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 
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 
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 
Thanks for the attention,
Instale a Barra de Ferramentas com Desktop Search e ganhe EMOTICONS para o 
Messenger! É GRÁTIS!
Felvtalk mailing list

Reply via email to