection are regarded as the dead end hosts. Possibilities of seasonal effect on introduction of Ebola virus infection have also been hypothesised. [14],[15] Besides this, stress due to alteration of diet, scarcity of diet as well as physiological conditions like pregnancy, all have been observed to increase viral replication and thereby increase the risk of virus transmission. [16]

Clinical features

The severity of different species has been found to be of variable grade. ZEBOV is the most severe and a case fatality rate approaching 90%, followed by Sudan EBOV (SEBOV) which has been associated with 53-66% mortality. [17],[18] The case fatality in Bundibugyo virus is estimated to be near 40%, whereas Tai Forest virus has been described only in a single case, who had recovered from the disease. [8],[19],[20]

The disease usually starts with an abrupt onset, after an incubation period of 2-21 days (average 4-10 days). [21] The initial manifestations are fever, chills and myalgia. Subsequently haemorrhagic manifestation sets in, which manifests with petechiae, ecchymoses, and finally subcutaneous/mucosal/internal bleeding occurs involving multiple organs. Appearance of maculopapular rash associated with erythema at around 5-7 days of illness is often considered as an important differential feature, which later isfollowed by desquamation. In the end stage, metabolic disturbances, diffuse coagulopathy and circulatory collapse supervene. [22],[23] The outcome of the disease in terms of death or recovery usually is observed during 6-11 days of illness. [24] Absence of haemorrhagic manifestations at the time of diagnosis was noted in majority of the patients during the present outbreak. This has highlighted the importance of the term "Ebola virus disease" instead of "Ebola haemorrhagic fever", which would help in early recognition of cases. [2]


The outbreak of EVD begins with the introduction of virus into human population from infected bats or non-human primates. Thereafter, the transmission from human to human occurs through close contact with patients or cadaver of Ebola-infected patients. The first part generates the outbreak, occurs due to spill over of zoonotic infection where the virus is acquired by close contact with bats or non-human primates through hunting, butchering, eating or handling organs or cells of these animals or through exposure to bat inhabited caves. [25],[26] The second part, i.e, the human to human transmission, is responsible for spreading the outbreak. This occursmainly through direct contact with patient's blood or various body fluids like urine, semen, genital secretion, sweat, bloody stool and vomitus and indirect contact with environment contaminated with infected body fluids. [27] The virus has been found in semen for up to 7 weeks after recovery from the illness, suggesting the possibility of sexual mode of transmission. [21]

Transmission through re-use of contaminated needles in hospitals had led to the first outbreak of Zaire and Sudan EBOV in 1976. [6] Exposure to infected monkey cells, blood and needle stick injury has also been reported. [28],[29],[30] Though evidences of aerosol transmission have been reported between monkeys in natural condition, proven in laboratory experiments and considered as an efficient route if given deliberately, the transmission pattern during outbreaks in humans does not suggest respiratory route of transmission. No evidence suggests the role of insects in disease transmission. [31],[32]

[Figure 3] depicts the various modes of Ebola virus transmission.
Figure 3: Modes of transmission of Ebola virus infection

Click here to view

The virus gains entry into the body through mucosa, skin abrasion or directly through blood. Monocyte, macrophage and dendritic cells, hepatocyte, adrenal cortical cells and endothelial cells are the target cells. The initial replication occurs in monocytes, macrophage and dendritic cells and via these cells dissemination of virus occurs to lymph nodes, spleen, liver and other organs. [33],[34] The infected macrophage and dendritic cells get activated and release various proinflammatory cytokines like TNF-α, IL6, IL1-β, IL-8, macrophage inflammatory protein (MIP)-α, MIP-β, monocyte chemotactic protein (MCP)-1, and growth-regulated protein (GRO)-α. [35] High level of TNF-α mediates the increase endothelial permeability leading to vascular leakage. [36]

Various viral glycoproteins; GP1, 2 and VP40 have also been associated with increased endothelial permeability by triggering the expression of intracellular and vascular adhesion molecules (ICAM1 and VCAM-1) and E-selectin by activation of endothelial cells. [35]

Besides the endothelial damage, apoptosis of lymphocytes, necrosis of liver and adrenal gland have also been shown to have important role in disease pathogenesis. Lymphoid depletion has largely been attributed to apoptosis. Significant lymphoid depletion and lymphopenia have been reported in severe fatal cases. The possible pathway of lymphocyte apoptosis might involve TRAIL (TNF-related apoptosis inducing ligand) or Fas-receptor pathway, or Ebola virus-induced impairment of dendritic cell function. [33],[37],[38] Cells that are infected by Ebola virus, show the features of necrosis and do not undergo apoptosis. [33] The necrosis of liver cells is thought to be responsible for decreasing clotting factor and dysfunction of coagulation system. Infection and necrosis of adrenal cortex lead to decreased synthesis of steroids, leading to hypovolumia and shock, which are important end stage feature in severe Ebola haemorrhagic fever. [24] Increased level of proinflammatory cytokines and high viral load have been associated with fatal outcome, whereas, survival has been associated with antibody response to viral nucleoprotein (NP) and VP40, cell-mediated immune response against viral glycoprotein (GP), clearance of virus and activation of cytotoxic T lymphocytes. Decreased D- dimers, IL6, IL10, TNF-α along with low viral load have been reported among survivors in experimental animal experiment. [35] The association of soluble CD40 ligand (sCD40L) level with non-fatal outcome has been shown in a recent study in patients, indicating the repair of damaged endothelium by activated platelets. [39]


Acute febrile illness is the usual presentation in the initial part of disease. In endemic countries, classical epidemiological history like travel to jungle, eating or hunting of bats or animals, exposure to cave, close contact with sick patients or dead bodies'helps in clinching the suspicion for Ebola virus infection. However, in absence of relevant epidemiological history, the clinical suspicion is difficult particularly during the initial part of illness without haemorrhagic manifestation, as the symptoms mimic other tropical infectious diseases like malaria, typhoid fever, leptospirosis, relapsing fever, anthrax, chikungunya, yellow fever, etc., which are also prevalent in these countries. Patient with haemorrhagic features may also be confused with Lassa fever. In non-endemic countries, patient with history of travel to endemic countries or outbreak affected localities, if develops acute febrile illness, should be suspected for Ebola virus infection.

Laboratory diagnosis is performed only in designated national and international laboratories. Blood, serum and tissues are the samples that are subjected for testing. While collecting the samples, the health care worker must follow (i) the use of appropriate barrier precautions, (ii) maintenance of sterility, (iii) proper disposal of materials after collection and (iv) avoidance of needle stick injury. The clinical materials are subjected for the test after rendering the samples non-infectious. Blood/serum samples for antibody detection are either gamma eradiated with Cobalt 60 or heat inactivated, whereas for nucleic acid detection, RNA isolation from clinical material can be done by treating with guanidiumisothiocyanate (GITC), a chaotropic agent that degrades the viral protein and makes the sample non-infectious. [24]

Detection of viral RNA, antigen and virus specific IgM and IgG are the major modalities of diagnosis. The diagnostic tests employed at various stage of illness are described in [Table 1]. Positive serology test helps in confirmation but negative result does not rule out the possibility of infection, as patient with severe fatal infection may not mount any antibody response. Among the other serological tests, Western blot and indirect immunofluorescence tests can be used for confirmation and screening, respectively. Sophisticated diagnostic tests like multiplex PCR and micro-array-based tests have also been developed based on the common clinical syndrome; however, the primitive facility in endemic countries makes them far from implementation. [31]
Table 1: Laboratory tests for Ebola virus diagnosis

Click here to view

Treatment and prevention

Management of patient is largely based on supportive and symptomatic treatment which constitutes, broad spectrum antibiotics, IV fluid administration and management of organ failure. The other important aspect is prevention of disease transmission by strict isolation of patients and practicing barrier nursing procedures. As the virus can also be transmitted from the dead bodies of the infected patients, disposal of dead bodies should be carried by cremation or burial in hermetically sealed casket, using personal protective equipment and surface decontamination, following the safety procedure as described by CDC guideline. [40]

So far, no specific anti-Ebola drug has the approval for human use. The non-availability was much felt during the current outbreak and raised the controversies regarding slow process of anti-Ebola drug trial. The uncontrolled nature of the currently ongoing Ebola outbreak in West Africa, however, compelled the WHO to approve the use of experimental treatments in infected patents. [41] Several compounds have been tried in the recent past in non-human primates and appears promising for human use in future.

Monoclonal antibody based therapy gained the attention of the entire world during current outbreak, when the antibody preparation (ZMapp) was given to the two American health workers, who acquired Ebola virus infection while working during the current West Africa Ebola outbreak. The preparation named as "Secret serum" by the media. ZMapp TM consists of three "humanised" monoclonal antibodies (MB-003) manufactured in tobacco plant, Nicotiana. [42] It is an optimized combination of MB-003 components (Mapp) and ZMAb (Defyrus/PHAC) and is a collaborative product of Mapp Biopharmaceutical, Inc, LeafBio (San Diego, CA), Defyrus Inc. (Toronto, Canada) and Public Health Agency of Canada (PHAC). [43] The survival rate of 100%, 67% and 43% have been reported with MB-003 in non-human primates when given at 1hour, 24-48 hours and 120 hours, respectively, post-infection after onset of viremia and fever. Both the Americans who had received the monoclonal antibodies have recovered from the disease. However, whether the recovery can be attributed to the use of drug is a matter of debate, as both of them had received the antibody late in the course of disease where the overall chances of survival increases, and can also be due to high quality medical care. Nevertheless, the anti-Ebola drug therapy for the first time has generated hope to combat the mortality in patients.

Small interfering RNA molecules (siRNA) have been made targeting Ebola virus VP24, VP35 and polymerase (L) genes. Recently the combination of these three siRNAs encapsulated in stable nucleic acid lipid particles (SNALPs) has been reported to provide 100% protection against Ebola virus when given 30 minutes post-infection. [44] Tekmira's siRNA preparation targeting L gene of EBOV (TKM-Ebola) has recently got the approval by US Food and Drug Administration for use in infected patients. [45] PMOPlus (Positively charged phosphorodiamidatemorpholino oligomers), [46] BCX 4430 anadenosine analogue, [47] T-705, (favipiravir) a pyrazinecarboxamide derivative, are the other promising candidates, acts by inhibiting viral replication.

Ebola in indian perspective

The Ministry of Health and Family Welfare, Government of India, has issued several guidelines for effective management of the situation in case the virus gets entry into the country. However, beyond guidelines, keeping the required logistics in place, adequate training of healthcare workers for proper use and disposal of personal protective equipment are also essential. In the recent past India has shown its capability in prompt and effective containment of a similarly fatal viral haemorrhagic fever, Crimean Congo Haemorrhagic fever. The challenge of Ebola if it enters the country would be much more than CCHF, as the introduction can occur at multiple sites simultaneously, demanding a countrywide preparedness.

The knowledge on Ebola virus has progressed significantly, but still large gaps remain. The elusive virus ecology still has the upper hand and no advances have been made to predict any impending outbreak. The West African countries, the poorest of the world, when affected by the deadliest of the dreadful virus, ZEBOV, the explosive uncontrollable situation probably would have been anticipated much earlier. The limitations of diagnostic facilities, medical care, logistic constraints along with the cultural differences and hostile environment have compounded the problem of disease containment. The International communities have joined hands to contain this ever expanding Ebola outbreak and stopping the helpless West Africans to die.

 ~ References Top

1.WHO: Ebola Response Roadmap Situation Report 25 September 2014: [Last accessed on 2014 Sept 07].  Back to cited text no. 1
2.Baize S, Pannetier D, Oestereich L, Rieger T, Koivogui L, Magassouba N, et al. Emergence of Zaire Ebola Virus Disease in Guinea-Preliminary Report. N Engl J Med 2014.  Back to cited text no. 2
3.Gire SK, Goba A, Andersen KG, Sealfon RS, Park DJ, Kanneh L, et al. Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak. Science 2014. Available from: 1259657.full.pdf [Last accessed 2014 Aug 31].  Back to cited text no. 3
4.Sanchez A, Trappier SG, Mahy BW, Peters CJ, Nichol ST. The virion glycoproteins of Ebola viruses are encoded in two reading frames and are expressed through transcriptional editing. Proc Natl Acad Sci U S A 1996;93:3602-7.  Back to cited text no. 4
5.Gatherer D. The 2014 Ebola virus disease outbreak in West Africa. J Gen Virol 2014;95:1619-24.  Back to cited text no. 5
6.Ebola haemorrhagic fever in Sudan, 1976. Report of a WHO/International Study Team. Bull World Health Organ 1978;56:247-70.  Back to cited text no. 6
7.Cox NJ, McCormick JB, Johnson KM, Kiley MP. Evidence for two subtypes of Ebola virus based on oligonucleotide mapping of RNA. J Infect Dis 1983;147:272-5.  Back to cited text no. 7
8.Le Guenno B, Formenty P, Wyers M, Gounon P, Walker F, Boesch C. Isolation and partial characterisation of a new strain of Ebola virus. Lancet 1995;345:1271-4.  Back to cited text no. 8
9.Towner JS, Sealy TK, Khristova ML, Albarino CG, Conlan S, Reeder SA, et al. Newly discovered ebola virus associated with hemorrhagic fever outbreak in Uganda. PLoS Pathog 2008;4:e1000212.  Back to cited text no. 9
10.Centers for Disease Control (CDC). Update: Filovirus infections among persons with occupational exposure to nonhuman primates. MMWR Morb Mortal Wkly Rep 1990;39:266-7; 273.  Back to cited text no. 10
11.Leroy EM, Kumulungui B, Pourrut X, Rouquet P, Hassanin A, Yaba P, et al. Fruit bats as reservoirs of Ebola virus. Nature 2005;438:575-6.  Back to cited text no. 11
12.Biek R, Walsh PD, Leroy EM, Real LA. Recent common ancestry of Ebola Zaire virus found in a bat reservoir. PLoS Pathog 2006;2:e90.  Back to cited text no. 12
13.Bausch DG, Nichol ST, Muyembe-Tamfum JJ, Borchert M, Rollin PE, Sleurs H, et al.; International Scientific and Technical Committee for Marburg Hemorrhagic Fever Control in the Democratic Republic of the Congo. Marburg hemorrhagic fever associated with multiple genetic lineages of virus. N Engl J Med 2006;355:909-19.  Back to cited text no. 13
14.Johnson BK, Wambui C, Ocheng D, Gichogo A, Oogo S, Libondo D, et al. Seasonal variation in antibodies against Ebola virus in Kenyan fever patients. Lancet 1986;1:1160.  Back to cited text no. 14
15.Lahm SA, Kombila M, Swanepoel R, Barnes RF. Morbidity and mortality of wild animals in relation to outbreaks of Ebola haemorrhagic fever in Gabon, 1994-2003. Trans R Soc Trop Med Hyg 2007;101:64-78.  Back to cited text no. 15
16.Groseth A, Feldmann H, Strong JE. The ecology of Ebola virus. Trends Microbiol 2007;15:408-16.  Back to cited text no. 16
17.Baron RC, McCormick JB, Zubeir OA. Ebola virus disease in southern Sudan: Hospital dissemination and intrafamilial spread. Bull World Health Organ 1983;61:997-1003.  Back to cited text no. 17
18.Towner JS, Rollin PE, Bausch DG, Sanchez A, Crary SM, Vincent M, et al. Rapid diagnosis of Ebola hemorrhagic fever by reverse transcription-PCR in an outbreak setting and assessment of patient viral load as a predictor of outcome. J Virol 2004;78:4330-41.  Back to cited text no. 18
19.MacNeil A, Farnon EC, Wamala J, Okware S, Cannon DL, Reed Z, et al. Proportion of deaths and clinical features in Bundibugyo Ebola virus infection, Uganda. Emerg Infect Dis 2010;16:1969-72.  Back to cited text no. 19
20.Wamala JF, Lukwago L, Malimbo M, Nguku P, Yoti Z, Musenero M, et al. Ebola hemorrhagic fever associated with novel virus strain, Uganda, 2007-2008. Emerg Infect Dis 2010;16:1087-92.  Back to cited text no. 20
21.Ebola virus disease. Available from: [Last accessessed on 2014 Sept 07].  Back to cited text no. 21
22.Bausch DG, Borchert M, Grein T, Roth C, Swanepoel R, Libande ML, et al. Risk factors for Marburg hemorrhagic fever, Democratic Republic of the Congo. Emerg Infect Dis 2003;9:1531-7.  Back to cited text no. 22
23.Feldmann H, Geisbert T, Kawaoka Y. Filoviruses: Recent advances and future challenges. J Infect Dis 2007;196 Suppl 2:S129-30.  Back to cited text no. 23
24.Feldmann H, Geisbert TW. Ebola haemorrhagic fever. Lancet 2011;377:849-62.  Back to cited text no. 24
25.Georges-Courbot MC, Sanchez A, Lu CY, Baize S, Leroy E, Lansout-Soukate J, et al. Isolation and phylogenetic characterization of Ebola viruses causing different outbreaks in Gabon. Emerg Infect Dis 1997;3:59-62.  Back to cited text no. 25
26.Centers for Disease Control and Prevention (CDC). Imported case of Marburg hemorrhagic fever-Colorado, 2008. MMWR Morb Mortal Wkly Rep 2009;58:1377-81.  Back to cited text no. 26
27.Dowell SF, Mukunu R, Ksiazek TG, Khan AS, Rollin PE, Peters CJ. Transmission of Ebola hemorrhagic fever: A study of risk factors in family members, Kikwit, Democratic Republic of the Congo, 1995. Commission de Lutte contre les Epidemies a Kikwit. J Infect Dis 1999;179 Suppl 1:S87-91.  Back to cited text no. 27
28.Ebola, lab accident death-Russia (Siberia), International Society for Infectious Diseases. 2004;2014.  Back to cited text no. 28
29.Francesconi P, Yoti Z, Declich S, Onek PA, Fabiani M, Olango J, et al. Ebola hemorrhagic fever transmission and risk factors of contacts, Uganda. Emerg Infect Dis 2003;9:1430-7.  Back to cited text no. 29
30.Ebola virus, needle stick injury - Germany: (Hamburg), International Society for Infectious Diseases; 2009.  Back to cited text no. 30
31.Sanchez A, Geisbert TW, Feldmann H. Marburg and Ebola viruses. In: Knipe DM, Howley PM, editors. Fields Virology. 5 th ed., Vol. 1. Philadelphia: Lippincott Williams and Wilkins; 2007. p. 1409-48.  Back to cited text no. 31
32.Mahanty S, Bray M. Pathogenesis of filoviral haemorrhagic fevers. Lancet Infect Dis 2004;4:487-98.  Back to cited text no. 32
33.Olejnik J, Ryabchikova E, Corley RB, Muhlberger E. Intracellular events and cell fate in filovirus infection. Viruses 2011;3:1501-31.  Back to cited text no. 33
34.Geisbert TW, Young HA, Jahrling PB, Davis KJ, Larsen T, Kagan E, et al. Pathogenesis of Ebola hemorrhagic fever in primate models: Evidence that hemorrhage is not a direct effect of virus-induced cytolysis of endothelial cells. Am J Pathol 2003;163:2371-82.  Back to cited text no. 34
35.Paessler S, Walker DH. Pathogenesis of the viral hemorrhagic fevers. Annu Rev Pathol 2013;8:411-40.  Back to cited text no. 35
36.Stroher U, West E, Bugany H, Klenk HD, Schnittler HJ, Feldmann H. Infection and activation of monocytes by Marburg and Ebola viruses. J Virol 2001;75:11025-33.  Back to cited text no. 36
37.Geisbert TW, Hensley LE, Jahrling PB, Larsen T, Geisbert JB, Paragas J, et al. Treatment of Ebola virus infection with a recombinant inhibitor of factor VIIa/tissue factor: A study in rhesus monkeys. Lancet 2003;362:1953-8.  Back to cited text no. 37
38.Mahanty S, Hutchinson K, Agarwal S, McRae M, Rollin PE, Pulendran B. Cutting edge: Impairment of dendritic cells and adaptive immunity by Ebola and Lassa viruses. J Immunol 2003;170:2797-801.  Back to cited text no. 38
39.McElroy AK, Erickson BR, Flietstra TD, Rollin PE, Nichol ST, Towner JS, et al. Ebola hemorrhagic fever: Novel biomarker correlates of clinical outcome. J Infect Dis 2014;210:558-66.  Back to cited text no. 39
40.Centers for Disease Control and Prevention and World Health Organization. Infection Control for Viral Haemorrhagic Fevers in the African Health Care Setting. Atlanta, Centers for Disease Control and Prevention 1998:1-198.  Back to cited text no. 40
41.Ethical considerations for use of unregistered interventions for Ebola viral disease (EVD): Summary of the panel discussion. WHO statement. 2014.  Back to cited text no. 41
42.Goodman JL. Studying "Secret Serums"-Toward Safe, Effective Ebola Treatments. N Engl J Med 2014.  Back to cited text no. 42
43.Z Mapp Information Sheet. [Last accessed on 2014 Sept 07].  Back to cited text no. 43
44.Geisbert TW, Lee AC, Robbins M, Geisbert JB, Honko AN, Sood V, et al. Postexposure protection of non-human primates against a lethal Ebola virus challenge with RNA interference: A proof-of-concept study. Lancet 2010;375:1896-905.  Back to cited text no. 44
45.Mullard A. Experimental Ebola drugs enter the limelight. Lancet 2014;384:649.  Back to cited text no. 45
46.Warren TK, Warfield KL, Wells J, Swenson DL, Donner KS, Van Tongeren SA, et al. Advanced antisense therapies for postexposure protection against lethal filovirus infections. Nat Med 2010;16:991-4.  Back to cited text no. 46
47.Falzarano D, Feldmann H. Possible leap ahead in filovirus therapeutics. Cell Res 2014;24:647-8.  Back to cited text no. 47


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


Print this article  Email this article


© 2004 - Indian Journal of Medical Microbiology
Published by Wolters Kluwer - Medknow

Online since April 2001, new site since 1st August '04