Tag Archives: pandemic

New Ebola virus disease case confirmed in a third DRC health zone

Alert, alert…

The Democtraic Republic of the Congo (DRC) Ministry of Health (MOH) today announced that 1 of 2 suspected EVD cases in the Mbandaka Health Zone has tested positive for Ebola virus.[1]

This weekend, two suspected cases of haemorrhagic fever were reported in the health zone of Wangata, one of the health zones of the city of Mbandaka. After analysis, one of the two samples was positive for Ebola virus disease.
-TRANSLATED from [1]

Zoomed in section of the adjacent DRC map highlighting the Wangata Health Zone (purple area) housing ta new EVD confirmed case, just below Mbandaka (Pin4), capital of Équateur Province.

What does it mean?

This is of particular concern as the cases lie adjacent to Mbandaka, the capital of Équateur province and a city of approximately 1 million people.[2]

Now is certainly a good time to have the experimental Ebola virus vaccine (V920) onsite and ready to be distributed to healthcare workers and contacts of cases in a ring vaccination format. This approach encircles cases with vaccinated people to prevent further spread from known foci of infection.[2]

New numbers

Case numbers have now changed again. As at the 15th May:

 

Table from DRC MOH.[1]

  • 44 total EVD cases (includes suspect, probable and confimred)
  • 2 new suspect cases, 1 each in Bikoro and Wangata health zones
    • 21 suspect cases
    • 20 probable cases
    • 3 confirmed cases
    • 23 deaths (proportion of fatal cases = 52%)

Case numbers are always changing so please use these as a guide only.

This latest turn of events is something to keep a close eye on. When EVD reaches more populated areas and transport hubs, we’ve seen how things can quickly spiral out of control. Hopefully the fast and collaborative response to date will stay on top of things.

It’s still too early to tell whether this outbreak is under control or not yet.

References…

  1. Special Communication from His Excellency the Minister of Health on May 16, 2018 on the evolution of the Ebola epidemic in the Democratic Republic of Congo
    https://us13.campaign-archive.com/?u=89e5755d2cca4840b1af93176&id=a902d8be0b
  2. Experimental Vaccine Will be Used against Ebola Outbreak in the DRC
    https://www.scientificamerican.com/article/experimental-vaccine-will-be-used-against-ebola-outbreak-in-the-drc/
  3. Effective Post-Exposure Treatment of Ebola Infection
    https://www.ncbi.nlm.nih.gov/pubmed/17238284
  4. Recombinant vesicular stomatitis virus vector mediates postexposure protection against Sudan Ebola hemorrhagic fever in nonhuman primates
    https://www.ncbi.nlm.nih.gov/pubmed/18385248
  5. Efficacy of Vesicular Stomatitis Virus-Ebola Virus Postexposure Treatment in Rhesus Macaques Infected With Ebola Virus Makona
    https://www.ncbi.nlm.nih.gov/pubmed/27496978
  6. Postexposure Treatment of Marburg Virus Infection
    https://wwwnc.cdc.gov/eid/article/16/7/10-0159_article
  7. Recombinant vesicular stomatitis virus vector mediates postexposure protection against Sudan Ebola hemorrhagic fever in nonhuman primates
    https://www.ncbi.nlm.nih.gov/pubmed/18385248

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Emerg. Infect. & Microbes: Novel Triple-Reassortant influenza Viruses In Pigs, Guangxi, China

Yikes!

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As pork production rises around the world – particularly in countries where there is poor biosecurity and little surveillance – the risks of seeing another novel swine flu virus emerge as a pandemic threat continues to grow. 

While we watch avian H5 & H7 flu viruses with particular concern – mainly due to their high mortality rates in humans – swine, or swine-avian-human triple reassortant viruses – are perhaps even more likely to emerge as a pandemic threat.

Two and a half years ago, Chen Hualan – director of China’s National Avian Influenza Reference Laboratory – gave an interview to Xinhua where she pegged the EA (Eurasian Avian-like) H1N1 swine virus (EAH1N1) as having perhaps the greatest pandemic potential of any of the novel viruses in circulation.

Avian-like H1N1 swine flu may “pose highest pandemic threat”: study

WASHINGTON, Dec. 28 (Xinhua) — The Eurasian avian-like H1N1 (EAH1N1) swine flu viruses, which have circulated in pigs since 1979, have obtained the ability to infect humans and may “pose the highest pandemic threat” among the flu viruses currently circulating in animals, Chinese researchers said Monday.

“Pigs are considered important intermediate hosts for flu viruses,” Chen Hualan, director of China’s National Avian Influenza Reference Laboratory, who led the study, said in an written interview with Xinhua.

“Based on scientific analysis and comprehensive comparison of the main animal flu viruses: H1N1, H3N2, H5N1, H7N9, H9N2 and EAH1N1, we found the EAH1N1 is the one most likely to cause next human flu pandemic. We should attach great importance to the EAH1N1.”

(Continue . . . )

And indeed, we’ve been following the evolution of EAH1N1, along with other novel swine-origin viruses in China, with considerable interest.  A few recent blogs include:

Emerg. Microbes & Infect.: Effect Of D701N Substitution In PB2 Of EAH1N1 Swine Flu Viruses

J. Virology: A Single Amino Acid Change Alters Transmissability Of EAH1N1 In Guinea Pigs

Emerg. Microbes & Inf.: Pathogenicity & Transmission Of A Swine Influenza A(H6N6) Virus – China

Lest anyone think this is strictly a Chinese problem, we’ve also spent considerable time looking at the evolution and emergence of North American, European, and South American swine flu viruses as well.  Regions not mentioned are likely to have little or no surveillance and reporting.

I&ORV: Triple-Reassortant Novel H3 Virus of Human/Swine Origin Established In Danish Pigs

EID Journal: Characterization of a Novel Human Influenza A(H1N2) Virus Variant, Brazil

MMWR: Investigation Into H3N2v Outbreak In Ohio & Michigan – Summer 2016

J. Virol: Novel Reassortant Human-like H3N2 & H3N1 Influenza A Viruses In Pigs

And as we discussed yesterday (see PNAS: Broad Receptor Engagement of PDCoV May Potentiate Its Cross-Species Transmissibility), influenza isn’t the only zoonotic disease concern when it comes to pigs.

Nature’s Scientific Reports carries two related studies (albeit by different authors) on influenza in China’s commercial swine production industry.  The first, which is linked below with a short quote, is an article on surveillance.

Prospective surveillance for influenza. virus in Chinese swine farms

Benjamin D. Anderson, Mai-Juan Ma, Guo-Lin Wang, Zhen-Qiang Bi, Bing Lu, Xian-Jun Wang, Chuang-Xin Wang, Shan-Hui Chen, Yan-Hua Qian, Shao-Xia Song, Min Li, Teng Zhao, Meng-Na Wu, Laura K. Borkenhagen, Wu-Chun Cao & Gregory C. Gray

Excerpt

Overall, these first year data suggest that IAV is quite ubiquitous in the swine production environment and demonstrate an association between the different types of environmental sampling used. Given the mounting evidence that some of these viruses freely move between pigs and swine workers, and that mixing of these viruses can yield progeny viruses with pandemic potential, it seems imperative that routine surveillance for novel IAVs be conducted in commercial swine farms.

The second study (below) tells us a lot more about the growing number of novel triple reassortant swine-origin flu viruses circulating in Guangxi, China over the past few years.

Out of 15 isolates selected, researchers found 10 novel reassortant viruses (see chart below), all hybrids of EAH1N1, H1N1/09, CS H1N1, and HL H3N2, and all reportedly replicated in mice without adaptation, with several proving to be lethal. 

https://www.nature.com/articles/s41426-018-0088-z

Being a snapshot in time, and taken from a single Chinese province (ranked 11th in population), this likely only reveals a fraction of the viral diversity on Chinese pig farms.

I’ve only posted the link, abstract, and as short excerpt from the discussion. Follow the link below to read it in its entirety.

Novel triple-reassortant influenza viruses in pigs, Guangxi, China 

Ping He, Guojun Wang, Yanning Mo, Qingxiong Yu, Xiong Xiao, Wenjuan Yang,
Weifeng Zhao, Xuan Guo, Qiong Chen, Jianqiao He, Mingli Liang, Jian Zhu, Yangbao Ding, Zuzhang Wei, Kang Ouyang, Fang Liu, Hui Jian, Weijian Huang,
Adolfo García-Sastre & Ying Chen

Emerging Microbes & Infections volume 7, Article number: 85 (2018)
doi:10.1038/s41426-018-0088-z


Published:16 May 2018

Abstract

Considered a “mixing vessel” for influenza viruses, pigs can give rise to new influenza virus reassortants that can threaten humans. During our surveillance of pigs in Guangxi, China from 2013 to 2015, we isolated 11 H1N1 and three H3N2 influenza A viruses of swine origin (IAVs-S). 

Out of the 14, we detected ten novel triple-reassortant viruses, which contained surface genes (hemagglutinin and neuraminidase) from Eurasian avian-like (EA) H1N1 or seasonal human-like H3N2, matrix (M) genes from H1N1/2009 pandemic or EA H1N1, nonstructural (NS) genes from classical swine, and the remaining genes from H1N1/2009 pandemic. 

Mouse studies indicate that these IAVs-S replicate efficiently without prior adaptation, with some isolates demonstrating lethality. Notably, the reassortant EA H1N1 viruses with EA-like M gene have been reported in human infections. Further investigations will help to assess the potential risk of these novel triple-reassortant viruses to humans.

       (SNIP)

Currently, influenza A H1N1 and H3N2 viruses are the circulating seasonal influenza A viruses subtypes in human. The H1N1/2009 pandemic became the current seasonal H1N1 virus.

Our EA H1N1 HAs share < 73.7 and 78.1% similarity with the H1N1/2009 pandemic vaccine strain (A/Michigan/45/2015 H1N1), at nucleotide level and amino acid level, respectively. Our H3N2 IAVs-S share < 94.1 and 91.5% similarity with the H3N2 vaccine strain (A/Hong Kong/4801/2014 H3N2), at nucleotide level and amino acid level, respectively.

Studies have reported that seasonal trivalent inactivated influenza vaccine induce poor cross-reactive antibodies to EA H1N1 virus23 and does not protect against swine H3N257. Importantly, according to the risk assessment tool, which is developed by the Centers for Disease Control and Prevention in the United States to evaluate the pandemic potential of different influenza strains58, we found that the EA H1N1 and swine H3N2 viruses are among the animal viruses with the highest risk score in Yang’s analysis26. Besides, at least one human infection with a similar reassortant IAV-S has been reported22.

We suggest that intensive surveillance of IAV-S and of swine-to-human infections with the IAV-S described in our study should be a priority for future research.

(Continue . . . .)

Human T-Lymphotropic Virus type 1 (HTLV-1): a primer

What is HTLV-1?

HTLV-1 is a human delta retrovirus assigned to the genus Deltaretrovirus, species Primate T-lymphotropic virus 1 [5]. It was first described in 1980.[10]

ViralZone:www.expasy.org/viralzone,
SIB Swiss Institute of Bioinformatics [6]

Soon thereafter Japanese researchers identified endemic virus, especially in southwestern Japan.[8,9]

These viruses infect a cell and make new DNA from their RNA genetic blueprint using an enzyme called reverse transcriptase.[7] This DNA then acts as a blueprint to manufacture more RNA and then viral proteins. The DNA form inserts into a random site in the host cell genome.[19] This form of HTLV-1 is called the provirus. The order of making RNA first then DNA is the reverse (retro) of the usual ‘direction’ of protein manufacture in human cells which is from DNA to RNA to protein.

HTLV-1 infects T and B lymphocytes, monocytes, endothelial cells, and fibroblasts, using a common molecular, ubiquitous cell surface molecule, the glucose transporter 1, as its receptor.[12]

HTLV-1 is established mostly in resource-limited regions of the world, infecting an estimated 10-20 million people.[9] Australia hosts the distinct HTLV-1c strain although little is known about its distribution.[1,17] It is predicted that HTLV-1c arrived and then divided into at least 2 further distinct groups (clades) around 3,000-9,000 years ago.[17,18]

In Australia, HTLV-1 infection occurs in the middle of the country (‘central Australia’ mostly reported in the Northern Territory but also Western Australia and South Australia) and antibodies in sera collected in 1956 from Aboriginal Australians in Cape York, Queensland.[20] In some communities, greater than 40% of Aboriginal Australian adults are HTLV-1 infected.[13]

An HTLV-1 timeline. Some discoveries of interest are shown. Click to enlarge.

What does HTLV-1 do?

Infection is generally without symptoms. In 3-5% of those infected develop a highly malignant T-cell neoplasm known as adult T-cell leukaemia/lymphoma (ATLL).[11] This can take decades to develop. There is an estimated 23.6 ATLL cases /100,000 population among Australian adult HTLV-1 carriers.[16]

Infection can also result in HTLV-1-associated-myeIopathy/tropical-spastic-paraparesis (HAM/TSP) and other inflammatory diseases involving the lungs, central nervous system and eyes.[1,10]

Crusted scabies has also been described as a marker for HTLV-1 infection.[2,3]

Bronchiectasis is the most common evidence of HTLV-1 infection among Aboriginal Australians.[1] 

How is HTLV-1 transmitted?

Epidemiological aspects and world distribution of HTLV-1 infection. Gessain & Cassar 2012. Front. Microbiol., 15 November 2012  [8]

The virus can be passed to a susceptible new host via prolonged breastfeeding, sexual transmission ( 4X more frequently male to female[9]),  via HTLV-1-contaminated blood or blood-product transfusion or intravenous drug use.[8]

Japan successfully deployed a program to reduce transmission methods to reduce mother-to-child-transmission.[14]

How do we test for HTLV-1?

Detecting the presence of antibody to viral proteins as a result of infection is a widely used and relatively inexpensive method that fits into the workflow of the modern serology laboratory. Specificity issues were an early and ongoing issue.[8]

The detection of proviral DNA using PCR methods is a sensitive way to identify infected blood cells. Enhanced methods can quantify how much provirus is present which is related to disease progression. A typical healthy infected person may have proviral DNA in 0.1-1% of peripheral blood cells.[10] Virus levels are generally stable but a rise has been associated with the development of HAM/TSP and proviral load is higher in bronchiectasis.[10,15] 

References…

  1. Human T-Lymphotropic Virus type 1c subtype proviral loads, chronic lung disease and survival in a prospective cohort of Indigenous Australians.
    http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0006281
  2. Crusted scabies: a clinical marker of human T-lymphotropic virus type 1 infection in central Australia.
    https://www.mja.com.au/journal/2014/200/11/crusted-scabies-clinical-marker-human-t-lymphotropic-virus-type-1-infection
  3. HTLV-I and scabies in Australian Aborigines
    https://www.thelancet.com/journals/lancet/article/PII0140-6736(93)91186-P/abstract
  4. Human T-lymphotropic virus 1: recent knowledge about an ancient infection
  5. https://talk.ictvonline.org/ictv-reports/ictv_9th_report/reverse-transcribing-dna-and-rna-viruses-2011/w/rt_viruses/161/retroviridae
  6. https://viralzone.expasy.org/59
  7. Retrovirus
    https://www.britannica.com/science/retrovirus
  8. Epidemiological aspects and world distribution of HTLV-1 infection
    https://www.frontiersin.org/articles/10.3389/fmicb.2012.00388/full
  9. HTLV-1 infections
    http://jcp.bmj.com/content/53/8/581
  10. Detection and isolation of type c retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC350514/
  11. HTLV-1 Infection and Adult T-Cell Leukemia/Lymphoma—A Tale of Two Proteins: Tax and HBZ
    http://www.mdpi.com/1999-4915/8/6/161
  12. The Ubiquitous Glucose Transporter GLUT-1 Is a Receptor for HTLV
    https://doi.org/10.1016/S0092-8674(03)00881-X
  13. The prevalence and clinical associations of HTLV-1 infection in a remote Indigenous community
    https://www.mja.com.au/journal/2016/205/7/prevalence-and-clinical-associations-htlv-1-infection-remote-indigenous
  14. Establishment of the milk-borne transmission as a key factor for the peculiar endemicity of human T-lymphotropic virus type 1 (HTLV-1): the ATL Prevention Program Nagasaki
    https://www.jstage.jst.go.jp/article/pjab/87/4/87_4_152/_article
  15. Higher Human T-Lymphotropic Virus Type 1 Subtype C Proviral Loads Are Associated With
    Bronchiectasis in Indigenous Australians: Results of a Case-Control Study
    https://academic.oup.com/ofid/article-lookup/doi/10.1093/ofid/ofu023
  16. Variant Human T-cell Lymphotropic Virus Type 1c and Adult T-cell Leukemia, Australia
    https://wwwnc.cdc.gov/eid/article/19/10/13-0105_article
  17. Human T-Cell Lymphotropic Virus Type 1 Subtype C Molecular Variants among Indigenous Australians: New Insights into the Molecular Epidemiology of HTLV-1 in Australo-Melanesia
    http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0002418
  18. Detailed phylogenetic analysis of primate T-lymphotropic virus type 1 (PTLV-1) sequences from orangutans (Pongo pygmaeus) reveals new insights into the evolutionary history of PTLV-1 in Asia
    https://www.sciencedirect.com/science/article/pii/S1567134816302180
  19. Nonspecific integration of the HTLV provirus genome into adult T-cell leukaemia cells.
    https://www.ncbi.nlm.nih.gov/pubmed/6328324
  20. Antibodies to HTLV‐I in populations of the southwestern Pacific
    https://ift.tt/2GqBKQG

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Ebola virus: wild and domestic animals, plants and insects…

IMPORTED POST*

Initial Ebola virus (EBOV) infection of humans is a rare zoonotic spillover event. 

Hypsignathus monstrosusEpomops franqueti and Myonycteris torquatebats, all fruit-eating megabats of the family Pteropodidae, are considered to be important reservoir hosts, yet they do not show signs of disease.[1] 

While a great deal remains unknown about the identity and spectrum of natural ebolavirus hosts,[1] zoonoses appear to co-occur with bat pregnancy.[2]

Animals that have died from ebolavirus infections include:[3,4]

  • Duiker (Cephalophus sp.; an antelope) 
  • Gorilla (Gorilla gorilla
  • Chimpanzee (Pan troglodytes)

Living animals found to harbour ebolavirus RNA include:[1,4,23]

  • Cynomolgus macaque monkey (Macaca fascicularis; RESTV) 
  • Franquet’s epauletted fruit bat (Epomops franqueti; EBOV) 
  • Hammer-headed bat (Hypsignathus monstrosus; EBOV) 
  • Little collared fruit bat (Myonycteris torquata; EBOV)

Those animals with only antibodies to EBOV in the absence of infectious virus, suggesting past exposure include:[5,6]

  • Domestic dogs (Canis lupus familiaris
  • Peter’s lesser epauletted fruit bat (Micropterus pusillus; fruit-eating) 
  • Angolan free-tailed bat (Mops condylurus; insect-eating) 
  • Giant roundleaf bat (Hipposideros gigas; insect-eating) 
  • Egyptian fruit bat (Myion; fruit-eating) 
  • Geoffrey’s rosette (Rousettus amplexicaudatus; a bat species; fruit-eating) 
  • Lord Derby’s scaly-tailed squirrel (Anomalurus derbianus)

Porcupines (Hystrix cristata) have been implicated as a source for human EBOV exposure but virus-positive animals have not been documented.[4]

Between nine and 25% of 337 domestic dogs from various towns and villages in Gabon during an EBOV outbreak in 2001-2002 were identified as possible hosts for EBOV when found to be seropositive.[7,8] It was not known when they became seropositive nor has it been experimentally determined that dogs are able to host an active EBOV infection.[9,10] Dogs were observed in contact with suspected virus-laden fluids and with other animals during the Gabon outbreak but seropositive dog specimens did not contain EBOV antigen or viral RNA. Three specimens from these seropositive dogs did not yield infectious virus in cell culture either and thus there remains no documented evidence for a canine source of human EBOV infection. In 2014, two dogs owned by human cases of EBOV/Mak in Spain (euthanized without testing [11]) and the United States of America (tested negative for EBOV[12,13]) did not exhibit any signs of disease.

Domestic pigs have been found to be a natural host for the Reston ebolavirus[9,14] and antibodies to EBOV have also been found in guinea pigs, an animal that can also be experimentally infected.[15] Domestic dogs and guinea pigs appear to become infected without symptoms.[6,7] Horses, mice, guinea pigs and goats have been experimentally inoculated with EBOV to produce antisera or test therapeutic preparations.[16,17]

Pigs experimentally infected with a member of the Zaire ebolavirus become symptomatic.[8] NHP, guinea pigs and mice have been used to examine aspects of disease progression and exhibit various degrees of disease when experimentally infected.[18,19] 

On a few occasions in one study into possible hosts, a low viral load of EBOV could be sporadically recovered after inoculation of a snake (up to 11 days post inoculation), a mouse (up to nine days later) and a spider (21 days later) but the authors of this study concluded that these results could have represented residual inoculum.[21]

Plants, arthropods, cows, cats and sheep have not been found to naturally carry or host ebolavirus infection but only small numbers of some species have been examined.[3,20-22]

References…

  1. Leroy EM, Kumulungui B, Pourrut X, et al. Fruit bats as reservoirs of Ebola virus. Nature 2005;438:575-6. 
  2. Plowright RK, Eby P, Hudson PJ, et al. Ecological dynamics of emerging bat virus spillover. Proc Biol Sci 2015;282:20142124. 
  3. Olson SH, Reed P, Cameron KN, et al. Dead or alive: animal sampling during Ebola hemorrhagic fever outbreaks in humans. Emerg Health Threats J 2012;5 
  4. 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. 
  5. Marsh GA, Haining J, Robinson R, et al. Ebola Reston virus infection of pigs: clinical significance and transmission potential. J Infect Dis 2011;204 Suppl 3:S804-9
  6. Gonzalez JP, Herbreteau V, Morvan J, Leroy EM. Ebola virus circulation in Africa: a balance between clinical expression and epidemiological silence. Bull Soc Pathol Exot 2005;98:210-7. 
  7. Allela L, Boury O, Pouillot R, et al. Ebola virus antibody prevalence in dogs and human risk. Emerg Infect Dis 2005;11:385-90. 
  8. Weingartl HM, Nfon C, Kobinger G. Review of Ebola virus infections in domestic animals. Dev Biol (Basel) 2013;135:211-8. 
  9. Stansfield SK, Scribner CL, Kaminski RM, Cairns T, McCormick JB, Johnson KM. Antibody to Ebola virus in guinea pigs: Tandala, Zaire. J Infect Dis 1982;146:483-6. 
  10. Connolly BM, Steele KE, Davis KJ, et al. Pathogenesis of experimental Ebola virus infection in guinea pigs. J Infect Dis 1999;179 Suppl 1:S203-17
  11. Why Dallas Won’t Kill The Dog Of The Texas Nurse With Ebola. Business Insider, 2014. (Accessed 27/4/2015, at http://www.businessinsider.com.au/what-will-happen-to-dallas-nurses-dog-2014-10 ) 
  12. Starting today, Dallas Animal Services will begin testing Nina Pham’s year-old dog Bentley for Ebola. The Dallas Morning News, 2014. (Accessed 17/4/2015, at http://thescoopblog.dallasnews.com/2014/10/starting-today-dallas-animal-services-will-begin-testing-nina-phams-year-old-dog-bentley-for-ebola.html/.) 
  13. EBOLAVIRUS, ANIMAL RESERVOIR (05): USA, DOG, NOT. 2014. (Accessed 01/05/2015, at http://promedmail.org/direct.php?id=20141026.2901733 ) 
  14. Barrette RW, Metwally SA, Rowland JM, et al. Discovery of swine as a host for the Reston ebolavirus. Science 2009;325:204-6. 
  15. Rouquet P, Froment JM, Bermejo M, et al. Wild animal mortality monitoring and human Ebola outbreaks, Gabon and Republic of Congo, 2001-2003. Emerg Infect Dis 2005;11:283-90. 
  16. Kudoyarova-Zubavichene NM, Sergeyev NN, Chepurnov AA, Netesov SV. Preparation and use of hyperimmune serum for prophylaxis and therapy of Ebola virus infections. J Infect Dis 1999;179 Suppl 1:S218-23
  17. Bray M, Davis K, Geisbert T, Schmaljohn C, Huggins J. A mouse model for evaluation of prophylaxis and therapy of Ebola hemorrhagic fever. J Infect Dis 1998;178:651-61. 
  18. Ebihara H, Takada A, Kobasa D, et al. Molecular determinants of Ebola virus virulence in mice. PLoS Pathog 2006;2:e73. 
  19. Geisbert TW, Young HA, Jahrling PB, Davis KJ, Kagan E, Hensley LE. Mechanisms underlying coagulation abnormalities in ebola hemorrhagic fever: overexpression of tissue factor in primate monocytes/macrophages is a key event. J Infect Dis 2003;188:1618-29. 
  20. Turell MJ, Bressler DS, Rossi CA. Short report: lack of virus replication in arthropods after intrathoracic inoculation of Ebola Reston virus. Am J Trop Med Hyg 1996;55:89-90. 
  21. Swanepoel R, Leman PA, Burt FJ, et al. Experimental inoculation of plants and animals with Ebola virus. Emerg Infect Dis 1996;2:321-5. 
  22. Ebola haemorrhagic fever in Sudan, 1976. Report of a WHO/International Study Team. Bull World Health Organ 1978;56:247-70. 
  23. Miranda ME, Ksiazek TG, Retuya TJ, Khan AS, Sanchez A, Fulhorst CF, Rollin PE, Calaor AB, Manalo DL, Roces MC, Dayrit MM, Peters CJ. Epidemiology of Ebola (subtype Reston) virus in the Philippines. J Infect Dis. 1999 Feb;179 Suppl 1:S115-9.
  • *IMPORTED POST
    This post from 03JUL2015 was posted over on my old blog platform virologydownunder.blogspot.com.au and has now been moved to here and lightly updated. 

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