Game Warden

FIV: feline immunodeficiency virus

60 posts in this topic

Just a few more papers detailing more recent studies investigating possible morbidity in lions testing positive for FIV etc.Unfortunately the first one is only available to purchase unless you have access via an institutional log in (so if anyone has friends or relatives currently studying at Uni!). However the abstract sounds interesting.

 

Worth bearing in mind not only the date of publication of papers but also the time lag between submission of paper by it's authors and it's actual publication by journals. This can take up to two years or more in some cases.

 

Melody E. Roelke et al. Pathological manifestations of feline immunodeficiency virus (FIV) infection in wild African lions. Virology 390 (1) July 2009 pp 1-12

available from:

 

http://www.sciencedirect.com/science?_ob=A...d0a02b6af1d194f

 

Abstract:

 

Feline immunodeficiency virus (FIV) causes AIDS in the domestic cat (Felis catus) but has not been explicitly associated with AIDS pathology in any of the eight free-ranging species of Felidae that are endemic with circulating FIV strains. African lion (Panthera leo) populations are infected with lion-specific FIV strains (FIVple), yet there remains uncertainty about the degree to which FIV infection impacts their health. Reported CD4+ T-lymphocyte depletion in FIVple-infected lions and anecdotal reports of lion morbidity associated with FIV seroprevalence emphasize the concern as to whether FIVple is innocuous or pathogenic. Here we monitored clinical, biochemical, histological and serological parameters among FIVple-positive (N = 47) as compared to FIVple-negative (N = 17) lions anesthetized and sampled on multiple occasions between 1999 and 2006 in Botswana. Relative to uninfected lions, FIVple-infected lions displayed a significant elevation in the prevalence of AIDS-defining conditions: lymphadenopathy, gingivitis, tongue papillomas, dehydration, and poor coat condition, as well as displaying abnormal red blood cell parameters, depressed serum albumin, and elevated liver enzymes and gamma globulin. Spleen and lymph node biopsies from free-ranging FIVple-infected lions (N = 9) revealed evidence of lymphoid depletion, the hallmark pathology documented in immunodeficiency virus infections of humans (HIV-1), macaques, and domestic cats. 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).

 

This one by Slattery et al is open access. Genomic organization, sequence divergence, and recombination of feline immunodeficiency virus from lions in the wild. Available from:

 

http://www.biomedcentral.com/1471-2164/9/66

 

Abstract:

 

Background

Feline immunodeficiency virus (FIV) naturally infects multiple species of cat and is related to human immunodeficiency virus in humans. FIV infection causes AIDS-like disease and mortality in the domestic cat (Felis catus) and serves as a natural model for HIV infection in humans. In African lions (Panthera leo) and other exotic felid species, disease etiology introduced by FIV infection are less clear, but recent studies indicate that FIV causes moderate to severe CD4 depletion.

 

Results

In this study, comparative genomic methods are used to evaluate the full proviral genome of two geographically distinct FIV subtypes isolated from free-ranging lions. Genome organization of FIVPle subtype B (9891 bp) from lions in the Serengeti National Park in Tanzania and FIVPle subtype E (9899 bp) isolated from lions in the Okavango Delta in Botswana, both resemble FIV genome sequence from puma, Pallas cat and domestic cat across 5' LTR, gag, pol, vif, orfA, env, rev and 3'LTR regions. Comparative analyses of available full-length FIV consisting of subtypes A, B and C from FIVFca, Pallas cat FIVOma and two puma FIVPco subtypes A and B recapitulate the species-specific monophyly of FIV marked by high levels of genetic diversity both within and between species. Across all FIVPle gene regions except env, lion subtypes B and E are monophyletic, and marginally more similar to Pallas cat FIVOma than to other FIV. Sequence analyses indicate the SU and TM regions of env vary substantially between subtypes, with FIVPle subtype E more related to domestic cat FIVFca than to FIVPle subtype B and FIVOma likely reflecting recombination between strains in the wild.

 

Conclusion

This study demonstrates the necessity of whole-genome analysis to complement population/gene-based studies, which are of limited utility in uncovering complex events such as recombination that may lead to functional differences in virulence and pathogenicity. These full-length lion lentiviruses are integral to the advancement of comparative genomics of human pathogens, as well as emerging disease in wild populations of endangered species.

 

And following on from the earlier paper from virology posted the other day this paper also looks at possibilities of cross species infection and development

 

Troyer et al. FIV cross-species transmission: an evolutionary prospective

 

Available from:

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2442884/

 

Abstract:

 

Feline and primate immunodeficiency viruses (FIVs, SIVs, and HIV) are transmitted via direct contact (e.g. fighting, sexual contact, and mother-offspring transmission). This dynamic likely poses a behavioral barrier to cross-species transmission in the wild. Recently, several host intracellular anti-viral proteins that contribute to species-specificity of primate lentiviruses have been identified revealing adaptive mechanisms that further limit spread of lentiviruses between species. Consistent with these inter-species transmission barriers, phylogenetic evidence supports the prediction that FIV transmission is an exceedingly rare event between free-ranging cat species, though it has occurred occasionally in captive settings. Recently we documented that puma and bobcats in Southern California share an FIV strain, providing an opportunity to evaluate evolution of both viral strains and host intracellular restriction proteins. These studies are facilitated by the availability of the 2X cat genome sequence annotation. In addition, concurrent viral and host genetic analyses have been used to track patterns of migration of the host species and barriers to transmission of the virus within the African lion. These studies illustrate the utility of FIV as a model to discover the variables necessary for establishment and control of lentiviral infections in new species.

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Posted (edited)

1

Edited by russell

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Posted (edited)

Russell: you asked these questions:

 

"I would have to question why you attack other researchers work on a public forum?

 

Your arguments on FIV sound interesting, though I was wondering what level of peer review they have subjected to?

 

I feel this is important as you seem to publicly peer review the work of others through this site."

 

All publications listed on FIV on this site have been peer reviewed. In fact, many of the publications result from one research group that seems to be rapidly changing their own minds as to the consequences of FIVple infection. They are doing this themselves, as they were the primary proponents of FIVple non-pathogenicity and now changing their minds.

 

"You have asked me to prove that FIV does not cause big issues, I can simply turn the debate around without even researching FIV.

 

'Prove that in the remaining 98% of the lion population that it does have an effect"

 

Really? You can simply turn the debate around against all scientific evidence? How amazing. So you are of the belief that the researchers, by great coincidence , sampled only those lions that showed a negative response to infection? So for you to be convinced, all 20,000 lions or less remaining would need to be sampled? Let's put it this way. Say you have a human population susceptible to breast cancer. Genetic determinants for risk are established from a smaller subsample than the entire human population. Would you, as someone who acknowledges they use statistics in everyday life, argue that therefore, as it is a subsample, the genetic parameters established as risk factors of breast cancer cannot be extrapolated to any but the sampled population? Or take the established risk factors associated with smoking with lung and other cancers. This was also based on a subsample of the human population. Would you say that the risk of smoking cannot be proved until every smoker was analysed?

 

"Sadly, I do not have the time to sift through academic papers on FIV"

 

That is sad. You otherwise might actually gain some credence on this thread.

 

So, to summarize: all articles offered as examples of the consequences of FIVple infection on this thread have been peer reviewed. There has been no cherry picking, and others have contributed material. Subsampling a population is standard procedure and allowed by all scientific standards. If you do not read the papers, you will, sadly, not be informed. Others are making the effort in terms of reading and expanding the knowledge base on this thread.

 

By the way, I did not compare you to creationists. I used that association to illustrate the differences of opinion on subjects we might encounter.

Edited by Lion Aid

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Posted (edited)

...

Edited by russell

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Being facetious? How artfully you attempt to retreat Russell. So it was just a joke, a bit of humour? All can see that you were not being facetious in the slightest. You mention again Lion Aid for example. Give us all a break please.

 

You are not adding anything meaningful to this issue.

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zzzzzzzzzzz...............

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Posted (edited)

Sorry for your boredom Pangolin. (Edited, Matt)

 

Immunodeficiency viruses, and all viruses actually, are fascinating entities. We cannot call them organisms like pathogenic bacteria, but they are a step above prions - proteins - that cause mad cow disease etc. Imagine yourself as a virus for a few minutes. You have a protein envelope surrounding either DNA or RNA. In the case of the latter, you either bring with you to tools to convert the RNA into DNA and insert your sequence into the host cell, or the host cell provides this for you. That is how you replicate, the host cell you have invaded will provide what you need in terms of replication (many times) of your genetic sequence and a new protein envelope for further invasion of other host cells, either within the current host or new hosts.

 

What is interesting is that generations of viruses have left their signature (sequences) within host DNA. This is perhaps comparable to a fossil record in terms of past human viral invasions.

 

Back to you as a virus. What you need to be able to do is to recognize specific host cells among the vary many types present to invade. FIV and other immunodeficiency viruses attack host cells specifically involved in immune defense, while rabies, another RNA virus, targets nerve cells in contrast. You recognize those cells by their surface proteins, attach, and dump your RNA content. In the case of FIV, this is converted into DNA and integrated into the host cell DNA. The host cell is thereby turned into a virus "factory", and because of the integration of "proviral" sequences into the host cell, the lifetime of that cell is compromised. In the case of immunodeficiency viruses, specific cells involved in host immune responses are therefore not only adding to the viral burden of the host, but also dying off before their expected lifespan.

 

I can be accused of oversimplification here, as there are are very many other factors involved in HIV and FIV viral invasions of susceptible hosts. But those are the basics... and the current medicinal defenses largely involve means to prevent the conversion of RNA into DNA and subsequent genomic integration. That is another oversimplification perhaps...

Edited by Game Warden

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I don't know what has happened in this thread which has led to contributors editing posts, members wanting to leave etc, as I have not been able to be here these part couple of days whilst this discussion was evolving. However, whatever has transpired I feel very unhappy about, especially if there have been robust exchanges which have led to this: I want to remind all members of the following line in the Safaritalk Vision:

www.safaritalk.net is not an animal rights website nor is it a pro hunting website. However it encourages balanced informed and respectful discussion and debate which may surround such issues, where every member may have a right to voice his/her opinion, and such views are respected and listened to.

I want to see any further posts in this topic, adhering to the above, whether or not you agree/disagree with statements or opinions voiced. I'm not inviting any responses on this thread to my post here, but should anyone wish to contact me via PM, feel free to do so.

 

Matt

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To lend some life to this topic, let me offer this Abstract available at:

 

http://www.ncbi.nlm.nih.gov/pubmed/19896220

 

"Molecular epidemiology of feline immunodeficiency virus in the domestic cat (Felis catus).

Hayward JJ, Rodrigo AG.

 

Bioinformatics Institute, Allan Wilson Centre for Molecular Ecology and Evolution, School of Biological Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand. jjh276@cornell.edu

 

Abstract

Studying the evolutionary mechanisms of feline immunodeficiency virus in the domestic cat (Felis catus), FIV(Fca), provides a good comparison to other lentiviruses, such as HIV and FIV(Pco) in the cougar (Puma concolor). We review the current epidemiological and evolutionary findings of FIV(Fca). In addition to the five accepted FIV(Fca), subtypes, several recent phylogenetic studies have found strains that form separate clades, indicative of novel subtypes. In New Zealand cats, these strains of unknown subtype have been found to be involved in complex patterns of intergenic recombination, and whole genome sequences are required to resolve these. Evidence of recombination events has been documented with the highest levels in the env gene, the region involved in host cell receptor recognition. Several cases of FIV(Fca) multiple infections, both inter- and intra-subtype, have been reported. The findings of both unknown subtypes and relatively high levels of recombination suggest the need for further testing of the current vaccine. Limited studies on the evolutionary rate of FIV(Fca) document a value twice to three times that of FIV in the cougar, a result suggesting the different levels of co-adaptation between the viruses and their respective hosts. We studied the tissue distribution of FIV(Fca) in feral domestic cats, finding the first case of FIV compartmentalisation, a phenomenon well documented in HIV-1 patients."

 

Dense language? You bet. Let me interpret – this is part of Jennifer Hayward’s PhD thesis at the University of Auckland.

 

She says this in the full paper:

 

The global prevalence of FIVfca – the domestic cat feline immunodeficiency virus variant, is 4-12% in what she calls “companion cats” – those who have a home. The highest level of infection comes from Japan, where up to 44% of home cats might be infected. There are also “feral” cats – living in the suburban wilds and elsewhere – a limited study showed they were infected at a level of 8-19%, with male cats at highest risk.

 

What Dr Hayward adds is that domestic cats can be infected with multiple strains of the virus. Retroviruses like FIV have a tendency to recombine, shuffle their genetic components. They do this at amazing rates – especially in terms of expression of their “envelope” proteins – how the immune system of the host recognizes the virus. Different FIV virus strains resulting from multiple infections do this particularly well – it is not really equivalent, but why do you think we need a different flu vaccination every year? Rearrangement, shuffling – it is like taking your favourite novel and rearranging the contents every year. John Grisham knows all about this!

 

The point here is that the virus can make amazing and rapid changes. Viruses measure evolutionary change in hours and days – hosts measure that in generations. A stop watch versus a sandglass.

 

Serengeti lions have also been shown to be infected by multiple viral strains….

 

“Compartmentalization” refers to the virus being able to “hide” in different body tissues less actively patrolled by the host immune system, and from which further challenges can be launched. These include the genitourinary tract, the central nervous system, the lymph nodes, and lungs among HIV patients.

 

So in summary the article say this – the virus changes rapidly in a short amount of time to avoid host immune system defences. The virus maintains itself in an infected host by selecting tissues less monitored by the immune system. Rapid changes in virus genetics can result in new and more virulent strains within a short amount of time compared to a host generation. Oh, and the reference to vaccines? The abstract answers that for itself.

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