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Feline Leukemia Virus
David S. Bruyette, DVM, DACVIM (SAIM)

Anivive Lifesciences, Long Beach, CA, USA

Etiology/Pathophysiology usually no viral RNA is detectable in peripheral blood
cells. In addition, some cats seem to abort infection prior
Like all retroviruses, feline leukemia virus (FeLV) is an to provirus integration and an antibody response may be
enveloped RNA virus. It carries an enzyme (reverse tran- the only sign of previous FeLV exposure.
scriptase) that transcribes the viral RNA genome into After FeLV exposure, some, mostly young, cats develop
DNA (the FeLV provirus), which is then integrated into progressive FeLV infection, characterized by persistent
the host’s cell genome. Exogenous FeLV isolates are antigenemia/viremia. Cats with progressive infection
grouped into four major subcategories: FeLV‐A, ‐B, ‐C, shed high copy numbers of FeLV and pose an infection
and ‐T. The dominant FeLV‐A subgroup is horizontally risk to other cats. Progressive infection is usually con-
transmitted and is found in all FeLV‐infected cats; it is firmed by repeated testing for antigenemia of the cat sev-
the most infectious but low in pathogenicity. FeLV‐B and eral weeks or a few months apart; only repeated positive
particularly FeLV‐C are less prevalent. They arise within antigen testing verifies the presence of a progressive
the individual cat after FeLV‐A infection: FeLV‐B devel- infection, which is linked to a poorer prognosis than
ops via recombination of FeLV‐A with endogenous regressive FeLV infection. Cats with progressive FeLV
FeLV‐related sequences and FeLV‐C and FeLV‐T evolve infection are at high risk to die within a few months to
from FeLV‐A via mutations or insertions in the surface years with FeLV‐associated diseases (see Prognosis).
glycoprotein gene. If a cat tests positive for FeLV p27 antigen, but upon
Feline leukemia virus is shed in large quantities via later retesting becomes FeLV antigen negative, it has
saliva, but it can also be found in feces, urine, and milk. developed a regressive FeLV infection. Cats with regres-
FeLV is unstable in the environment and transmission is sive infection have mounted an effective immune
thought to require intimate friendly (or aggressive) con- response and recovered from FeLV viremia. Fortunately,
tact between infected and uninfected cats. Contact with most adult cats are found to develop regressive infections.
infectious saliva or, less probable, infectious feces may Cats with regressive infection usually do not develop
also be sufficient to transmit the infection (sharing of FeLV‐associated disease. Clearance of antigenemia is
food bowls or litterboxes). In addition, FeLV can be observed mostly within a few (2–8) weeks, but in rare
transmitted vertically from the queen to her kittens. cases it can also occur after many months although the
Feline leukemia virus infection usually starts at the chance for recovery decreases with increasing time.
mucosa of the oropharynx. Subsequently, viral replica- Following recovery from antigenemia (regressive infec-
tion takes place in the adjacent tonsils and local lymph tion), latent infection can be identified for a few months
nodes. The virus is spread in the lymphoid tissues to years by culturing bone marrow cells in the presence of
throughout the body via lymphocytes and monocytes. corticosteroids. Provirus polymerase chain reaction
Replication in the bone marrow and infection of neutro- (PCR) from peripheral blood or bone marrow is positive
phil and platelet precursors favor the initiation of sec- in these cats and viral plasma RNA detected by reverse
ondary viremia and systemic infection. Cats that undergo transcriptase (RT)‐PCR may be positive. Infection may be
bone marrow infection usually develop progressive reactivated in latently FeLV‐infected cats. The potential
infection. In cats that do not undergo bone marrow for reactivation seems to be associated with the FeLV iso-
infection, only lymphocytes are provirus positive and late and generally decreases with increasing timespan.

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical