Thanks for sharing this bit of research, Hebert.

I suspect it would be very helpful for us all to be able to learn the
specific viral subgroup(s) infecting our cats so we could customize their
diets/meds accordingly, where possible!

I wonder if vets will eventually use this test in their practices?

Best,
Giselle


> Message: 1
> Date: Thu, 4 Sep 2008 09:45:06 -0300
> From: hebert ferrarezzi <[EMAIL PROTECTED]>
> Subject: [Felvtalk] FeLV diversity
> To: <felvtalk@felineleukemia.org>
> Message-ID: <[EMAIL PROTECTED]>
> Content-Type: text/plain; charset="iso-8859-1"
>
> I found the following introductory paragraph of an article from The Journal
> of Virology very interesting (and not excessively technical), to be posted
> here. It provides some possible explanations to the differences regarding
> latency period, survival time, associate malignancies and other disease
> outcomes that we have witnessed, which could be related to different kinds
> of FeLV viruses recognizable by means of molecular sequence comparisons:
>
>  "Feline leukemia virus (FeLV) is a naturally occurring gammaretrovirus of
> the domestic cat. FeLV is endemic in free-roaming urban domestic cats,
> serological survey of which shows that at least 50% of adult animals have
> been infected. The disease outcome of natural FeLV infection is variable and
> rather unpredictable. Among persistently infected animals, the majority
> succumb to degenerative diseases, including anemia or immunodeficiency;
> however, a substantial minority develop neoplastic or proliferative
> diseases, including lymphoma, leukemia, or myeloproliferative disorder. The
> determinants of disease outcome in natural FeLV infection have not been
> clearly defined but probably involve a combination of host, viral, and
> environmental factors. While there is little doubt that the genetic
> heterogeneity of the outbreeding mammalian host exerts an influence on
> disease outcome, the genetic heterogeneity of FeLV in nature clearly has an
> impact as well.
> Like other natural retrovirus populations, FeLV is not a single genomic
> species but represents a family of closely related viruses. Four natural
> subgroups of FeLV (A, B, C, and T) have been described on the basis of
> sequence differences in the surface glycoprotein (SU) and on receptor
> interactions required for entry.
> Subgroup A FeLV (FeLV-A) includes the ecotropic, weakly pathogenic viruses
> that are horizontally transmitted in nature. Infection with FeLV-A is
> associated with prolonged, asymptomatic persistent infection that may lead
> to malignant lymphoma, typically of T-cell origin. For example, infection
> with FeLV-A/61E in several studies induced thymic lymphoma in some animals
> after prolonged latency for up to 2 years, but other animals remained
> healthy for even longer periods of observation. FeLV-A is present in all
> natural infections and gives rise to the other subgroups by envelope (env)
> gene mutation, insertion, or recombination events de novo.
> FeLV-B is a polytropic virus that arises by recombination with endogenous
> FeLV-related sequences. The disease association of FeLV-B infection remains
> unclear; however, FeLV-B is unusually common in animals with lymphoid
> malignancy and thus may be linked to the induction of that disease.
> FeLV-C is also a polytropic virus that arises by mutation in the SU gene.
> FeLV-C is strongly associated with aplastic anemia in infected animals.
> FeLV-T has recently been classified and includes T-cell-tropic cytopathic
> viruses that cause lymphoid depletion and fatal immunodeficiency disease in
> infected cats. FeLV-T evolves from FeLV-A by mutation and insertion in the
> SU gene.
> The association of particular outcomes with FeLV subgroups as described
> above suggests that the nature of the virus isolate is the major disease
> determinant in FeLV infection. In fact, in the case of anemia or
> immunodeficiency induced by FeLV-C or FeLV-T, the genetic regions
> responsible for directing disease outcome have been localized to mutations
> or insertions in the FeLV SU gene. By comparison, the viral determinants of
> neoplastic disease have not been as clearly defined."
>  Chandhasin et al. full text is available at
> http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15827142
>
> Thanks for the attention,
> Hebert
>
>
>
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> End of Felvtalk Digest, Vol 3, Issue 4
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