[Frontiers in Bioscience 7, d504-518, Feburary 1, 2002]

INFECTIONS OF FELINE LEUKEMIA VIRUS AND FELINE IMMUNODEFICIENCY VIRUS

Takayuki Miyazawa

Research Center for Emerging Infectious Diseases, Research Institute for Microbial Diseases, 3-1 Yamadaoka, Suita-city, Osaka 565-0871, Japan

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Classification of feline retroviruses
3.1. RD-114 virus
3.2. Endogenous FeLV-related sequences
3.3. Mac-1
3.4. FeLV
3.5. FIV
3.6. FeFV
4. General feature of FeLV infection
4.1. The genomic structure of FeLV
4.2. Immune responses to FeLV
5. Subgroups of FeLV
6. Natural resistance to FeLV-B
7. Receptors of FeLV-A, B and C
8. Cofactor for infection of FeLV-T
8.1. FeLIX
8.2. Paradox of FeLIX
9. Discordant clinical samples
10. General feature of FIV infection
10.1. The genomic structure of FIV
10.2. Immune responses to FIV
11. Receptors of FIV
12. Concluding remarks
13. Acknowledgements
14. References

1. ABSTRACT

Feline retrovirus infections have been extensively studied for more than 30 years as an animal model for the persistent infections and pathogenesis caused by retroviruses in general. Two retroviruses, feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV), have been recognized as causative agents of a variety of diseases including proliferative and degenerative diseases. Recent studies revealed the receptors of FeLV, its variants and FIV. FeLVs utilize at least three distinct receptors, two of which have been successfully cloned and characterized. Furthermore, an FeLV variant which induces severe immunodeficiency, utilizes a truncated envelope of the endogenous FeLV as coreceptor or cofactor for viral entry. FIV utilizes as receptor one of the chemokine receptors, CXCR4 which also is a coreceptor for the T-lymphotropic human immunodeficiency virus. This review provides an overview to the infections of FeLV and FIV, specifically focuses on the viral genomic structures, FeLV variants, the immune responses and recent findings on the receptors for FeLV and FIV. Better understanding of retroviral persistence and pathogenesis will aid the development of prophylactic vaccines and therapeutic medicine to interfere with retrovirus infections.