Game Warden

FIV: feline immunodeficiency virus

60 posts in this topic

Following on from the discussion centred around FIV which arose in the LIONAID, Ask some questions of lionaid topic, I have copied across relevant posts in a chronological order so we can continue this interesting discussion with Dr. Kat separately. (Should I have missed any posts from the original topic, let me know: also if everyone is in agreement, I shall delete the original posts in the Lion Aid topic.)

 

Please feel free to suggest a more appropriate title for the topic if need be.

 

Matt

Share this post


Link to post
Share on other sites
In answer to your link:-

 

A lion lentivirus related to feline immunodeficiency virus: epidemiologic and phylogenetic aspects.

 

To date, there is no clear evidence of FIV-Ple-associated pathology, raising the possibility of a historic genetic accommodation of the lion lentivirus and its host leading to a coevolved host-parasite symbiosis (or commensalism) in the population similar to that hypothesized for endemic simian immunodeficiency virus without pathology in free-ranging African monkey species

See Link Here¬

 

 

Thanks again

Zimbo_Mukiwa - Jul 27 2010, 11:37 PM

Share this post


Link to post
Share on other sites
Zimbo:

 

The article you quote on lion lentivirus is old and reflects the thinking at that time. Things have moved on from there. Even SIV among among primates is now showing to have negative effects on their immune systems. The very considerable literature on the consequences of FIV infection among domestic cats (laboratory animals) is the best model we have for FIV infection among lions. More recent papers that actually examine the CD4/CD8 ratios among lions show many parallels with the domestic cat studies - i.e. over time, the immune system is eroded among infected lions. There is no way that a fast-evolving lentivirus would become a "commensal" with a host as there is no selection for less pathogenic strains. The problem with looking at CD4/CD8 ratios among infected lions is that the approach necessarily needs to be "coarse grained" - as there is no information as to when the lion was infected. Therefore, lions are grouped by age when they are sampled, and older lions all clearly show loss of immune competence.

 

Worrying aspects of the domestic cat studies indicate that infected queens (female domestic cats) have smaller litters, more stillbirths, and less survivorship among kittens than their negative counterparts. There is thus a good possibility that infected lions could show similar trends in terms of reproduction.

 

FIV among lions will necessitate careful and long-term studies of lion cohorts in the wild, and this has very limited possibility of occurring, so at present we must be satisfied with drawing parallels from domestic cat studies coupled with snapshot analyses among lion populations.

Lion Aid - Jul 28 2010, 12:02 PM

Share this post


Link to post
Share on other sites
Just to give an indication of how the debate surrounding the significance of FIV is, to put it delicately so as to not cause offence, unresolved here is an exert taken from an abstract from a paper which includes Craig Packer amongst its co-authors.

 

"Results from FIV-infected lions and pumas parallel human and Asian monkey CD4+ diminution in HIV and SIV infection, respectively, and suggest there may be unrecognised immunological consequences of FIV infection in these two species of large cats."

 

The paper: T-LYMPHOCYTE PROFILES IN FIV-INFECTED WILD LIONS AND PUMAS REVEAL CD4 DEPLETION can be found at:

 

http://www.jwildlifedis.org/cgi/content/full/42/2/234

 

Packer and colleagues had published prior to this paper studies on distemper outbreaks in the Serengeti and had been dismissive of the disease burden related to FIV infection.

 

But then, that's the wonderful thing about science, we can revise our opinions based on the testing and revision of evidence and not be stuck in a dogmatic rut!!

 

p.s. the paper concludes with the following advice:

 

"it would be prudent to discourage the translocation of seropositive animals into naive populations."

 

Furthermore, from Roelke et al 2009

 

"We conclude that over time FIVple infections in free-ranging lions can lead to adverse clinical, immunological, and pathological outcomes in some individuals that parallel sequelae caused by lentivirus infection in humans (HIV), Asian macaques (SIV) and domestic cats (FIVfca)."

 

Paper can be found here:

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771374/

John Peter - Jul 28 2010, 01:03 PM

Share this post


Link to post
Share on other sites
Matt:

 

FIV is a "political" disease. I cannot go into much detail here, but the "research" done on FIVple by one group in particular was motivated to gain funding from HIV programs - what was required was a species infected with an immunodeficiency virus that showed no adverse effects. Too bad it all went wrong in the end when the facts had to be admitted - the erosive effects of FIV on lion immune systems was known well before the latest papers were published - Suzanne Kennedy-Stoskopf published on CD4/CD8 ratios among infected lions long ago, and Alessandro Poli performed an extensive autopsy on a lion that was infected with FIVple to show that many of the identical pathologies among domestic cats infected with FIVpca were also present in this lion. This information was not mentioned in the headlong rush to proclaim FIVple innocuous - a rush that has now hit a brick wall.

 

Perhaps it would be good to have a discussion on FIV, call it FIVgate.

Lion Aid - Jul 29 2010, 01:24 PM

Share this post


Link to post
Share on other sites
Just had a read of Poli's paper. Interesting stuff. It would have been particularly interesting to have had some idea of where/how the lion was infected.

 

I can see how this issue of FIV could have implications for those seeking to implement long term conservation strategies for the lion as most papers published recently on the subject suggest infection rates of up to 90% in wild populations. Given the increased pressure on these populations from habitat loss and the possible increased exposure to other pathogens I assume the presence FIV in shrinking populations could be more significant than previously thought?

 

In relation to Dr Kat's work with ALERT I seem to recall reading that he was utilising the lions at Antelope Park and other sites run under the Lion Encounter umbrella to study the progression of FIV. Is there any signs of anything interesting emerging from this collaboration? I appreciate that it may not be possible to give any insights at this stage or particular forum.

 

However, it would be interesting to know how some of these captive bred lions (well, doesn't have to be specifically these lions but in general) are FIV positive while others are negative? Are they from the same breeding pool or drawn from different origins? Does the transmission of FIV in lions follow a similar pattern to that of HIV in humans whereby infected mothers do not necessarily pass on infection if intervention takes place?

John Peter - Jul 29 2010, 04:28 PM

Share this post


Link to post
Share on other sites
John peter:

 

You are apparently a born diplomat. I find it quite interesting how the likes of Steve O’Brien, Craig Packer, etc can for years deny any influence of FIVple on lions, and then do a complete U-turn without any reference to their many former papers and previous statements. You put it delicately when you say “we can revise our opinions based on the testing and revision of evidence and not be stuck in a dogmatic rut!!” In fact, the dogma about FIVple ruled for many years and dissuaded many from taking an alternative view based on the very extensive domestic cat studies as well as lion studies. They knew that their grant proposals would be reviewed by those stuck in the rut, and therefore rejected. Suzanne Kennedy-Stoskopf and Marta Bull did some very good work on CD4/CD8 ratios of free-ranging lions in Kruger and clearly showed an effect of the infection, but were dismissed. Poli was never referred to. Neils Pedersen, who discovered the FIV virus, urged me to keep working in this area, and Brian Willett at Glasgow also was very encouraging. But to apply for a research grant under the “old regime” was about as useful as trying to breathe underwater.

 

Now that things have relaxed a bit, I would expect more balanced research to be done on FIVple, including the use of cohorts of lions with known natural infection dates that can be directly compared to those not infected. The problem is that you are dealing with a lentivirus, and infected individuals might take years to develop consequential symptoms.

 

You seem to be well informed about FIVple, and will have noticed that all the “rut” papers were based on two main premises. 1. FIVple is characterized by a number of different strains with some considerable genetic divergence. This led researchers to propose that the virus had been present among lion populations for very many thousands of years. 2. Lion populations in the Serengeti, Kruger, Botswana were infected to a very high degree, but they were not apparently dying off in great numbers (though “wasting” was very apparent among older lions in Bots – 10-12 years old). Put 1. and 2. together, and throw in some fanciful suppositions about virus-host interactions, and there you have the formula – lions are immune. This came about because of a lack of understanding about how lentiviruses operate (despite all the available information from domestic cats and humans with HIV), and a lack of understanding about viral evolution. Yes, with some viruses an attenuated strain might be selected for because if the host dies before being able to spread the virus, then that viral strain is selected against.

 

But look at rabies. That virus has been around for many thousands of years as well, and that virus has not become less deadly. There are very many strains of rabies – domestic dog rabies is essentially European fox rabies that spread all over the world by introduction of domestic dogs. However, there are many strains of that virus, including endemic strains in Nigeria (host unknown), South Africa (yellow mongooses have their own strain), Botswana (yellow mongoose but different), and China (host unknown) at least. Those have nothing to do with domestic dogs – and were present long before domestic dogs ever came to South Africa for example. And then there are all the various bat rabies viruses that diverged long ago from fox/dog/mongoose virus. But if you get infected by any of those it is goodnight.

 

So basically, FIVple research was based on bad science, specific agendas that “needed” lions to be resistant, and, shall we say, a calculated ignorance of lentiviral evolution and modi operandi.

 

http://www.ncbi.nlm.nih.gov/pubmed/14596469

 

http://www.jwildlifedis.org/cgi/reprint/31/1/70.pdf

Lion Aid - Jul 29 2010, 04:53 PM

Share this post


Link to post
Share on other sites
John peter:

 

At Antelope park, there was a natural infection of a number of females by a male brought into the program. Whether captive or wild, I always urge testing for a panel of diseases. All these FIV+ lions have now been quarantined. FIV testing these days can be done very simply by using a commercial test kit. They are quick and easy to use, and since they are based on the presence of antibodies to "core proteins" (slow evolving) as opposed to "envelope proteins" (fast evolving) of the virus, a positive result is very reliable. Comparing this commercial test kit to specific tests carried out in laboratories with blood samples from Botswana, there were no false positives and no false negatives. However, the test kits are made by very many manufacturers, and I found IDEXX the most reliable. Laboratory confirmation of these initial results, however, should always be done in cases where extreme accuracy is required for lion populations.

Lion Aid - Jul 29 2010, 05:08 PM

Share this post


Link to post
Share on other sites
John peter:

 

FIV can be communicated by bite, by semen, by milk, transplacentally, by cubs/kittens ingesting blood during the birth process, etc. I would also imagine that contact between saliva and blood in terms of one lion licking/cleaning another one with a wound would also constitute exposure? A very limited survey of cubs born to positive females indicates that about 50% are born positive, roughly similar to domestic cat data. In Botswana I found that young negative females seroconverted soon after being mated.

 

I you want to open up a whole new level of complication, ask me about FIV and hormones such as estrogen and progesterone....???

 

An interesting article that gives insight into the eventual dogma:

 

http://discovermagazine.com/1995/jul/thekillercatviru533

Lion Aid - Jul 29 2010, 05:20 PM

Share this post


Link to post
Share on other sites
Lion Aid:

 

Thanks for that background on the development of the FIV research paradigm. I suspected as much as though I have only a lay persons knowledge of virology I did find some of those papers dismissing the pathogenicity of FIV odd particularly in how they make casual reference to SIV and HIV without acknowledging the huge variation in how different strains varied in terms of time elapsed before disease became apparent.

 

It also seems disingenuous to state in a paper, well here we have lions with multiple viral and bacterial infections but their simultaneous infection with FIV is just a coincidence and not relevant, and not elaborate on why or how.

 

Thanks also for the info from the Antelope Park studies I was interested when I heard about these as it seems to offer a good opportunity to have at least two groups to study over a reasonable time scale.

 

I'm no diplomat but I have studied conservation from a social science perspective so that perhaps is an influence!!!

 

Once again thanks very much for the information!

John Peter - Jul 29 2010, 05:43 PM

Share this post


Link to post
Share on other sites
LionAid:

 

One other thing, do you have any insights as to whether there is any relationship between FIV and hormones such as estrogen and progesterone??

 

This is great participating on an internet forum and actually gaining knowledge and insight, who'd have thought it possible.

John Peter - Jul 29 2010, 05:48 PM

Share this post


Link to post
Share on other sites
John peter:

 

Well, since you ask, let me give you a brief overview. Estrogen stimulates the immune system, and contrary to popular belief, it is not an exclusive female hormone. Estrogen levels in males are present in variable quantities. Progesterone, however, is purely female and immunosuppressive - it has to be since the immune system of a pregnant female has to be told to take things easy for a bit as her body should not reject a foreign body (the fetus) trying to thrive within her.

 

From the point of an immunodeficiency virus, a pregnant female is thus a nice place to live and thrive. But let me back up a bit. On first infection, the immunodeficiency virus is happily exploring fertile ground and infecting the white blood cells that have the right surface proteins to be recognized by the virus (basically the CD4 cells). When the host immune system kicks in after this initial infection, the virus then lies dormant as it inserts its RNA (turned into DNA) into the host cell genome. In fact, while you can test positive for antibodies to immunodeficiency viruses after the initial infection, it is often difficult to isolate active virus from the host. Basically the virus reproduces on a go-slow program, but it is still there, and interfering with the production and/or longevity of CD4 cells because of the inserted DNA. Release of new viral particles is ongoing, and really kicks in when the immune system and antibody production is depressed either as a result of pregnancy and/or collapse due to the slow but relentless action of the virus itself.

 

Now, pregnant females are sort of important to population reproduction, but are also sort of vulnerable to the actions of an immune deficiency virus. That is why in humans, domestic cats, and probably lions, there is a much higher incidence of spontaneous abortions, stillbirths, and low levels of offspring survival. I cannot yet post an article about this on the LION AID website as the current setup will not allow sufficient graphs to illustrate my point.

 

It has always been accepted that lions have high cub mortality - about 60% of cubs born do not reach age 2. But this is the tip of the iceberg. In my Botswana study, I was able to differentiate between females who were pregnant and then lost their pregnancies, females who denned but produced no cubs, and females who did produce cubs from their dens. The 60% mortality rate only applies to the latter, although there was no way of establishing how many cubs were either stillborn or died before they emerged from their dens. Thus 60% is a very minimal estimate.

 

So are FIVple-infected lions fragile in other ways besides being more vulnerable to diseases like bTB and canine distemper? You bet. FIV has a considerable impact on reproduction among domestic cats, and it is no different among lions.

Lion Aid - Jul 29 2010, 08:11 PM

Share this post


Link to post
Share on other sites
Lion Aid:

 

That's a very interesting insight and would be great to explore in more detail, you need to get the website updated for those graphs!!

 

I remember reading a while back about the effects of oestrogen and progesterone on the bodies capacity to defend itself from viral infection and the implications of this for pregnant women and as a route for possible mechanisms to prevent infection with HIV. But I hadn't considered it in this context at all...duuh!

 

Have you any plans to take the research further?

 

It's a great pity that it has taken so long for the routine dismissal of FIV in lion morbidity to be re-evaluated, bearing this in mind I wonder if any consideration is being given to the possible effects of the virus on decreasing lion populations that may become bottle-necked as it were? It's a coincidence that this reassessment occurs just as the effects of SIV in primates has also recently been revised.

John Peter - Jul 29 2010, 08:58 PM

Share this post


Link to post
Share on other sites
Matt, I am very interested in the FIV discussion and other viral implications for lions and any other wildlife for that matter. I vote YES to start a new thread and get the factual and interesting and educational discussion to the forum where it belongs so we can learn and contribute in a positive manner. The scientific discussion which has developed is interesting and needs its own focus.

Twaffle - Jul 30 2010, 02:20 AM

The debate/discussion on FIV is very enlightening and I agree we should split to another thread.

Dik dik - Jul 30 2010, 08:25 AM

Share this post


Link to post
Share on other sites
I have found the scientific discussion very interesting and one of the great benefits of Safari talk.

Wild Dog - Jul 30 2010, 10:11 AM

Share this post


Link to post
Share on other sites
It is no wonder that as general readers of scientific studies we get confussed as to the significance or not of various factors affecting conservation strategies and interventions as this discussion of the role of FIV has illustrated. For example:

 

I have just been reading a report of the implications of climate fluctuations on disease prevalence in lions written by M. E. Roelke, J. Pecon-Slattery S. Taylor, S. Citino, E. Brow, C. Packer, S. VandeWoude and S. J. O’Brien published in 2008 and available here:

 

http://www.jwildlifedis.org/cgi/content/full/42/2/234#T1

 

Now this paper basically finds that extreme drought followed by exceptional rains affected the exposure of lions to babesiosis, which coupled with cdv outbreaks caused high mortality and dramatic die offs.

 

Now, the paper states in relation to FIV that:

 

"feline immunodeficiency virus (FIV) infection was ruled out as a co-factor because nearly all of the adult Serengeti and Crater lions have been FIV+ each year since at least 1984, and FIV-infection in lions has never been linked with mortality" citing two papers published in 1992 and 1999.

 

All well and good you might say but I then remembered that three of the authors of this paper Roelke, Packer, and O'Brien published a study in 2006 stating that they had idendified:

 

"Results from FIV-infected lions and pumas parallel human and Asian monkey CD4+ diminution in HIV and SIV infection, respectively, and suggest there may be unrecognized immunological consequences of FIV infection in these two species of large cats."

 

The paper is available here:

 

http://www.jwildlifedis.org/cgi/content/full/42/2/234#T1

 

As samples studied in this 2006 paper were collected from Serengeti lions I checked back to the 2008 paper to examine whether the samples came from the same collection.

 

However, what I found reviewing the 2008 paper was that I couldn't find any mention of the blood samples having being tested for FIV or any investigation of CD4 levels being tested. I found this rather odd as the same authors two years earlier suggest that the influence of FIV should be considered when investigating disease outbreaks. Yet the only reference to FIV in the 2008 paper is the dismissal qouted above which is only supported by references to two papers published in the 1990s. This despite the fact that both the 2006 and 2008 papers were based on the studies including Serengeti lions by the same researchers.

 

Now this may all be down to editorial decisions rather than the researchers themselves but either way it seems there are some very mixed messages being sent out!

John Peter - Jul 30 2010, 12:14 PM

Share this post


Link to post
Share on other sites
John peter:

 

Good for you for wading through all these papers, as a result of which you are now aware of the many internal contradictions that seem to have slipped past the editors and the reviewers. Earlier papers on the CDV outbreak basically said the same thing about a relationship between CDV and FIV – there is no correlation. Now, as FIV negative lions in the Serengeti are a bit thin on the ground, the only way that statement could have been made is by invoking the fact that (A) not all FIV-infected lions died during the CDV outbreak; and ( FIV-infected lions that survived were able to mount an antibody response to CDV.

 

I mentioned earlier the long-term process involved between initial FIV infection and eventual immune system compromise and collapse. As with humans infected with HIV, the immune system is perfectly capable of dealing with a variety of challenges in the early stages. In fact, in Botswana, anti-retroviral drugs are not issued to patients until CD4/CD8 ratios fall below a certain level indicative of a threatening level of immune competence loss. As I also mentioned, the FIV status among lion populations is based on antibody presence. All that antibodies can tell you is that the lion was exposed and now life-long infected. It tells you nothing about immune competence. So therefore, in a population of infected animals, you would expect some with still functional immune systems, some with immune systems being compromised, and some with immune systems in a bad state.

 

With that diversity of immune system competence you would expect a diversity of possible responses to a CDV outbreak, and a lack of direct correlation between FIV infection as measured by antibodies and CDV-related mortality.

 

Another bit of interesting information about the CDV outbreak among the lions in the Serengeti was that the authors blamed the mortality on a virulent and variant strain of CDV. Their evidence was based on differences between the CDV virus recovered from the Serengeti lions and a strain of CDV from the Onderstepoort laboratories in South Africa. Given the geographic distance between the sources of the virus, and the likelihood of independent strains developing among different virus populations, differences would be expected. The conclusion of exceptional virulence is conjecture – for all we know, the eastern African strain of CDV recovered from the lions might long have been present as a “normal” variant of CDV? Claims of exceptional virulence were not evaluated scientifically, although the possibility that it was cannot be ruled out. Canine distemper is a virus with a very wide host range including dogs and lesser pandas!

 

More tip of the iceberg stuff. I hope Matt will soon establish the FIV discussion section to have what will be a very interesting discussion on FIV and other disease aspects threatening not only lions but a variety of susceptible carnivores. Thanks again for your input, I hope others will join in soon with their contributions?

Lion Aid - Today, 12:59 PM

Share this post


Link to post
Share on other sites

Matt:

 

Thanks for making this a new topic. Timely and much-needed.

Share this post


Link to post
Share on other sites

Thanks Matt. Will re read all the posts in chronological order to come to grips with the issue.

Share this post


Link to post
Share on other sites

I thought I would add this link.

 

New insights into lions genetic evolution

 

An international team of researchers has successfully traced the evolutionary history of the world's lions in unprecedented detail. The researchers' findings published online in the journal Public Library of Science (PLoS), indicate that there are 11 genetic subsets in today's lions that not only distinguish African from Asian populations but also separate genetic strands within the African population.

 

In this regard, the feline immunodeficiency virus (FIV), a retrovirus analogous to the human immunodeficiency virus (HIV), was particularly useful because, the authors explain, 'the virus is quite genetically diverse in lions, offering a unique marker for assessing ongoing lion demographic processes.' According to the analysis, today's population of 50,000 free-ranging lions in sub-Saharan Africa and Asia derive from several habitats in Eastern and Southern Africa in the Pleistocene epoch (about 324,000 to 169,000 years ago). These genetically distinct populations spread into Central and Northern Africa and into Asia during the Late Pleistocene (about 100,000 years ago).

 

six distinct FIV-Ple subtypes among lion populations, refute the hypothesis that African lions consist of a single panmictic population.'

 

What would interest me is what appropriate action can be taken to stop the spread of FIV?

Share this post


Link to post
Share on other sites

Posted (edited)

I read that paper in 2008 when it was published, and admit to being puzzled by the conclusions drawn by the authors and the data on which their conclusions were based.

 

Let me back up a bit. This is basically a paper on population genetics. Such papers in the past have drawn conclusions about how different populations are from each other based on what are called genetic distances. Such distances are established among non-interbreeding populations over time, so the greater the distance, the less interbreeding there has been. On the basis of that data, it is possible to construct "trees" of resemblance of one population to another, and thereby derive a picture of how closely (or not) populations of a species are related to each other. It would not surprise you that geographically distant populations were usually genetically distinct, especially if those populations were separated by some kind of geographic or habitat barrier that prevented interbreeding.

 

Population genetics also revealed aspects of the evolutionary history of the species - for example, during the Pleistocene glaciations (ice ages), populations of African species were separated by great distances as suitable habitats were confined. You might associate ice ages with glaciers, and that is true. But so much water was tied up in ice that formerly tropical and subtropical areas were also greatly affected. If you were a monkey dependent on a rainforest habitat you would have been severely challenged - rainforests shrank to very small and distant patches during the Ice Ages.

 

So during that time monkey and other species' populations were isolated and diverged, and genetic analyses can reveal that.

 

Now. Next topic. Genetic analyses are based on various techniques. Obviously, for population genetics, you need to examine regions of the nuclear DNA that evolve rapidly. You are not interested in the difference between a wildebeest and an eland - you want to know about wildebeest east and west of the Rift Valley in Kenya, for example. But such analyses give no answer based on nuclear DNA - rate of change is too slow. So you turn to mitochondrial DNA.

 

Now here is an interesting thing. Mitochondria are present in every cell, especially cells that need lots of energy. Mitochondia are what are called "organelles" - very much like chloroplasts in plant cells responsible for photosynthesis. Both mitochondria and chloroplasts are thought to have been free-living organisms way back when, and "captured" by early single-celled organisms to form a mutually beneficial relationship.

 

Thus from an organism, you can recover both nuclear and mitochondial DNA, and especially the "D-loop" region of mitochondrial DNA has been very useful for population genetics as it accumulates changes much faster than the nuclear DNA. Early analyses of human evolution and human population genetics were based on mitochondrial DNA to differentiate populations. One problem though - mitochondria and thus their DNA are inherited through maternal lines, and recently there have been sequence analyses of the Y-chromosome (obviously paternally inherited) to fill in the picture.

 

Still with me? Sometimes, however, even with data from nuclear DNA, Y-chromosome information, and mitochondrial DNA sequences, fine-scale population differentiation remains obscure.

 

So this is where the viruses come in. They evolve much faster than the host organism - the generation time of a virus can be measured in hours or days versus many years for the host. So the thought was why not look at viral genetics to determine host population differentiation? Very specific viruses like FIVple only infect lions, communication of the disease among lions is bound to be local, so an examination of infective viruses can tell you a lot about host population differences.

 

Right? Well..... maybe. Viruses have their own evolutionary trajectories that can be very seperate from their host populations. Viruses have their own selective forces acting on them. Viruses can accomodate changes within their genetic makeup that are not in any way associated with their hosts. It might well be that one can argue for local virus populations being characteristic of local hosts, but there are problems with that. A virus can make significant genetic changes over a short time and then none for years. Viruses dont really obey population genetic parameters.

 

So is it possible to draw conclusions from virus genetics in terms of host genetics? Maybe, but one has to be careful. The authors of this paper might not have been...

Edited by Lion Aid

Share this post


Link to post
Share on other sites

Thank you Lion Aid. Makes perfect sense and I can understand why scientists are trying to find other ways to analyse population differences. In the long term it may be critical for conservation efforts to understand why certain individuals should not be relocated into different areas. Not just for genetic reasons if sub species have evolved (even when their phenotype may look the same to us) but for disease resistance amongst other things.

 

Although the viral markers may be being used for determining genetic difference in a way which may not hold up in the long term, useful information could come out of the research for different reasons. But that is just a layman's view of what is quite a complex issue and I only completed 1st year uni genetics so it gies way beyond my learning.

Share this post


Link to post
Share on other sites

As a lay person, may I casually punch out some thoughts and questions - some may be silly, but it would help my understanding.

 

I heard that FIV was because lions ate some people once and got infected. Is this true? So the virus can pass from human to feline?

 

I was also under the impression that only Kruger lions were infected, yet it seems that lions all over are infected and there is no way that they could have past the virus to each other. Including Pumas. So how did the virus spread?

 

It seems that FIV has been around for a lot longer than we think, and could have been present in lions before we started to look for it. Is it possible that lions have been living with FIV for a lot longer first believed?

 

Then domestic cats are also infected, yet I don't see domestic cat numbers plummeting and pet owners panicking. So why should we be worrying about an impact on the lion populations?

 

If the Virus was so bad, then wouldn't Kruger have considered culling all the infected lions? They have culled many buffalo, and unlike buffalo - lion numbers recover quickly.

 

Then what, (if any) plans or suggestions are there to combat the virus?

Share this post


Link to post
Share on other sites

Posted (edited)

It is known that immunodeficiency viruses can make host transitions, but very rarely. It is actually thought that one of the original immunodeficiency viruses occurs among bovines, not surprisingly called BIV. Somewhere along the line (and it is conjecture as to when, but certainly very many thousands of years ago) this virus was able to skip into felines by a necessary mutation to begin FIV. Then, so the reconstruction goes, an African feline bit a monkey and that was the start of Simian Immunodeficiency Virus. And then, a human in West Africa either ate or was bitten by a monkey, and hence the emergence of HIV.

 

I must emphasize strongly that these transitions between original hosts and new hosts are extremely rare. You will not get SIV by dining on a monkey, nor will you get FIV by being bitten by your infected domestic cat. A transition requires a greatly altered virus that is capable of dealing with a completely new host environment - almost as drastic as a fish suddenly being able to survive on land. Very occasionally it happens... not the fish, but the virus that is....

 

So no, the lions did not get FIV by eating humans with HIV, that is just a (popular) rumour.

 

When FIV was discovered in domestic cats in 1986 by Neils Pedersen at the University of California Veterinary School in Davis, a survey was taken among other cat species and the virus was already very widespead among wild cat species all over the world. And all had their own strain or strains, and subsequent surveys showed that virtually all lions in the Serengeti were positive. So yes, the virus is old, and has probably been among lions for a very long time. This is where the concept of a happy coexistence came from in early days of research. Not true as is now known.

 

How the virus spread among all those species in the Americas, Asia, Africa is also unknown. But wherever it was that the virus initially infected lions in Africa, it is clear that it spread through almost all eastern and southern African populations. What is interesting is that some populations remain negative - like Etosha. To date, I have not seen a publication on the presence of the virus among western African lions - there are research projects in place, so I hope we will soon have information from there - it will give us much more perspective on the spread of the virus among lions. It is possible that the Etosha lions were a very isolated population cut off from immigrating lions and thus avoided infection. It is important to remember that Etosha was originally a very harsh environment until water holes were put in....

 

As for the domestic cats. First, it is important to remember that domestic cats come in two categories - feral and the ones living comfortably in homes. Among the feral cats, FIV is much more prevalent. And also remember that infection with FIV takes time to take effect. Among domestic cats, this might be seven to ten years before their immune system is destroyed after initial infection - analogous to the time frame among humans. Domestic cats also have accessible veterinary care, good food, and there is even now a vaccine that seems to be helping. I sort of doubt the latter, but veterinarians believe it is doing good while we await an HIV vaccine?

 

The point here is that infection with FIV, for cats and lions, is not an immediate death sentence, but they are on death row. Lions can live with the virus, reproduce to some extent, and maybe maintain populations. As I said in earlier posts, the real threat comes when an immunologically challenged population is faced with invading viruses like canine distemper and invading bacteria like bovine tuberculosis. That is when the losses will mount. Always remember - FIV and HIV do not kill by themselves - they just make the host less and less capable of dealing with challenges to the immune system that uninfected individuals might be able to deal with.

 

There are no plans to combat the virus - it is impossible at present; there is no cure. Vaccinating lions with a domestic cat vaccine with limited reliability? Forget it. The domestic cat FIV is genetically different from lion FIV, and what would be needed is an experiment where vaccinated lions and unvaccinated lions are challenged with the FIVple virus in all its different strains - no way could that experiment take place, imagine the outrage among various groups. Adult Kruger lions are infected at very high percentages, and culling is not an option - remember that for many years the virus was considered a bit of an irritation the lions could deal with.

 

So what we must accept, in Kruger, Serengeti, Uganda, Kenya, Botswana, Zimbabwe, Zambia, Tanzania - is that we are dealing with a lion population that is fragile, and to do all we can to prevent a flow of diseases into those populations, especially from domestic sources. That will help.

Edited by Lion Aid

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!


Register a new account

Sign in

Already have an account? Sign in here.


Sign In Now

  • Recently Browsing   0 members

    No registered users viewing this page.


© 2006 - 2017 www.safaritalk.net - Talking Safaris and African Wildlife Conservation since 2006. Passionate about Africa.