Chapter 8 Feline Leukemia Virus
ETIOLOGY
Structure of the Virus
Certain structural components of the FeLV virion have clinical implications.
• Core contains the viral RNA and reverse transcriptase enzyme that allows DNA copies of the virus to be transcribed and inserted into the genome of infected host cells.
• Core protein (p27) is the group-specific FeLV antigen detected by conventional FeLV diagnostic tests.
• Envelope glycoprotein (gp70) defines the FeLV antigenic subgroup as A, B, C, or combinations of these; determines infectivity, host range, and pathogenicity; and elicits the protective host neutralizing-antibody response that occurs with natural exposure or vaccination. Only subgroup A is infectious.
Prevalence
• In highly endemic households with many viremic cats—30% to 70% of unvaccinated kittens compared with only 10% to 20% of unvaccinated adult cats
Transmission
• Persistently viremic cats continuously shed large amounts of virus in saliva and, to a lesser extent, in naso-ocular secretions. Infected queens shed large amounts of virus in milk. Feces, urine, and fleas are less likely sources of infection.
• Transmission most often occurs through direct oronasal contact with infectious saliva during mutual grooming and sharing of food and water bowls or through bite wound inoculation of saliva.
• Transplacental transmission can occur, but milk-borne infection in nursing kittens is more common.
• Iatrogenic transmission of FeLV can occur through contaminated blood transfusions, needles, surgical and dental instruments, and endotracheal tubes.
• FeLV usually does not survive more than a few hours outside of the cat, up to a maximum of 48 hours under optimal temperature and moisture conditions. Heat, drying, detergents, and disinfectants readily destroy FeLV.
PATHOGENESIS
Sequence of FeLV Infection
• After oronasal or percutaneous inoculation, FeLV replicates in local lymphoid tissues and then in systemic lymphoid tissues throughout the body, such as lymph nodes, spleen, and thymus. Viral antigen may first become detectable in the blood (antigenemia) at this stage with enzyme-linked immunosorbent assay (ELISA) tests (see “Diagnosis”). A successful immune response may terminate the infection at this stage or even before antigenemia is detectable.
• If infection progresses, FeLV infects the bone marrow, leading to circulation of virus-infected leukocytes and platelets (cell-associated viremia) that are detectable in the blood by the immunofluorescent antibody (IFA) test (see “Diagnosis”). This usually indicates that FeLV has overwhelmed the host immune response and that the infection is likely to persist indefinitely.
• Concurrent with the development of viremia, FeLV infects glandular cells throughout the body (e.g., salivary glands, lacrimal glands, mammary glands, and mucosal epithelial glands). This leads to shedding of virus in most body secretions, with especially high concentrations of virus in saliva and the milk of lactating queens. At this stage, FeLV-infected cats are contagious to other cats in close contact, and queens can infect their nursing kittens.
Host Immune Response
• Antiviral response is mediated by neutralizing antibody directed against FeLV envelope antigens. Transient infection and recovery occur if the immune response is successful, whereas bone marrow infection and persistent viremia occur if the virus overwhelms the host immune response.
• Antitumor response is mediated by antibody directed against FeLV-associated antigens on the surface of FeLV-induced neoplastic cells.
Transient Infection
• Transiently infected cats usually eliminate the virus swiftly within 4 to 6 weeks after exposure, with either no detectable antigenemia or a transient antigenemia lasting 1 to 5 weeks. However, FeLV-infected cats can potentially eliminate the virus at any stage, rarely even after many months or years as a persistent carrier.
• Many cats are vaccinated against FeLV, and upon exposure, most will resist persistent infection and instead go through a brief transient infection (see “Vaccination”).
Latent Infection
• In latent FeLV infection, non-replicating FeLV provirus remains dormant within the DNA genome of bone marrow and lymphoid cells of the cat. This can only be detected by specialized virus culture techniques or polymerase chain reaction (PCR) assays (see “Diagnosis”); thus, it is difficult to distinguish cats that have truly cleared the virus from cats with latent infection.
• In most transiently infected cats, the latent stage of infection eventually is eliminated uneventfully within 6 to 9 months as part of the normal recovery process, but it sometimes can take a year or more. Latent infection persists indefinitely in an estimated 10% of “recovered” cats.
• The clinical significance of FeLV latency is the rare possibility of reactivation to a replicating infection, either spontaneously or in response to immunosuppression (e.g., corticosteroid-induced). In addition, reactivation of infection in latent-infected queens may rarely transmit FeLV to kittens in utero or during nursing.
Persistent Infection
• Persistent infection eventually leads to fatal FeLV-related disease in most cats after a variable disease-free interval. The mortality rate in persistent FeLV-positive cats is 30% at 6 months, 60% at 2 years, and 90% at 4 years.
• Persistent infection will develop in approximately 10% to 30% of unvaccinated cats that receive continuous heavy exposure, such as living in an endemically infected household. In this situation, kittens less than 4 months of age are most susceptible, and the persistent infection rate can reach 70% in this group.
CLINICAL DISEASE SYNDROMES
Lymphoma and Leukemia
FeLV can be a primary cause of lymphoma, leukemia, and myelodysplasia. For additional information regarding diagnosis and treatment of these neoplastic conditions, see Chapters 26 and 27. In the mid-1970s, 70% of cats with lymphoma and leukemia were FeLV positive. Virus-negative alimentary lymphoma was uncommon. However, with the decline in prevalence of FeLV infection, FeLV-negative lymphomas now comprise 85% to 90% of the lymphomas seen in cats, and alimentary lymphoma is the predominant form. Some of these FeLV-negative lymphomas have molecular evidence of FeLV provirus, but most feline lymphomas are now caused by factors other than FeLV.
Alimentary Lymphoma
• Intestine—Diffuse infiltrative thickening of the intestinal wall or palpable obstructing mass (weight loss, vomiting, diarrhea, and inappetence)
• Liver—Diffuse hepatomegaly or nodular tumor masses within the liver (icterus, weight loss, vomiting, and abnormal liver tests)
Leukemia and Myelodysplasia
FeLV infection of bone marrow hemopoietic cells can result in acute lymphoid leukemia, non-lymphoid leukemia, or myelodysplasia (preleukemia). Clinical signs include pallor (anemia), petechial and ecchymotic hemorrhages (thrombocytopenia), fever, lethargy, weight loss, hepatosplenomegaly, and mild lymphadenopathy. Abnormal blast cells are usually identified in the blood and bone marrow. For additional information, see Chapters 22 and 27.
Acute Lymphoid Leukemia
• Acute lymphoblastic leukemia is characterized by extensive infiltration of the bone marrow with neoplastic lymphoblasts, often accompanied by neoplastic infiltration of the liver, spleen, and lymph nodes.
Acute Myeloid (Non-lymphoid) Leukemia
• This group of neoplastic diseases is characterized by the proliferation of one or more cell lines in the bone marrow at the expense and to the eventual exclusion of normal hemopoietic cells. These disorders are classified on the basis of the cellular origin of the abnormal cells as acute myeloblastic leukemia, acute myelomonocytic leukemia, acute monocytic leukemia, and erythroleukemia.
• Diffuse hepatomegaly, splenomegaly, and lymphadenopathy occur from extramedullary hematopoiesis and/or neoplastic infiltration. Neoplastic infiltration of the liver may cause jaundice.
• Anemia and thrombocytopenia are common, and the diagnosis is based on identification of neoplastic blast cells in the blood and bone marrow.
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