PATHOGENESIS

          
The pathogenesis varies in cats, depending on immune status of the cat, virulence of the virus, and dose of virus the cat came into contact with. 

There are several stages in the disease process:

1) INITIAL ORONASAL INFECTION

            The virus replicates in oropharyngeal lymphoid tissue. 

2) IMMUNE FUNCTION

What happens next depends on the cat’s immune system:

a) An immunocompetent cat uses its cell-mediated immunity to inhibit further viral replication and eliminate it from the body.  The cat develops high levels of neutralizing antibody so the virus cannot become systemic.  If blood is tested, FeLV is not detected, but high levels of anti-FeLV antibody are found.  These cats are called REGRESSOR cats (3).  They are free of infection and are now immune to further FeLV infection.

OR

b) An immunosuppressed cat cannot prevent viral replication and the infection becomes systemic by virus traveling in lymphocytes and monocytes through the circulation.  A blood sample will reveal detectable FeLV p27 protein (3).

 

path flow chart

(3)

3) VIREMIA

A cat with systemic virus is viremic.  This occurs 2-4 weeks post-infection.  The virus is carried to the thymus, spleen, lymph nodes, and salivary glands.  At this stage, the cat shows signs of malaise, fever and lymphadenomegaly (5).

If the cat has a transient viremia, the virus can be removed completely from the cat within 3-6 weeks on average (maximum of 16 weeks).  While the cat’s immune system is trying to remove the virus, cats are infectious and shed the virus (3).  The virus has not yet infected the bone marrow at this stage. 

***70% of infected cats show transient viremia.  Once it is cleared, they are immune to recurrent infection of FeLV (5).           

4) BONE MARROW INFECTION

The longer viremia persists, the harder it is to clear.  When the virus infects hematopoietic cells of the bone marrow at ~3 weeks, the condition worsens.  All granulocytes are infected as well as platelets because the hematopoietic cells are precursors for these cell lines (5).

Cats can still remove the viremia at this stage, but they cannot completely clear the virus since the provirus has inserted into the bone marrow stem cell DNA.  They end up with a latent infection.  No virus is produced at this time because the proviral DNA is not translated, so the cats will test negative for FeLV (5).  Latent infections are not really clinically significant to the veterinarian because these cats cannot spread the infection.

Latent infections can eventually be eliminated at 9 – 16 months.  If not eliminated, a latent infection can reactivate under various stimuli such as stress, glucocorticoid administration, and other immunosuppressive drugs (3).  Upon reactivation, the cat becomes viremic once again and sheds the virus.  The longer the virus remains latent, the harder it is to reactivate because the provirus is slowly being deleted from the precursor blood cells (5).

In ~30% of cats, the viremia persists for longer than 16 weeks.  It is not cleared and so becomes a persistent viremia.  Cats are unable to mount a good enough immune response to remove the virus.  This is a permanent and eventually fatal condition within 3 years of initial infection.  They die of FeLV-related diseases.  These cats remain infectious throughout life and only have low levels of circulating neutralizing antibodies.  A cat exposed to the virus once has a low chance of developing persistent viremia.  A cat that is continually being exposed to contagious cats has an increased risk of developing persistent viremia (3).

5) EPITHELIAL INFECTION

The virus spreads to epithelium of lacrimal glands, salivary glands, intestine, and urinary bladder at 3-4 weeks.  At this stage, cats can have up to 1 million virus particles per milliliter of saliva (3).

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