Calicivirus

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Vet. Res. 38 (2007) 319–335 c INRA, EDP Sciences, 2007 DOI: 10.1051/vetres:2006056

319

Review article

Feline calicivirus
Alan D. R*, Karen P. C, Susan D, Carol J. P, Rosalind M. G
University of Liverpool Veterinary Teaching Hospital, Leahurst, Chester High Road, Neston, S. Wirral, CH64 7TE, United Kingdom (Received 23 June 2006; accepted 25 September 2006)Abstract – 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 andhas 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. Aproportion 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 haseffectively 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 necessarilyfocus on how to control the variability of this virus particularly in relation to emerging virulent strains and vaccination. calicivirus / evolution / feline / vaccination / virulence

Table of contents 1. Aetiology.......................................................................................................... 320 2. Clinicalsigns..................................................................................................... 321 3. Pathogenesis ..................................................................................................... 322 3.1. FCV-associated oral and upper respiratory tract disease ...................................... 322 3.2. FCV-associated lameness.............................................................................. 322 3.3.FCV-associated virulent systemic disease ......................................................... 322 3.4. Molecular pathogenesis ................................................................................ 324 4. The FCV carrier state .......................................................................................... 325 5. Epidemiology.................................................................................................... 325 6. Prevention, control and vaccination ........................................................................ 326 6.1. Vaccines ................................................................................................... 326 * Corresponding author: alanrad@liv.ac.uk

Article available at http://www.edpsciences.org/vetres orhttp://dx.doi.org/10.1051/vetres:2006056

320

A.D. Radford et al.

6.2. Treatment.................................................................................................. 328 6.3. Management of FCV-associated respiratory disease ............................................ 329 6.4. Control of outbreaks of FCV-associated VSD.................................................... 329 7....
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