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Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

C

Chicagogal

Well-known member
From "A top scientist worries that Ebola has mutated to become more contagious" (Vox)

http://www.vox.com/2014/10/13/6959087/ebola-outbreak-virus-mutated-airborne

JB: A higher viral load means this Ebola virus can spread faster and further?

PJ: Yes. I have a field team in Monrovia. They are running [tests]. They are telling me that viral loads are coming up very quickly and really high, higher than they are used to seeing. It turns out that in limited studies with the evacuated patients, they continued to express virus in blood and semen. What does that mean? Right now, we just don't know.
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Lots of information in this article which contradicts everything else we've been hearing about Ebola.
I would wonder if the fact that they are using different testing methods with this outbreak is a factor in picking up increased viral loads.

What does this mean? "It would appear there have been multiple introductions [from animals to people]. This is not all human to human transmission. It's coming from animals again and again." That statement contradicts everything previously stated about the outbreak.

He thinks it will "burn out" ?
He thinks it is unlikely to perpetuate in humans?

What?
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

It seems certain that the initial transmission in each of the separate outbreaks has been from an animal reservoir, but if he's implying that any significant transmission since then has been from animals, then I think he's way off base. And such a statement only feeds into the suggestions that it can be spread by rodents, mosquitos and cockroaches, claims that keep showing up on the more extremist blogs.
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Are the bodies and bodily fluids of those who die at home completely protected from rodents? In some parts of the world, rats occasionally bite people (especially children) sleeping on mats or low beds.

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Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

AlaskaDenise said:
Are the bodies and bodily fluids of those who die at home completely protected from rodents? In some parts of the world, rats occasionally bite people (especially children) sleeping on mats or low beds.

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Click to expand...
Yes, but have rodents (or mosquitos et al) been identified as vectors? With as many outbreaks as have occurred now, I would think there would have been some hint of that if they were a significant factor. Not saying they aren't, but I've seen no serious suggestion of it.
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Lizw said:
Yes, but have rodents (or mosquitos et al) been identified as vectors? With as many outbreaks as have occurred now, I would think there would have been some hint of that if they were a significant factor. Not saying they aren't, but I've seen no serious suggestion of it.
Click to expand...

Since most local testing is after-the-fact, it has usually been impossible to ascertain with 100% certainty exactly which non-human species have been carrying ebola in any capacity. One study that did find some is

Identification of Ebola virus sequences present as RNA or DNA in organs of terrestrial small mammals of the Central African Republic.


Abstract


The life cycle of the Ebola (EBO) virus remains enigmatic. We tested for EBO virus in the organs of 242 small mammals captured during ecological studies in the Central African Republic. EBO virus glycoprotein or polymerase gene sequences were detected by reverse transcription PCR in RNA extracts of the organs of seven animals and by PCR in DNA extract of one animal. Neither live virus nor virus antigen was detected in any organ sample. Direct sequencing of amplicons identified the virus as being of the Zaire/Gabon subtype. Virus-like nucleocapsids were observed by electron microscopy in the cytoplasm of the spleen cells of one animal. The animals belonged to two genera of rodents (Muridae; Mus setulosus, Praomys sp1 and P. sp2) and one species of shrew (Soricidae; Sylvisorex ollula). These preliminary results provide evidence that common terrestrial small mammals living in peripheral forest areas have been in contact with the EBO virus and demonstrate the persistence of EBO virus RNA and DNA in the organs of the animals. Our findings should lead to better targeting of research into the life cycle of the EBO virus.


PMID: 10580275

(study was done by the Pasteur Inst.)

-------------------------------------------------------------

Unfortunately, much of the desired ebola study had to wait for another outbreak!.

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Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Bull Soc Pathol Exot. 2000 Jul;93(3):172-5.

[Forest ecosystems and Ebola virus].

[Article in French]

Morvan JM1, Nakoun? E, Deubel V, Colyn M.


Author information

1Laboratoire des arbovirus, Institut Pasteur, Bangui, R?publique Centrafricaine. morvan@intnet.cf


Abstract


Despite data collected since the emergence of the Ebola virus in 1976, its natural transmission cycle and especially the nature of its reservoirs and means of transmission are still an enigma. This means that effective epidemiological surveillance and prevention are difficult to implement. The location of outbreak areas has suggested that the reservoir and the transmission cycle of the Ebola virus are closely linked to the rainforest ecosystem. The fact that outbreaks seldom occur suggests the presence of a rare animal reservoir having few contacts with man. Paradoxically, various serological investigations have shown a high prevalence in human beings, especially in forest areas of the Central African Republic (CAR), with no pathology associated. This would appear to suggest a circulation of both pathogenic and non-pathogenic strains as well as frequent contacts with man. The ecological changes resulting from human activity (agriculture and logging) account for the modification of the fauna (movement of rainforest fauna, introduction of savannah species) and could explain a multiplication of contacts. Likewise, it is interesting to note that the centre of outbreaks has always been in areas bordering on forests (ecotone foreset-savannah in the Democratic Republic of Congo, savannah in Sudan). All these considerations have led us to establish a permanent "watch" in areas bordering on forests in the CAR, involving a multidisciplinary approach to the virological study (strain isolation, molecular biology) of the biodiversity of small terrestrial mammals. The results of a study conducted on 947 small mammals has shown for the first time the presence of the Ebola virus genome in two species of rodents and one species of shrew living in forest border areas. These animals must be considered as intermediary hosts and research should now focus on reservoirs in the ecosystem of forest border areas where contacts with man are likely to be more frequent.


PMID: 11030051

-----------------------------------------

I assume this paper is referring to the same study as the prior on posted.

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Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Perhaps rodents fall into the same category as bats, in that the "gold standard" to define "vector/reservoir" is finding LIVE virus in the animal, which has not yet occured. The dead virus and antibodies don't meet the "gold standard." But, once again... the absence of evidence is not evidence of absence!

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Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

AlaskaDenise said:
Perhaps rodents fall into the same category as bats, in that the "gold standard" to define "vector/reservoir" is finding LIVE virus in the animal, which has not yet occured. The dead virus and antibodies don't meet the "gold standard." But, once again... the absence of evidence is not evidence of absence!

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Click to expand...
That's what I took from the study too, that antibodies and dead virus particles were evidence of exposure, not necessarily of active infection. But there is so much we still don't know.
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Lizw said:
That's what I took from the study too, that antibodies and dead virus particles were evidence of exposure, not necessarily of active infection. But there is so much we still don't know.
Click to expand...

Antibodies without an infection???

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(see post #19 for Emily's explanation of how this can happen!)

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Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Chicagogal said:
Early immune responses accompanying human asymptomatic Ebola infections
Click to expand...

Good paper. Thanks. It does discuss the fact that asymtomatic cases clearly do get infected.

What I found most interesting/alarming was the testing of the asymptomatic cases showed active infections (countered by inflammatory reponse) only a few days after exposure - much earlier than I expected. So there must be a point at which those infected cells transition from simple reproduction within a person to actively shedding/transmission.

Perhaps one of the reasons for the apparent increase in viral loads is that the stress of the overall situation is producing enough cortisol in "exposed" patients that it dampens the immune system to th epoint it cannot minimize the viral load.

From Wikipedia:

Cortisol can weaken the activity of the immune system. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor (IL-2).[18] Cortisol also has a negative-feedback effect on interleukin-1.[19]
Click to expand...

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Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

I think a higher virus load, earlier and less detectable by non-intrusive observation, is the mutation/cjange we should worry about rather than going airborne. If we lose the ability to screen effectively at airports and walk-in clinics, or can no longer assume asymptomatic = non-infectious...
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

AlaskaDenise said:
Antibodies without an infection???

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Click to expand...
Sorry, that wasn't clear. In the same sense that one can tell whether a person has ever been exposed to tuberculosis, for example. Yes, infection clearly has to have been present, but the person's immune system overcame it, and only the specific antigen still present in the blood indicates that the infectious organism was ever there. I see that as different from asymptomatic, but I could be mistaken :)
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

AlaskaDenise said:
Perhaps rodents fall into the same category as bats, in that the "gold standard" to define "vector/reservoir" is finding LIVE virus in the animal, which has not yet occured. The dead virus and antibodies don't meet the "gold standard." But, once again... the absence of evidence is not evidence of absence!

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Click to expand...

"The sudden outbreak of bat die-offs in Spain that precipitated this study destroyed several bat colonies in less than 10 days."

This article shows that bats sometimes are not at all a reservoir or vector for filovirus but -at least until now- definitely the endstation.

Article: http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002304
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Interesting - death by LLOV - "...genetically distinct from other marburgviruses and ebolaviruses and is the first filovirus detected in Europe that was not imported from an endemic area in Africa."

So filoviruses have many different "strains". How does their mutation to a new strain compare to other pathogens & is it similar in diversity to all the many permutations of influenza, i.e., all the H & N combinations?

The article did not make mention of the ebola in Indonesian orangutangs - but the paper was from 2011.

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Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Lizw said:
Sorry, that wasn't clear. In the same sense that one can tell whether a person has ever been exposed to tuberculosis, for example. Yes, infection clearly has to have been present, but the person's immune system overcame it, and only the specific antigen still present in the blood indicates that the infectious organism was ever there. I see that as different from asymptomatic, but I could be mistaken :)
Click to expand...

Antigenic stimulation can produce antibodies without causing true infection. Think of the killed virus vaccines like whooping cough. During a primate ebola outbreak, there is a lot of environmental contamination. The live virus lives only a few hours to days at most in its endemic environment after drying. However the particles are still there to stimulate the immune system.

I think live ebola virus similar to the human strain has been found in bats, just not during a human outbreak.

The viral sequences that are found in genomes are not equivalent to virus particles found in blood, saliva, etc found by PCR that indicate infection by live virus.

The genome incorporated sequences are part of a species' evolutionary history, thought to be just the "junk in our trunk" until relatively recently.

Humans have ebola sequences in their genome, so do guinea pigs but they are resistant to ebola infection unless the virus is adapted to that species via 'serial passage' in a laboratory. Ancient infections incorporating the virus into the host's genome seem to confer resistance - why did this change for humans in the late 1970's, which is about the same time HIV was gaining traction in Africa - we don't know for sure, but unintentional serial passage was going on through the unsafe use of injections.

Unexpected Inheritance: Multiple Integrations of Ancient Bornavirus and Ebolavirus/Marburgvirus Sequences in Vertebrate Genomes
 
Re: Peter Jahrling: virus load may be higher in these patients [today] than what we have seen before

Thanks Emily. Now I understand antigenic stimulation - that a person can have antibodies without an infection -just like I have a positive TB test from a known exposure to someone with TB, but I never had TB (that I know of).

Once again, it seem to come down to the robustness of an individual's immune system!

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