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| | ==Pathogenesis== | | ==Pathogenesis== |
| − | *Receptor: CD134, found on monocyte-derived macrophages and activated T cells
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| − | **Net effect: disruption of acquired immune response
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| − | *Infected cats develop antibody whether or not they are able to clear the virus
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| − | Two versions:
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| − | *'''Avirulent''':
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| − | **Transient infection with no CD4 decline
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| − | *'''Virulent''':
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| − | **Progressive CD4 decline with three stages (may present indistinct)
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| − | **#'''High circulating virus''' for 1-10 weeks with resulting lymphoid depletion and CD8CD4 double positive Tcell destruction, '''thymic aplasia''' esp in kittens
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| − | **#'''Remission''': decrease in circulating virus as immune response increases, followed by '''immune exhaustion'''
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| − | **#*Increase in CD8+ production and antibody response
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| − | **#*Paracortical T cells and lymphoid follicles expand in primary and secondary lymph tissue and may be visible as '''white nodules'''
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| − | **#'''Rapidly progressing infection''' with high virus present
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| − | **#*Feline AIDS presents in a minority of cases
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| − | **#*Nonregenerative anemia
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| − | **#*Leucopenia
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| − | **#*Neutropenia
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| − | **#*[[Viral skin infections - Pathology#Other viruses|Skin infections]]
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| − | **#*Usually followed by secondary infection as a result of '''immunosuppression'''
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| − | **#*Virus-ridden T cell destroy normal T cells, causing chronic immunosuppression
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| | ==Signalment== | | ==Signalment== |