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
Chandhasin et al. full text is available at
Thanks for the attention,
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