Showing posts with label feline infectious peritonitis. Show all posts

Thursday, January 10, 2013

Evolving insights into FIP virulence

Terada Y, Shiozaki Y, Shimoda H, et al. Feline infectious peritonitis virus with a large deletion in the 5'-terminal region of the spike gene retains its virulence for cats. The Journal of general virology. 2012; 93: 1930-4.

The acquisition of macrophage tropism appears to be an essential step in the transformation of feline enteric corona virus (FECV) to feline infectious peritonitis virus (FIPV).This is a transformation from a largely non-pathogenic and localized enterocyte pathogen to a highly virulent and systemic monocyte/macrophage pathogen. Therefore, determining the critical genetic mutation(s) leading a change in tropism is required for understanding the pathogenic phenomena of feline coronavirus (FCoV) infections. Although various viral proteins such as 3c and 7b have been considered to be involved in the transformation, the spike (S) protein may also play a role in a switch toward macrophage tropism and enhanced virulence.

In coronaviruses, the S protein functions in cell entry and is responsible for receptor attachment and membrane fusion. While the receptor-binding site is located in the N-terminal part of the protein, fusion is mediated by its membrane proximal part. Surprisingly, previous studies have suggested virulence mutation(s) in the S protein occur in the membrane-proximal domain of the protein and not in the N-terminal region.

In the present study, a type I FCoV strain, C3663, was found to have a large deletion of 735 bp within the gene encoding for the S protein, resulting in an estimated 245 amino acid loss in the N-terminal region of the protein. FIP developed in three out of four cats that were infected with strain C3663, suggesting that the 5’-terminal region of the S gene is not essential for pathogenic transformation. If the S protein is indeed involved in the transformation and development of FIP, then this result is consistent with the localization of the determinant for macrophage tropism lying in the domain responsible for membrane fusion suggesting a role for fusion function rather than for receptor binding. [GO]

See also: Rottier PJ, Nakamura K, Schellen P, Volders H and Haijema BJ. Acquisition of macrophage tropism during the pathogenesis of feline infectious peritonitis is determined by mutations in the feline coronavirus spike protein. J Virol. 2005; 79: 14122-30.

Related blog articles:
Understanding FIP virulence (October 2012)
Development of new therapies for FIP (March 2012)

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Understanding FIP virulence

Chang HW, Egberink HF, Halpin R, Spiro DJ and Rottier PJ. Spike protein fusion peptide and feline coronavirus virulence. Emerg Infect Dis. 2012; 18: 1089-95. [free, full text article]

Coronaviruses are enveloped RNA viruses known for their potential to change their cellular tropism. Tropism refers to the specificity of a virus for a particular host tissue, determined in part by the interaction of viral surface structures with receptors present on the surface of unique host cell (e.g., endothelial cells, macrophages). Whether tropism switching leads to cross-species transmission as happened with severe acute respiratory syndrome (SARS-CoV) jumping from bats to humans or, as in the case of feline coronaviruses, switching leads from a relatively low virulence enteric virus (FECV) to a systemic pathogenetic form (FIPV), it is clear that this family of viruses is an important public health concern and feline pathogen. In the case of FECV, identifying the genetic mutation(s) leading to this tropism switching still remains a quandary for researchers, veterinarians, and cat owners alike.

The researchers in this study compared full genome sequenced data from 11 viruses in each pathotype and identified the most distinctive site(s) by further refining sequence variation between the two pathotypes around those site(s). Two putative sites that both code for regions in the fusion peptide domain of the spike protein were found to distinguish FECV from FIPV, accounting for > 95% of cases. The S protein functions in cell entry via receptor attachment (involving the N terminus) and membrane fusion (membrane-proximal domain). These researchers further speculate that these two mutations in addition to other mutations likely within the accessory 3c gene account for switching to the virulent FIPV form. [GO]

See also: Pedersen NC, Liu H, Scarlett J, et al. Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats. Virus Research. 2012; 165: 17-28.

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Chang HW, Egberink HF, Halpin R, Spiro DJ and Rottier PJ. Spike protein fusion peptide and feline coronavirus virulence. Emerg Infect Dis. 2012; 18: 1089-95. [free, full text article]

Revealing more about FIP

Pedersen NC, Liu H, Scarlett J, et al. Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats. Virus Research 2012;165:17-28.

Feline infectious peritonitis (FIP) is a complex disease involving a mutant coronavirus. The specific mutation that occurs allowing this normally innocuous virus to cause a fatal disease remains unclear. A particular virus protein, the 3c protein, has been investigated as a possible viral mutational site contributing to disease development. These investigators found that this protein appears to be involved with the ability of the virus to replicate in the intestines. Mutations in the gene for this protein lead to the virus being unable to replicate in the intestinal tract and thus unable to be shed in feces. More than half of the FIP viruses they analyzed had a mutation in the 3c gene. This may explain why FIP outbreaks with cat-to-cat transmission of the mutant virus rarely occurs – it is simply no longer shed in feces once this mutation occurs. While we still don’t know what makes the FIP virus so nasty, we have gained a better understanding of its strange epidemiology. [MK]

See also: Brown MA. Genetic determinants of pathogenesis by feline infectious peritonitis virus. Vet Immunol Immunopathol 2011;143:265-268.

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Risk factors for FIP in Australian cats

Worthing KA, Wigney DI, Dhand NK, et al. Risk factors for feline infectious peritonitis in Australian cats. J Feline Med Surg 2012;14:405-412.

The purpose of this study was to determine whether patient signalment (age, breed, sex, and neuter status) is associated with naturally-occurring feline infectious peritonitis (FIP) in cats in Australia. FIP is a feline coronavirus-induced disease. There have been several risk factors discussed in association with the development of FIP. The disease is more frequent in cats less than 2 years of age, cats that reside in multi-cat environments, and in pedigreed cats. Early studies suggested FIP has a bimodal age distribution, though recent studies do not support this observation. In this study, the patient signalment of 382 confirmed cases of FIP were compared with a general cat population. Younger cats were significantly over-represented among FIP cases and a bi-modal age distribution was not found. Pedigreed cats were significantly over-represented and domestic crossbreeds under-represented in FIP cases. Several breeds were over-represented, including British Shorthair, Devon Rex, and Abyssinian. Male cats had a significantly higher proportion of representation than female cats. Domestic crossbred, Persian, and Himalayan cats were significantly under-represented in the FIP cohort of this study. [VT]

See also: Pesteanu-Somogyi L, Radzai C, Pressler B. Prevalence of feline infectious peritonitis in specific cat breeds. J Feline Med Surg 2006;8:1-5.

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Worthing KA, Wigney DI, Dhand NK, et al. Risk factors for feline infectious peritonitis in Australian cats. J Feline Med Surg 2012;14:405-412.

Ultrasound Findings in Cats with FIP

Lewis KM, O'Brien RT: Abdominal ultrasonographic findings associated with feline infectious peritonitis: a retrospective review of 16 cases, J Am Anim Hosp Assoc 46:152, 2010.

Feline enteric coronavirus (FeCV) is especially contagious and present throughout the domestic cat population. Feline infectious peritonitis virus (FIPV) is considered to be a mutated form of FeCV. Risk factors for FIP include cats living in multicat households or a cattery, being sexually intact, being less than 5 years of age, and being purebred. There are two forms of FIP that have been described. An effusive form is an immune-mediated vasculitis with the subsequent loss of protein-rich fluid into such areas as the pleural or peritoneal cavities. The non-effusive form involves pyogranulomatous or granulomatous inflammation in multiple organs. This study was a retrospective review of 16 cases analyzing abdominal ultrasonographic results where necropsy or findings were highly suggestive of FIP. This study found that 75% of diagnosed FIP cases had abdominal effusion. Renomegaly was also a frequent finding in this study, while the majority of the feline livers examined in this study were described as normal on ultrasound. In the majority of cases with FIP, the spleen also had a normal ultrasonographic appearance while the spleen is found to be diffusely affected. Almost half of the study population did not have abdominal lymphadenopathy. None of the ultrasonographic findings were found to be specific for FIP, a combination of findings should increase the index of suspicion for FIP when considered along with appropriate clinical signs. On the other hand, a normal abdominal ultrasound does not exclude the possibility of FIP. [VT]

Feline Coronavirus Persistence in Healthy Cats

Kipar A, Meli ML, Baptiste KE, et al. Sites of feline coronavirus persistence in healthy cats. J Gen Virol March 17, 2010.

Feline coronavirus (FCoV), the agent of FIP, is transmitted by the fecal-oral route. Some cats infected with FCoV do not clear the virus, and shed the virus either persistently or intermittently. These cats are important sources of the virus in cat populations. These investigators examined the tissues of infected cats in order to identify the organ site of viral persistence in healthy carriers. Overall, the colon tested positive for virus more than any other tissue over time. Interestingly, all organs, including brain and skin, tested positive for virus in at least one cat during the investigatory period, indicating that FCoV infection disseminates to many organs during infection, even in healthy cats. Cats shedding the virus were found to be infected not only in the colon, but also in the small intestine (jejunum and ileum); in addition, the amount of virus present was an important determinant of shedding in feces, with higher amounts leading to viral shedding as one would expect. While the colon was the primary site for viral persistence and the source of continued shedding over the long-term, spread of the virus to the small intestines appears to be necessary for detectable fecal shedding. This would explain the intermittent nature of virus shedding in carrier cats. In addition, it was found that other tissues outside the gut may remain persistently infected as well, and could serve as a source for recurrent viremia. Most commonly, the mesenteric, or abdominal lymph nodes, and liver were sites of viral persistence. In these tissues, it appears that the resident macrophages are the specific cells involved. Thus, even cats that clear the virus from the intestines may remain virus-infected. [MK]

Related articles:
Goodson TL, Randell SC, Moore LE. Feline infectious peritonitis. Compend Contin Educ Vet 2009;31.

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Genetics of Feline Infectious Peritonitis Virus

Chang HW, de Groot RJ, Egberink HF et al.: Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene, J Gen Virol 91:415, 2010.

The virus of the lethal disease, feline infectious peritonitis (FIP), is closely related to the relatively innocuous form of feline coronavirus (FCoV). There is genetic and animal experimental evidence to indicate that the disease-causing form evolves time and time again from the harmless one by mutation in individual infected cats. What this specific mutation in the virus is remains unknown. One possible gene that may be involved, termed the “3c” gene, encodes a viral protein of unknown function. Previous studies have identified mutations in this gene that may be associated with FIP development. In this report, the investigators examined the 3c gene in the coronavirus infecting 27 healthy cats and 28 cats diagnosed with FIP in order to compare the viruses in this genetic region. Interestingly, the 3c gene in the virus of healthy cats was always intact, with no mutations. However, in cats with FIP, the majority (20/28) of viruses had mutations in this gene, varying from minor changes in a few amino acids to major changes leading to lack of function of the encoded protein. The researchers also tested the feces of cats with FIP for coronavirus. Virus was found in only 6 of 17 cats, indicating that in most cats with FIP, coronavirus has been cleared from the intestines and is only present in the tissues. In samples from 6 cats in which virus were detected, the 3c gene either had no mutations (5/6) or only one amino acid change (1/6). These investigators proposed the following scenario: Cats become infected by circulating virus that replicates in the gut. Replication in this compartment and efficient fecal shedding strictly require an intact viral 3c gene. A mutation in the virus occurs continually, one or more of which incidentally provides the virus with the ability to replicate in macrophages and monocytes, which then spread the – now FIPV – infection to organs throughout the body. Once in this new environment, virus propagation no longer requires the 3c gene; thus, mutations readily occur in the gene that may even improve the virus’ replication in tissue. The result is the disease feline infectious peritonitis. [MK]

Related articles:
Brown MA, Troyer JL, Pecon-Slattery J et al.: Genetics and pathogenesis of feline infectious peritonitis virus, Emerg Infect Dis 15:1445, 2009.

Pedersen NC: A review of feline infectious peritonitis virus infection: 1963-2008, Journal of Feline Medicine & Surgery 11:225, 2009.

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Characterization of FIP Mutants

Pederson N, Liu H, Dodd K, Pesavento P. Significance of coronavirus mutants in feces and diseased tissues of cats suffering from feline infectious peritonitis. Viruses. 2009;1(2):166-184.

This article describes viral characterization of the feline coronavirus found in feces versus diseased tissues of cats with feline infectious peritonitis (FIP). The researchers found that within a single cat, the viruses found in the intestinal tract and diseased tissue were almost 100% identical genetically. Minor differences were found in several of the genes of feline coronaviruses. Notably, the gene encoding a virus protein whose function remains unknown, the 3c protein, was almost always mutated in viruses found in FIP lesions. These mutations, while minor, are predicted to lead to a dysfunctional protein product. Viruses from the feces of these same cats however, almost always had intact, functional 3c genes. While the 3c mutation is not universal among FIP virus isolates, it does occur in the majority, and is speculated to play a significant role in FIP development. From this study, it also appears that the FIP mutants arose separately in each affected cat, rather than spreading cat-to-cat. Thus, horizontal transmission of FIP does not readily occur. More research into the function of the 3c gene product is needed to define its role in FIP. [MK]

Related articles:
Pedersen NC. A review of feline infectious peritonitis virus infection: 1963-2008. Journal of Feline Medicine & Surgery. 2009;11(4):225-258.

Vennema H, Poland A, Foley J, Pedersen NC. Feline infectious peritonitis viruses arise by mutation from endemic feline enteric coronaviruses. Virology. Mar 30 1998;243(1):150-157.

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Potential Treatment for FIP

Legendre, A.M. and J.W. Bartges, Effect of polyprenyl immunostimulant on the survival times of three cats with the dry form of feline infectious peritonitis. Journal of Feline Medicine & Surgery, 2009. 11(8): p. 624-626.

Feline infectious peritonitis (FIP) is a baffling and clinical important disease of cats caused by a virulent biotype of feline coronavirus. Despite the fact that the disease is relatively common, veterinarians are faced with a frustrating dilemma because there are no individual tests that are reliable for the diagnosis of FIP, the clinical picture is highly variable, and there is no known effective treatment. Polyprenyl immunostimulant (PI) is an investigational veterinary biologic manufactured by Sass & Sass, Inc and is comprised of a mixture of phosphorylated, linear polyisoprenols. This case series from the University of Tennessee describes three cats with the dry (non-effusive) form of FIP treated with PI. The cats were treated with varying doses of the drug, and by both subcutaneous and oral routes. Two of the three cats were still on treatment and were alive and well 2 years after diagnosis. The third cat survived 14 months but was treated for only 4.5 months. The investigators conclude that further studies to assess the therapeutic efficacy of PI for the treatment of FIP are warranted. [SL]
>> PubMed Abstract

Related Articles:
Addie, D., et al., Feline infectious peritonitis ABCD guidelines on prevention and management. J Feline Med Surg, 2009. 11(7): p. 594-604.
>> Full text article

Pedersen, N.C., A review of feline infectious peritonitis virus infection: 1963-2008. Journal of Feline Medicine & Surgery, 2009. 11(4): p. 225-258.
>> PubMed Abstract

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Pathogenesis of Feline Coronavirus Infection

Pedersen, N.C., C.E. Allen, and L.A. Lyons, Pathogenesis of feline enteric coronavirus infection. Journal of Feline Medicine & Surgery, 2008. 10(6): p. 529-541.

The importance of feline enteric coronavirus (FECV) as a primary intestinal pathogen is considered minimal. The importance of FECV is that this virus can mutate in vivo. At least one mutant form causes the highly fatal disease called feline infectious peritonitis (FIP). Initially, this study had been designed to demonstrate that resistance and susceptibility to FECV infection were under genetic control, just as genetics appear to play a significant role in FIP resistance. With more than 3 years of study results, it became apparent that genetics would not readily define this initial goal. The investigators made a decision to concentrate their efforts on what was learned about FECV pathogenesis. A distinct primary stage of infection was identified that lasted from 7 to 18 months, with the highest level of virus shedding during this phase. This primary stage resolved in one of the three following ways: 1) recovery, 2) persistent shedding, or 3) recurrent or intermittent shedding. During the primary phase, shedding levels were significantly higher in kittens than in adult cats. As kittens might be infected before their immune systems mature, FECV replication would be more frequent and increase the potential for FECV to FIP mutations. FIP is known to be more common in kittens than adult cats. The investigators also looked at the role of stress on reactivating latent or subclinical infection, or increasing virus shedding. They evaluated the role natural stress such as pregnancy, parturition, and lactation might play. Stress was also simulated by giving a series of corticosteroid injections using methylprednisolone acetate. No increase in virus shedding was reported in any of the scenarios. Virus shedding and serum antibody titers had a significant relationship to each other. Cats shedding virus usually had titers of 1:100 or higher. Cats that were not shedding virus usually had titers of 1:25 and lower. Additional observations on immunity to FECV infection found that immunity during the primary phase of infection was slow to develop, intermittent, and tenuous in duration. Immunity during re-infection tended to mirror that occurring during primary infection, indicating this immunity lacks memory. This pattern of infection and immunity is strongly influenced by environmental factors. [MK]
>> PubMed Abstract

Related articles:
Pedersen, N.C., A review of feline infectious peritonitis virus infection: 1963-2008. Journal of Feline Medicine & Surgery, 2009. 11(4): p. 225-258.
>> PubMed Abstract

Addie, D., et al., Feline infectious peritonitis ABCD guidelines on prevention and management. J Feline Med Surg, 2009. 11(7): p. 594-604.
>> Free full text article

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Understanding FIP

Regan, A.D., R.D. Cohen, and G.R. Whittaker, Activation of p38 MAPK by feline infectious peritonitis virus regulates pro-inflammatory cytokine production in primary blood-derived feline mononuclear cells. Virology, 2009. 384(1): p. 135-43.

Feline infectious peritonitis (FIP) is a fatal disease of cats associated with feline coronavirus (FCoV) infection, a common enteric virus of cats. How this virus leads to the lethal disease is not clear, as most infected cats do not develop disease. Cytokines are proteins secreted from cells, including cells of the immune system, that are important in mediating an effective immune response. Cats with FIP have abnormal cytokine production that may contribute to the disease FIP. In this study, the investigators examined the effects of the FIP virus on certain white blood cells collected from cats, in a laboratory environment. These cells are the target of the FCoV in cases of FIP. The investigators showed that an important cellular pathway responsible for inducing inflammation is activated by the virus, and is a key contributor to the disease observed in cats with FIP. The raises the possibility that inhibitors of this pathway may be beneficial in the treatment of FIP. [MK]
>> PubMed Abstract

Related articles:
Takano, T., et al., Neutrophil survival factors (TNF-alpha, GM-CSF, and G-CSF) produced by macrophages in cats infected with feline infectious peritonitis virus contribute to the pathogenesis of granulomatous lesions. Arch Virol, 2009.
>> PubMed Abstract

Giordano, A. and S. Paltrinieri, Interferon-gamma in the serum and effusions of cats with feline coronavirus infection. Vet J, 2009. 180(3): p. 396-8.
>> PubMed Abstract

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Skin Lesions Associated with FIP

Declercq, J., H. De Bosschere, et al. (2008). "Papular cutaneous lesions in a cat associated with feline infectious peritonitis." Vet Dermatol 19(5): 255-8.

This paper describes unusual lesions associated with a case of feline infectious peritonitis (FIP)– slightly raised intradermal papules that were not painful nor itchy. The 7 month old intact male domestic shorthair cat also had other indicators of FIP, such as fever, anterior uveitis, respiratory distress, and kidney abnormalities. The skin lesions were on the neck and thorax and difficult to see in these haired areas. Histopathologic analysis of these lesions along with immunohistochemistry revealed typical FIP lesions. If detected early in the disease process, analysis of similar skin lesions may help provide a diagnosis. [MK]
>> PubMed Abstract

Related articles:
Cannon, M. J., M. A. Silkstone, et al. (2005). "Cutaneous lesions associated with coronavirus-induced vasculitis in a cat with feline infectious peritonitis and concurrent feline immunodeficiency virus infection." J Feline Med Surg 7(4): 233-6.
>> PubMed Abstract

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Immunity and Feline Infectious Peritonitis

Giordano, A. and S. Paltrinieri (2009). "Interferon-gamma in the serum and effusions of cats with feline coronavirus infection." Vet J 180(3): 396-8.

Investigators from the University of Milan studied and compared the quantity of interferon-gamma concentrations in the serum of clinically normal cats infected with feline coronavirus (FCoV) with the concentrations in the sera and effusions of cats with feline infectious peritonitis (FIP), a disease associated with infection with a mutated form of FCoV. Interferon-gamma is a cytokine and an important modulator of cell mediated immunity. Cats with strong cell mediated immunity (CMI) either do not become infected with FCoV or develop the non-effusive form of FIP. Investigators divided cases into two major groups: Group A included cats with clinical FIP and Group B included FCoV infected clinically normal animals. Group A was further subdivided into two groups, those with non-effusive FIP (A1) and effusive FIP (A2). Group B was also subdivided into 2 groups where subgroup B1 included cats from catteries with a high prevalence of FIP and group B2 included cats from catteries with a low prevalence of FIP. Clinically normal FCoV-infected cats from catteries with a high prevalence of FIP had the highest level of serum interferon-gamma. The serum concentration of interferon-gamma was not significantly different in cats with FIP and the clinically normal FCoV-infected cats from catteries with a low prevalence of FIP. The effusions from cats with FIP had a significantly higher level (40 fold) of interferon-gamma than the serum in these cats. This suggests that cells within FIP lesions produce the interferon-gamma present in effusions. The investigators believe the results indicate that CMI is also likely to be involved in the pathogenesis of FIP, and interferon-gamma prevents the onset of FIP in some instances and could contribute to development of disease in others. [VT]
>> PubMed Abstract

Related articles:
Kipar, A., M. L. Meli, et al. (2006). "Natural feline coronavirus infection: differences in cytokine patterns in association with the outcome of infection." Vet Immunol Immunopathol 112(3-4): 141-55.
>> PubMed Abstract

Paltrinieri, S., C. Metzger, et al. (2007). "Serum alpha1-acid glycoprotein (AGP) concentration in non-symptomatic cats with feline coronavirus (FCoV) infection." J Feline Med Surg 9(4): 271-7.
>> PubMed Abstract

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Diagnosis of FIP

Winn funded research

Kennedy, M. A., M. Abd-Eldaim, et al. (2008). "Evaluation of antibodies against feline coronavirus 7b protein for diagnosis of feline infectious peritonitis in cats." American Journal of Veterinary Research 69(9): 1179-1182.

Feline infectious peritonitis (FIP) is a lethal, complex, and clinically important disease of cats caused by feline coronavirus (FCoV). FCoV occurs in two biotypes: one that is virulent and causes FIP, and one that is nonvirulent. FIP occurs in an effusive form characterized by pleural effusion or ascites, as well as a granulomatous form that may affect several organs. No consistent genetic difference has been identified that can distinguish all virulent from nonvirulent FCoVs. As a result, antemortem diagnosis of FIP is difficult because no test that is specific and sensitive for the FIP virus is available. It has been suggested that the product of the 7b gene is a virulence factor. If expression of the 7b protein consistently leads to FIP, cats infected with virulent FCoV would be expected to have measurable antibodies against this protein, whereas cats infected with the nonvirulent FCoV would not. This would allow differentiation of cats infected with virulent FCoV from those infected with a nonvirulent strain. The purpose of this study was to determine specific antibody concentrations against the 7b protein in cats with FIP or other diseases and healthy cats. Serum samples from 95 cats submitted for various diagnostic tests as well as 20 samples from specific pathogen free cats used as negative controls were tested for antibodies against the 7b protein. Serum from cats with FIP had antibodies against the 7b protein. However, some healthy cats, as well as cats with other diseases, were seropositive for the 7b protein. The researchers conclude that seropositivity for the 7b protein is not specific for the FCoV virulent biotype or a diagnosis of FIP.
>> PubMed abstract

Related articles:
Hartmann, K., C. Binder, et al. (2003). "Comparison of different tests to diagnose feline infectious peritonitis." J Vet Intern Med 17(6): 781-90.
>> PubMed abstract

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Feline Interferon as a Treatment for FIP

Ritz, S., H. Egberink, et al. (2007). "Effect of feline interferon-omega on the survival time and quality of life of cats with feline infectious peritonitis." J Vet Intern Med 21(6): 1193-7.

Feline infectious peritonitis (FIP) is a devastating disease of young cats with no known effective treatment. Feline interferon-omega (Virbagen Omega, Virbac) has been used in Europe and other parts of the world to treat FIP, but its efficacy is unknown. The drug is currently not available in North America. This study evaluated the efficacy of feline interferon-omega on the survival time and quality of life in 37 privately owned cats with naturally occurring FIP. The study was designed as a placebo-controlled double-blind trial. There was no statistical difference in the survival time or other variables in cats receiving feline interferon-omega compared to cats receiving placebo.
>> PubMed abstract

Winn Feline Foundation funds 3 new studies on FIP in 2008

Bria Fund for FIP Research

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Health News

Pages

Thursday, January 10, 2013

Evolving insights into FIP virulence

Thursday, October 25, 2012

Understanding FIP virulence

Monday, July 9, 2012

Revealing more about FIP

Thursday, June 28, 2012

Risk factors for FIP in Australian cats

Tuesday, July 13, 2010

Ultrasound Findings in Cats with FIP

Thursday, May 27, 2010

Feline Coronavirus Persistence in Healthy Cats

Monday, March 22, 2010

Genetics of Feline Infectious Peritonitis Virus

Monday, January 11, 2010

Characterization of FIP Mutants

Friday, August 14, 2009

Potential Treatment for FIP

Wednesday, July 29, 2009

Pathogenesis of Feline Coronavirus Infection

Wednesday, July 22, 2009

Understanding FIP

Monday, May 18, 2009

Skin Lesions Associated with FIP

Thursday, April 9, 2009

Immunity and Feline Infectious Peritonitis

Monday, October 20, 2008

Diagnosis of FIP

Tuesday, March 4, 2008

Feline Interferon as a Treatment for FIP