Effect of primary-stage feline immunodeficiency virus infection on subsequent feline calicivirus vaccination and challenge in cats

Dawson, Susan; Smyth, Neil; Bennett, Malcolm J.; Gaskell, Rosalind M.; McCracken, Christina; Brown, Aileen; Gaskell, C. J.

doi:10.1097/00002030-199106000-00016

Cited by 45 publications

(27 citation statements)

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“…Some have suggested an immunemediated contribution to the pathogenesis for FCV-associated VSD [15,28], partly based on the fact that adult cats seem to develop more severe disease than young animals [43]. A possible immune-mediated pathogenesis has been shown for other FCV infections such as lameness [4], and in some cases, vaccination appears to potentiate FCV infection [17].…”

Section: Fcv-associated Virulent Systemic Diseasementioning

confidence: 99%

“…It is certainly true that existing vaccines do not prevent infection. Indeed there is a small amount of experimental data to suggest that under some circumstances, challenge virus may be shed for longer and at a higher titre by cats with some previous immunity when compared to naïve cats [17]. Whether this can also occur with commercial vaccines is not known.…”

Section: Vaccinesmentioning

confidence: 99%

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Feline calicivirus

et al. 2007

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-Feline calicivirus (FCV) is an important and highly prevalent pathogen of cats. It belongs to the family Caliciviridae which includes other significant pathogens of man and animals. As an RNA virus, high polymerase error rates convey upon FCV a high genome plasticity, and allow the virus to respond rapidly to environmental selection pressures. This makes the virus very adaptable and has important implications for clinical disease and its control. Being genetically diverse, FCV is associated with a range of clinical syndromes from inapparent infections to relatively mild oral and upper respiratory tract disease with or without acute lameness. More recently, highly virulent forms of the virus have emerged associated with a systemic infection that is frequently fatal. A proportion of FCV infected cats that recover from acute disease, remain persistently infected. In such cats, virus evolution is believed to help the virus to evade the host immune response. Such longterm carriers may only represent a minority of the feline population but are likely to be crucial to the epidemiology of the virus. Vaccination against FCV has been available for many years and has effectively reduced the incidence of clinical disease. However, the vaccines do not prevent infection and vaccinated cats can still become persistently infected. In addition, FCV strain variability means that not all strains are protected against equally. Much progress has been made in understanding the biology and pathogenesis of this important feline virus. Challenges for the future will necessarily focus on how to control the variability of this virus particularly in relation to emerging virulent strains and vaccination.

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Section: Fcv-associated Virulent Systemic Diseasementioning

confidence: 99%

Section: Vaccinesmentioning

confidence: 99%

Feline calicivirus

et al. 2007

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“…Following acute infection, some cats remain persistently infected with the virus (11,40,48,59). Such carriers appear to be relatively common in the general population, with prevalences ranging from 15 to 91%, and they play an important role in the epidemiology of the disease (1,3,7,8,21,22,42).…”

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confidence: 99%

Evolutionary Mechanisms of Persistence and Diversification of a Calicivirus within Endemically Infected Natural Host Populations

Coyne¹,

Gaskell

Dawson³

et al. 2007

J Virol

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In order to understand the evolutionary mechanisms of persistence and diversification within the Caliciviridae, we have been exploiting endemic infection of feline calicivirus within five geographically distinct household groups of cats. By sequencing immunodominant and variable regions of the capsid gene, we identified the relative contribution of the different evolutionary processes employed by the virus to ensure its long-term survival in the host population. Such strategies included progressive evolution of a given variant of a strain through mutation accumulation within an individual, sequential reinfection with either a variant of the same strain or with a different strain, and mixed infection. Recombination between different strains in this study has been reported in detail elsewhere (K. P. Coyne et al., J. Gen. Virol. 87:921-926, 2006). Here, we provide evidence to suggest that true long-term persistent infection in individuals is relatively rare, with the majority of apparent viral carriers undergoing a combination of progressive evolution and cyclical reinfection. Progressive evolution at the individual level and variant reinfection at both the individual and population levels were associated with positive selection. Two measures of evolution rate were determined; for a virus progressively evolving within an individual (1.32 ؋ 10 ؊2 to 2.64 ؋ 10 ؊2 substitutions per nucleotide per year, i.e., no transmission) and for a strain circulating within a population (3.84 ؋ 10 ؊2 to 4.56 ؋ 10 ؊2 substitutions per nucleotide per year, i.e., including transmission). Reiteration of both progressive evolution and variant reinfection appeared to lead to a gradual increase in the diversity of a given strain of virus, both in the individual and in the population, until eventually new strains emerged.The Caliciviridae are an important group of human and animal RNA pathogens, causing a wide range of diseases, including acute outbreaks of gastroenteritis in humans (noroviruses and sapoviruses) and vesicular and other diseases in animals (vesiviruses and lagoviruses) (19). The Caliciviridae are a highly variable family of small positive-strand RNA viruses, demonstrating considerable antigenic and genetic diversity both between and within genera. Such variability has been associated with the emergence of highly transmissible globally dominant strains of human caliciviruses (36) and hypervirulent animal caliciviruses that are frequently lethal (9,33,39). Despite the obvious significance of such variation, the origins of this diversity and the evolutionary mechanisms by which new, and possibly more virulent strains evolve remain unclear.Feline calicivirus (FCV) belongs to the genus Vesivirus and is a highly infectious oral and respiratory pathogen of domestic cats (18). Following acute infection, some cats remain persistently infected with the virus (11,40,48,59). Such carriers appear to be relatively common in the general population, with prevalences ranging from 15 to 91%, and they play an important role in the epidemiolog...

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“…Certainly, FIV infection has an early direct effect upon T-cell subsets in the cat [2], with a selective loss of the CD4+ cells [3]. Thus, FIV severely impairs the immune response and increases the susceptibility to opportunistic secondary pathogens [9,44]. Our finding has demonstrated that antioxidants could contribute to the preservation of T-lymphocytes, tending to improve the immunosuppression in FIV-infected cats.…”

Section: Discussionmentioning

confidence: 77%

Inhibition of Apoptosis and Virus Replication in Feline Immunodeficiency Virus-Infected Cells by N-Acetylcysteine and Ascorbic Acid.

Mórtola

Okuda

Ohno

et al. 1998

The Journal of Veterinary Medical Science

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ABSTRACT. Infection of feline immunodeficiency virus (FIV) has been shown to induce apoptosis that might be associated with the lymphocyte depletion in the infected cats. To investigate the inhibitory effect of antioxidants on FIV-induced apoptosis, we examined the effect of N-acetylcysteine (NAC) and ascorbic acid (AA) on apoptosis and virus replication in feline lymphoblastoid (Fel-039) and fibroblastoid (CRFK) cell lines infected with FIV. The treatment with NAC or AA induced a significant inhibition of viral replication and apoptosis in Fel-039 cells and tumor necrosis factor α (TNF-α) -treated CRFK cells infected with FIV. Both cell lines in the presence of noncytotoxic concentrations of NAC or AA showed an increase of intracellular glutathione (GSH) level, which might protect the cells against oxidative stresses exerted by FIV infection and TNF-α treatment. On the basis of these in vitro results, we suggest that antioxidant therapies aimed at restoring depleted GSH level might be effective for inhibition of viral replication and cell death associated with the development of immunodeficiency. -KEY WORDS: apoptosis, ascorbic acid, FIV, N-acetylcysteine.

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Effect of primary-stage feline immunodeficiency virus infection on subsequent feline calicivirus vaccination and challenge in cats

Cited by 45 publications

References 0 publications

Feline calicivirus

Feline calicivirus

Evolutionary Mechanisms of Persistence and Diversification of a Calicivirus within Endemically Infected Natural Host Populations

Inhibition of Apoptosis and Virus Replication in Feline Immunodeficiency Virus-Infected Cells by N-Acetylcysteine and Ascorbic Acid.

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