Feline Leukemia virus
Information 02-01-2012.

The feline leukemia virus (FeLV) is a type C Oncornavirus, belonging to the family Gammaretroviridae. There are three main subgroups of FeLV clinical significance. The subgroup A is found in all naturally infected cats, FeLV-A, it is the original form of the virus and is effective transmission between cats. The FeLV-A subtype tends to be less pathogenic viruses from other subgroups, but some strains of FeLV-A cause severe immunosuppression.

Almost all naturally infected cats are initially infected with FeLV-A. FeLV-B is in ~ 50% of cats naturally infected with FeLV-A. The FeLV-A and FeLV-B presence is more associated with neoplastic diseases single FeLV-A. FeLV-C virus is isolated on 1% of naturally infected cats, with FeLV-A and sometimes accompanied by coinfection of FeLV-A and FeLV-B. The presence of FeLV-C in an infected cat is strongly associated with the development of erythroid hypoplasia and severe anemia accordingly.

Viruses are detected the 3 subgroups (but not distinguishable) by the common use of diagnostic kits FeLV. The incidence of FeLV infection is directly related to the population density of cats. Infection rates are higher in nurseries and foster care of these animals, especially cats have access to
the outdoors. Healthy carriers Cats are the primary reservoir for the virus. Carriers excrete large amounts of virus in saliva, and smaller amounts tears, urine and feces.

The oronasal contact with infected saliva or urine is the most common mode of transmission. Nose to nose contact, mutual grooming, as well as sharing litter trays and plates facilitate transmission. Bite wounds are infected cats, cats uncommon in household transmission effectively. Bites can be an important mode of transmission in cats living free. Adult cats are more resistant to infection, young cats are much more susceptible. The virus can be transmitted via transuterine vertically or milk, or horizontally secretions and excretions.

After oronasal inoculation, the virus replicates in the oropharynx lymphoid tissue. From there, the virus is transported by mononuclear cells to
the spleen, lymph nodes, intestinal and bladder epithelial cells, salivary gland and bone marrow. The virus appears later in secretions and excretions of such tissues and peripheral blood leukocytes and platelets. Viremia is usually evident 2 to 4 weeks after infection.

The acute phase of infection with this virus (2 to 6 weeks) may go unnoticed. It is characterized by mild fever, malaise, and lymphadenopathy blood cytopenias. In ~ 70% of adult cats, viremia and virus shedding is transient, lasting 1 to 16 weeks. Few cats continue
to spread the virus (weeks or months) in secretions after viremia. The virus can persist in the bone marrow for a longer period, but usually disappears within 6 months.

Some cats exposed to FeLV (~ 30%) do not have an adequate immune response and happen to have persistent viremia. The viremic cats persistence in developing deadly diseases after a period of time is variable.

- related disorders are numerous and include immunosuppression, neoplasia, anemia, immune - mediated diseases, reproductive problems, and enteritis.

Immunosuppression caused by FeLV is similar to that caused by feline immunodeficiency virus. There
is an increased susceptibility to infections by fungi, protozoa , bacteria and other viruses. The number of neutrophils and lymphocytes in the peripheral blood of affected cats can be reduced, and cells present can be dysfunctional. Much of the immunodeficiency caused by FeLV is believed to be due to the high degree of viral antigenemia.

Lymphoid or myeloid tumors (eg lymphoma, lymphoblastic leukemia, erythremic myelosis) develop in up to 30% of persistently infected cats with FeLV. However, the persistence of FeLV antigen increases the risk of lymphoma in up
to 60 fold compared to a negative FeLV cat. Lymphoma is the most common cancer diagnosed in cats. Renal and gastrointestinal forms of lymphoma are more likely to be negative FeLV cats.

Anemia caused by FeLV is usually non
- regenerative and normochromic. There is often an idiosyncratic macrocitosis.

Immune complexes formed in
the presence of moderate excess antigen can cause systemic vasculitis, glomerulonephritis polyarthritis, and a variety of other immune disorders.

Reproductive problems are common; 68-73% of infertile female cats has been reported that are FeLV-positive, and 60% of cats are aborting FeLV-positive. Fetal death, reabsorption, and placental involution may occur in the second trimester of pregnancy, presumably as
a result of intrauterine infection of fetuses virus transported through maternal placenta in leukocytes.

Enteritis, can develop resembling feline panleukopenia clinically and histologically both. Clinical signs include anorexia, depression, vomiting and diarrhea (which may be bloody). Because the concurrent immunosuppression associated with FeLV infection, sepsis can develop.

Diagnosis can be accomplished by immunofluorescence assay (IF) to detect the presence of FeLV structural antigens (e.g., p27 or core antigens) in the cytoplasm of cells suspected of being infected with FeLV. The peripheral blood smear is generally used for the IF, but cytological preparations from bone marrow or other tissues may also be used. IF positive cats are considered persistently viremic and have a poor long
- term prognosis.

ELISA can be performed in veterinary clinics and detect the presence of FeLV p27 soluble. ELISA test detects antigenemia instead of viremia. There
are several types of test equipment available and most have a sensitivity and specificity of 98%. Accuracy can be improved by running both the IFA and ELISA in the same cat.

It can also perform diagnosis by molecular biology techniques in samples of whole blood or bone marrow to detect viral genome by PCR (polymerase chain reaction), and is very useful for diagnosing cases of false negative by ELISA or IF you have symptoms consistent with FeLV disease.

In IVAMI we perform laboratory diagnosis
by detecting the RNA genome of the virus followed by a transcription amplification (RT-PCR).

Recommended sample: EDTA whole blood (2 to 5 mL); bone marrow (1 mL).