Broadening the use of antiretroviral therapy: the case for feline leukemia virus

Figures & data

Table 1 Description of feline leukemia virus (FeLV) subtypes, their tropism, and prevalence in infected cats

FeLV subtypea	Tropism	Receptor used for entry	Prevalence in infected cats	Other
A	Kidney, liver, T-cells, small intestines	THTR1 (thiamine transport protein)	100%	Considered original transmitted FeLV
B	Wide range of tissues	Pit1 and Pit2	Occurs with FeLV A in 49% of infected cats	Arose through recombination of FeLV A and endogenous sequences
C	Erythroid progenitor cells	FLVCR1 (heme exporting protein)	1%	Arose through mutations in FeLV A env
T	T cells	Pit1 in combination with co-receptor, FeLIX	Unknown	Arose from evolution of FeLV A (mutation and recombination)

Notes:

a The four subtypes of FeLV arose through mutation and recombination. Each subtype uses different host receptors for cell entry, resulting in different tissue tropism. For more information on FeLV subtypes, see text and references therein.

Figure 1 Pathogenesis of feline leukemia virus (FeLV) showing common entry route of virus, sites of viral replication, and pathological consequences of infection.