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PostPosted: Sun Aug 31, 2014 8:25 am 
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Joined: Mon Aug 04, 2014 5:45 pm
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Location: Lisbon, Portugal
Sometimes it pays to be stubborn as a mule.

http://t.co/9HDm1qS3jO

http://www.ncbi.nlm.nih.gov/pmc/article ... 2-0107.pdf


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PostPosted: Sun Aug 31, 2014 10:18 am 
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Joined: Wed Aug 19, 2009 10:42 am
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Location: Pittsburgh, PA USA
morning wrote:

Ebola, like virtually all infectious agents have a dose / response effect. Lower initial doses will have a longer incubation time and may produce sub-clinical infections. That is a given.

Similarly, the level of viral shedding will also be dependent on the host and in most cases asymptomatic cases will shed little virus.

Ebola is like most infectious agents.

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PostPosted: Sun Aug 31, 2014 11:25 am 
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niman wrote:
morning wrote:

Ebola, like virtually all infectious agents have a dose / response effect. Lower initial doses will have a longer incubation time and may produce sub-clinical infections. That is a given.

Similarly, the level of viral shedding will also be dependent on the host and in most cases asymptomatic cases will shed little virus.

Ebola is like most infectious agents.

This paper details some particulars on Ebola asymptomatic/mild cases:
.
Quote:
The Lancet
Human asymptomatic Ebola infection and strong inflammatory response


Dr EM Leroy DVM , S Baize PhD , VE Volchkov PhD , SP Fisher-Hoch MD , M-C Georges-Courbot MD ,
J Lansoud-Soukate PhD , M Capron PhD , P Debré MD , JB McCormick , AJ Georges MD

Summary

Background
Ebola virus is one of the most virulent pathogens, killing a very high proportion of patients within 5—7 days. Two outbreaks of fulminating haemorrhagic fever occurred in northern Gabon in 1996, with a 70% case-fatality rate. During both outbreaks we identified some individuals in direct contact with sick patients who never developed symptoms. We aimed to determine whether these individuals were indeed infected with Ebola virus, and how they maintained asymptomatic status.

MethodsBlood was collected from 24 close contacts of symptomatic patients. These asymptomatic individuals were sampled 2, 3, or 4 times during a 1-month period after the first exposure to symptomatic patients. Serum samples were analysed for the presence of Ebola antigens, virus-specific IgM and IgG (by ELISA and western blot), and different cytokines and chemokines. RNA was extracted from peripheral blood mononuclear cells, and reverse-transcriptase-PCR assays were done to amplify RNA of Ebola virus. PCR products were then sequenced.

Findings
11 of 24 asymptomatic individuals developed both IgM and IgG responses to Ebola antigens, indicating viral infection. Western-blot analysis showed that IgG responses were directed to nucleoprotein and viral protein of 40 kDa. The glycoprotein and viral protein of 24 kDa genes showed no nucleotide differences between symptomatic and asymptomatic individuals. Asymptomatic individuals had a strong inflammatory response characterised by high circulating concentrations of cytokines and chemokines.

Interpretation
This study showed that asymptomatic, replicative Ebola infection can and does occur in human beings. The lack of genetic differences between symptomatic and asymptomatic individuals suggest that asymptomatic Ebola infection did not result from viral mutations. Elucidation of the factors related to the genesis of the strong inflammatory response occurring early during the infectious process in these asymptomatic individuals could increase our understanding of the disease. .

Excerpt:
Quote:
These findings show that some individuals wereinfected with the virus without developing symptoms.
Results from previous outbreaks had only indicated thatsuch an asymptomatic infection was possible.
During the first three outbreaks of Ebola virus in Sudan and Zaire in 1976 and 1979, WHO teams noticed that
individuals had symptoms that ranged in severity, from mild (and probably asymptomatic) to rapidly fatal.16
Moreover, the immunofluorescence showed higher antibody prevalence among asymptomatic family members
who had had physical contact with clinical cases than among the general population who had no contact
with symptomatic patients.17,18 More recently, a cohort of 152 household contacts of convalescents
was studied for up to 21 months during the Kikwit outbreak in Republic Democratic of the Congo.19
Blood samples of only five such individuals were IgM and IgG positive. Although the authors could not
exclude the possibility of false positive (5 [3%] of 152),they suggested that mild cases may occur.

- - -

Reference 17 from paper above features a preliminary statistics on case severity
in the context of the 1976 Zaire epidemic: (2)

Quote:
Finally, a better method for measuring Ebola virus antibodies is needed in order to interpret the
serological findings reported here. That less than 20% of persons gave a history of acute illness
following contact with a fatal case was no surprise. Most of these persons had mild, self-limiting diseases,
these being highly endemic in the area. But if the IFA data are correct, at least 2.5 % of persons in contact
with fatal cases experienced subclinical infection.
In addition, the finding of antibodies in a few individuals in the absence of any known contact with
Ebola virus during the epidemic raises the possibility that the agent is in fact endemic in the Yambuku
area and is occasionally transmitted to man. A definitive answer is essential to further ecological exploration
of what is now a very mysterious agent.

1. The Lancet, 355, 9222, Pages 2210 - 2215, 24 June 2000
http://www.thelancet.com/journals/lance ... 40-6736(00)02405-3/fulltext

2. Bull World Health Organ. 1978; 56(2): 271–293.
Ebola haemorrhagic fever in Zaire, 1976
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2395567/


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