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Research Updates in Medical Sciences (RUMeS) 2015, Volume 3; Issue 1 page 75 – 76. Editorial Feline Infectious Peritonitis: The Fatal Disease of the Feline. Ahmad Naqib Shuid Institut Biosains, University Putra Malaysia, Serdang, Selangor, Malaysia Advanced Medical and Dental Institute (AMDI), Universiti Sains Malaysia, Kepala Batas, Pulau Pinang, Malaysia Correspondence should be addressed to Ahmad Naqib Shuid, [email protected] Received 8-01-2015; Accepted 15-01-2015 Copyright © 2014 Naqib et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. How to cite: Naqib et al., 2015, Feline Infectious Peritonitis: The Fatal Disease of the Feline. 3(1) : 75– 76. Feline coronavirus (FCoV) is a positive single stranded RNA virus that is ubiquitous in cat populations. Depending on FCoV strains, the virus is able to cause different types of diseases from asymptomatic mild enteritis to a highly systemic immune-mediated fatal infection called feline infectious peritonitis (FIP). FIP is caused by a virulent form of feline coronavirus known as feline infectious peritonitis virus (FIPV) that arises from mutation of feline enteric coronavirus (FECV). Meanwhile, FECV only caused mild enteritis in cats. It is believed that FECVs and FIPVs came from a common ancestry [1]. FIPV strain WSU 79-1146 and FECV strain WSU 79-1683 and several different strains of FIPV and FECV have been studied, respectively [2]. FECV infect the cell of the intestinal mucosa of kittens and can cause from mild to moderate transient enteritis [3]. This is in contrast to FIPV which can cause fatal systemic disease. FIP was first recognized in the 1950’s [4] and considered the leading cause of death among pedigree cats and cats from shelters [1]. In addition, it has been suggested that the presence of cat antibodies might have accelerated FIP development [5]. Despite over 40 years of research, the mechanisms of FIPinduced disease and immunity in cats are still not clear. FIPV utilize several immune evasion mechanisms to avoid clearance of infected cells by the humoral immune response [6]. As a result, FIPV may developed into two types of infection namely dry or wet FIP. High humoral response without cell mediated immunity (CMI) resulted in the most common form of FIP referred to as wet FIP. Wet FIP causes inflammation of the linings of the abdominal viscera, and less commonly of the thoracic organs. On the other hand, poor CMI response leads to dry forms of FIPV, characterized by type IV hypersensitivity [7]. Dry FIP is the more chronic form of the disease that often ends up with jaundice, weight loss, diarrhea, ataxic and fever. Innate and adaptive immunity are two equally important component of the immune system. Innate immunity is rapid and nonspecific while adaptive immunity is specific but requires time to produce response after infection. Helper T cells or CD4+ lymphocytes are mediators in adaptive immune response. There are two major subtypes of effector CD4+ T helper cell known as the Type 1 helper T cells (Th1) and Type 2 helper T cells (Th2) [8]. Th1 dominates CD4+ T lymphocytes response in virus infection, which is influenced by the presence of interferon gamma (IFN-g) and interleukin 12 (IL-12). Th2 with the help of interleukin-10 (IL-10) promote humoral immunity in response to viral infections. However, the role of humoral immunity in protection against FIPV is controversial and apart from that FIPV infection also impairs CMI responses. Antibody-dependent enhancement (ADE) might play a role in FIPV infection which is likely to be mediated by opsonisation of the virus facilitating viral uptake by macrophages [9] that enables the virus to infect and replicates in the macrophages [3]. However, the role of ADE in natural infection is not clear as in the 75 fields, cats were most likely to develop FIP on first exposure to FCoV [10]. 2744. FIP can be treated with cytotoxic drugs and steroids. These drugs merely improve the quality of life and may prolong the cat’s life for a few months, but the prognosis is still poor. References 1. Vennema H., Poland A., Foley A. and Pedersen N. Feline infectious peritonitis viruses arise by mutation from en- demic feline enteric coronaviruses. Journal of Virology 1998. 243(1): 150–157. 2. Pedersen N.C., Allen C. E. and Lyons L. A. Pathogenesis of feline enteric coronavirus infection. Journal of Feline Medicine and Surgery 2008. 10(6): 529–541. 3. Rottier P., Nakamura K., Schellen P., Volders H. and Haijema B. Acquisition of macrophage tropism during the pathogenesis of feline infectious peritonitis is determined by mutations in the feline coronavirus spike protein. Journal of Virology 2005.79(22): 14122–14130. 4. Holzworth J. Some important disorders of cats. Cornell Veterinary Medicine 1963. 53:157–160 5. Dewerchin, H. L., Cornelissen, E. and Nauwynck, H. J. Feline infectious peritonitis virus–infected monocytes internalize viral membrane–bound proteins upon antibody addition. Journal of General Virology 2006. 87: 1685–1690. 6. Cornelissen E., Dewerchin H.L., Van Hamme E., Nauwynck H.J. Absence of surface expression of feline infectious peritonitis virus (FIPV) antigens on infected cells isolated from cats with FIP. Veterinary Microbiology 2007. 31;121(1–2):131–137 7. Paltrinieri S., Cammarata Parodi M., Cammarata G., Mambretti M. Type IV hypersensitivity in the pathogenesis of FIPV–induced lesions. Zentralblatt Veterinary Med B Journal 1989. 45(3):151–159. 8. Whitmire J.K., Asano M.S., Murali–Krishna K., Suresh M. and Ahmed R. (1998). Long–term CD4 Th1 and Th2 memory following acute lymphocytic choriomeningitis virus infection. Journal of Virology 72(10):8281–8228 9. Corapi W.V., Darteil R.J., Audonnet J.C. and Chappuis G.E. Localization of antigenic sites of the S glycoprotein of feline infectious peritonitis virus involved in neutrali- zation and antibody–dependent enhancement. Journal of Virology 1995. 69(5): 2858–2862. 10. Addie D.D., Schaap I.A., Nicolson L. and Jarrett O. Persistence and transmission of natural type I feline coronavirus infection. Journal of General Virology 2003. 84(10):2735– 76