**Feline Immunodeficiency**

Fabiana Alves and Jenner Karlisson Pimenta dos Reis

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/51631

**1. Introduction** 

356 Immunodeficiency

[231] Overbaugh, J., et al., Variation in simian immunodeficiency virus env is confined to V1

[232] Shibata, R., et al., Infection and pathogenicity of chimeric simian-human immunodeficiency viruses in macaques: determinants of high virus loads and CD4 cell

[233] Thigpen, M.C., Kebaabetswe, P.M., Smith, D.K., Segolodi,T.M. , Soud, F.A., Chillag, K., Chirwa, L.I., Kasonde, M., Mutanhaurwa, R., Henderson, F.L., Pathak, S., Gvetadze, R., Rose,C.E., Paxton, L.A., for the TDF2 Study Group. Daily oral antiretroviral use for the prevention of HIV infection in heterosexually active young adults in Botswana: results from the TDF2 study. in 6th IAS Conference on HIV

[234] Microbicide Trials Network Statement on Decision to Discontinue Use of Tenofovir

[235] MTN Statement on Decision to Discontinue Use of Oral Tenofovir Tablets in VOICE, a

[236] Hirsch, V.M., et al., Simian immunodeficiency virus infection of macaques: end-stage disease is characterized by widespread distribution of proviral DNA in tissues. J Infect

[237] Dewhurst, S., et al., Sequence analysis and acute pathogenicity of molecularly cloned

[238] Dewhurst, S., et al., Molecular clones from a non-acutely pathogenic derivative of SIVsmmPBj14: characterization and comparison to acutely pathogenic clones. AIDS Res

[239] Benveniste, R.E., et al., Isolation of a lentivirus from a macaque with lymphoma: comparison with HTLV-III/LAV and other lentiviruses. J Virol, 1986. 60(2): p. 483-90. [240] Benveniste, R.E., et al., Characterization of clones of HIV-1 infected HuT 78 cells defective in gag gene processing and of SIV clones producing large amounts of

[241] Benveniste, R.E., et al., Inoculation of baboons and macaques with simian immunodeficiency virus/Mne, a primate lentivirus closely related to human

[242] Kimata, J.T., A. Mozaffarian, and J. Overbaugh, A lymph node-derived cytopathic simian immunodeficiency virus Mne variant replicates in nonstimulated peripheral

[243] Kimata, J.T. and J. Overbaugh, The cytopathicity of a simian immunodeficiency virus Mne variant is determined by mutations in Gag and Env. J Virol, 1997. 71(10): p. 7629-

and V4 during progression to simian AIDS. J Virol, 1991. 65(12): p. 7025-31.

killing. J Infect Dis, 1997. 176(2): p. 362-73.

Major HIV Prevention Study in Women, 2011.

SIVSMM-PBj14. Nature, 1990. 345(6276): p. 636-40.

Hum Retroviruses, 1992. 8(6): p. 1179-87.

Dis, 1991. 163(5): p. 976-88.

39.

Pathogenesis, Treatment and Prevention 2011. Rome, Italy.

Gel in VOICE, a Major HIV Prevention Study in Women 2011.

envelope glycoprotein. J Med Primatol, 1990. 19(3-4): p. 351-66.

immunodeficiency virus type 2. J Virol, 1988. 62(6): p. 2091-101.

blood mononuclear cells. J Virol, 1998. 72(1): p. 245-56.

Classic infectious causes of immunodeficiency in felines are the immunodeficiency by retroviruses, including feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV). Immunodeficiency caused by these infectious agents may result from disruption of normal host barriers or deregulation of cellular immunity.

The feline immunodeficiency virus and the feline leukemia virus are detected worldwide and are among the most common infectious diseases of domestic cats, others small felids and wild cats, and causes immunodeficiency, with increased risk for opportunistic infections, neurologic diseases, and tumors.

Feline immunodeficiency virus and feline leukemia virus are retrovirus, but they differ in their potential to cause disease. FIV is classified as a *Lentivirus* and, FeLV as a *Gamaretrovirus*. The high incidence of FIV and FeLV is associated with density of cat population.

FIV causes immune dysfunctions in cats similar to those observed in people infected with human immunodeficiency virus (HIV). Diseases associated with FeLV and FIV may affect some organ, and may cause among other disorders, lymphoma, blood dyscrasias, alterations in the function of central nervous system, and secondary and opportunistic infections, with a significant number of opportunistic pathogens of viral, bacterial, protozoal, and fungal origin. Therefore, infected animals may play a role in transmission of various pathogens to human beings.

Risk groups for infection with FIV and FeLV are different: FIV is mainly associated with males, free access to streets and bites inflicted during fights for territory, therefore, the risk of FIV transmission is low in socially well-adapted cats, while FeLV infection is associated with social contacts and thus the FeLV infection is found almost equally between males and females, at a rate slightly elevate in male cats.

© 2012 Alves and Pimenta dos Reis, licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2012 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The diagnosis of FIV and FeLV can not be done based solely on clinical signs, but should be based on the demonstration of anti-FIV and FeLV antigen in the serum of infected animals.

Feline Immunodeficiency 359

efficacy of colostral immunity is not known (Sellon & Hartmann, 2006; Medeiros et al.,

FIV has a tropism for T cells, macrophages, dendritic cells and central nervous system cells. The major targets for FIV infection are activated CD4+ T lymphocytes (Fig. 1). These cells typically function as T helper cells, which have a central role in immune functions, facilitating the development of humoral and cell-mediated immunity (Fig. 1) (Sellon and Hartmann, 2006; Hosie et al., 2009; Simões et al., 2012) . FIV does not use CD4 as a primary *binding* receptor, its gp120 glycoprotein binds to the CD134 (OX40) a member of the tumor necrosis factor receptor (TNFR)/nerve growth factor receptor family of molecules as the binding receptor in conjunction with the chemokine receptor CXCR4 as a cofactor for infection (Yuan et al., 2003; de Parseval et al., 2005; Willett et al., 2006b; Elder et al., 2010). The CD134 co-stimulatory pathway has been shown to be critical for T, B and antigenpresenting cell (APC) cell activation. Studies have shown that antigen stimulation of infected B-cells is increased compared with non-infected cells. FIV-infection in cats also results in a sustained polyclonal activation of B-cells with the production of antibodies to a

**2.2. Pathogenesis, immunity and clinical symptoms** 

variety of non-viral antigens (Yuan et al., 2003; Willett et al., 2006b).

**Figure 1.** Diagram illustrating the stages of the pathogenesis of FIV. Modified from Sellon and

2012).

Hartmann, 2006.

FeLV and FIV do not survive for long outside the host and are easily inactivated by disinfectants, heating and drying. As prophylaxis against infection of FIV and FeLV is recommended castration to reduce aggression and lessen the bite. The rapid and accurate diagnosis of any secondary diseases is essential. In shelters, infected cats should be housed individually to prevent infection. All animals should be tested before being placed in shelters and breeding. Vaccines are available for both viruses; however, identification and segregation of infected cats remains the cornerstone for preventing new infections.

Studies and research about these viruses are continuously necessary to define prophylactic, management, and therapeutic measures for stray, feral and owned cats.
