FIV associated neoplasms-A mini-review

被引:28
作者
Magden, Elizabeth [1 ]
Quackenbush, Sandra L. [1 ]
VandeWoude, Sue [1 ]
机构
[1] Colorado State Univ, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA
关键词
Feline immunodeficiency virus; FIV; Neoplasia; Tumorigenesis; Lymphoma; FELINE IMMUNODEFICIENCY VIRUS; KAPOSIS-SARCOMA; LEUKEMIA-VIRUS; MALIGNANT-LYMPHOMA; (FIV)-ASSOCIATED LYMPHOMA; INDUCED ONCOGENESIS; AUSTRALIAN CATS; AFRICAN LIONS; DNA-SEQUENCES; UNITED-STATES;
D O I
10.1016/j.vetimm.2011.06.016
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Retroviral induced neoplasms have been key to understanding oncogenesis and are important etiologic agents associated with cancer formation. Cats infected with feline immunodeficiency virus (FIV), the feline analogue to human immunodeficiency virus (HIV), are reported to be at increased incidence of neoplasia. This review highlights reported risk factors and tumor cell phenotypes associated with neoplasias arising in FIV-infected animals, differences in oncogenic disease in natural versus experimental FIV infections, and similarities between FIV- and HIV-related malignancies. The most common type of FIV-associated neoplasm reported in the literature is lymphoma, specifically of B-cell origin, with experimentally infected cats developing neoplastic lesions at an earlier age than their naturally infected cohorts. The mechanism of FIV-induced lymphoma has not been completely ascertained, though the majority of published studies addressing this issue suggest oncogenesis arises via indirect mechanisms. HIV-infected individuals have increased risk of neoplasia, specifically B cell lymphoma, in comparison with uninfected individuals. Additional similarities between FIV- and HIV-associated neoplasms include the presence of extranodal lymphoma, a synergism with other oncogenic viruses, and an apparent indirect mechanism of induced oncogenesis. This literature supports study of FIV-associated neoplasms to further characterize this lentiviral-neoplasia association for the benefit of both human and animal disease, and to advance our general knowledge of mechanisms for viral-induced oncogenesis. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:227 / 234
页数:8
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