5 research outputs found
Retroviral DNA—the silent winner: blood transfusion containing latent feline leukemia provirus causes infection and disease in naïve recipient cats
Additional File 7: Figure S5. Photo of a blood smear from cat R1 (group B) with lymphoblastic leukemia at the time of necropsy. Lymphoblast cells are marked with an arrow. a) The picture displays a large lymphoblast with moderate amounts of basophilic cytoplasm and a large, round nucleus with fine chromatin patterns and several large, indistinct nucleoli. There is also a medium-sized lymphocyte with moderate amounts of pale basophilic cytoplasm and a round nucleus with a coarse chromatin pattern. b) The picture shows a medium-sized to large lymphoblast with small amounts of basophilic cytoplasm and a large, round nucleus with a fine chromatin pattern and two prominent round nucleoli
Transmission of feline leukemia virus infection by provirus positive blood
Cats with suspicion of feline leukemia virus (FeLV) infection are commonly tested for antigenemia by p27 ELISA. However, many p27 negative cats test FeLV provirus positive in the blood. So far, the risk of a FeLV transmission via provirus-positive blood has not been evaluated. The aim of this study was to explore this risk. Fifteen ten-week old specified pathogen free (SPF) kittens were randomly assigned to three groups: five cats (group A) received blood from a FeLV provirus positive cat, five cats (group B) were transfused with blood from a provirus and viral RNA positive cat and five control cats (group C) received SPF blood. All cats in groups A and B turned provirus and plasma viral RNA positive post transfusion. Moreover, all cats in group A, and three cats in group B became p27 positive. All cats in group C stayed FeLV negative. Remarkably, cats in group A turned FeLV positive later than cats in group B but had a graver infection outcome (higher FeLV loads); two cats in group A became persistently infected. Our results demonstrate for the first time that FeLV infection can be transmitted via blood transfusion of blood from FeLV provirus positive, antigen negative cats to naïve recipients. Based on our results we highly recommend screening blood donors for FeLV provirus by PCR prior to blood transfusion
Retroviral DNA-the silent winner: blood transfusion containing latent feline leukemia provirus causes infection and disease in naïve recipient cats
BACKGROUND: The feline leukemia virus (FeLV) is a gamma-retrovirus of domestic cats that was discovered half a century ago. Cats that are infected with FeLV may develop a progressive infection resulting in persistent viremia, immunodeficiency, tumors, anemia and death. A significant number of cats mount a protective immune response that suppresses viremia; these cats develop a regressive infection characterized by the absence of viral replication and the presence of low levels of proviral DNA. The biological importance of these latter provirus carriers is largely unknown.
RESULTS: Here, we demonstrate that ten cats that received a transfusion of blood from aviremic provirus carriers developed active FeLV infections, some with a progressive outcome and the development of fatal FeLV-associated disease. The infection outcome, disease spectrum and evolution into FeLV-C in one cat mirrored those of natural infection. Two cats developed persistent antigenemia; six cats were transiently antigenemic. Reactivation of infection occurred in some cats. One recipient developed non-regenerative anemia associated with FeLV-C, and four others developed a T-cell lymphoma, one with secondary lymphoblastic leukemia. Five of the ten recipient cats received provirus-positive aviremic blood, whereas the other five received provirus- and viral RNA-positive but aviremic blood. Notably, the cats that received blood containing only proviral DNA exhibited a later onset but graver outcome of FeLV infection than the cats that were transfused with blood containing proviral DNA and viral RNA. Leukocyte counts and cytokine analyses indicated that the immune system of the latter cats reacted quicker and more efficiently.
CONCLUSIONS: Our results underline the biological and epidemiological relevance of FeLV provirus carriers and the risk of inadvertent FeLV transmission via blood transfusion and demonstrate the replication capacity of proviral DNA if uncontrolled by the immune system. Our results have implications not only for veterinary medicine, such as the requirement for testing blood donors and blood products for FeLV provirus by sensitive polymerase chain reaction, but are also of general interest by revealing the importance of latent retroviral DNA in infected hosts. When aiming to eliminate a retroviral infection from a population, provirus carriers must be considered
Molecular characterization and virus neutralization patterns of severe, non-epizootic forms of feline calicivirus infections resembling virulent systemic disease in cats in Switzerland and in Liechtenstein
Feline calicivirus (FCV) infections are associated with oral ulceration, chronic stomatitis and a limping syndrome. Epizootic outbreaks of virulent systemic disease (VSD) have been reported in the USA and Europe. Here, the molecular characterization and neutralization patterns of FCV isolates from cases of severe, non-epizootic infection associated with skin ulceration and edema are presented. Samples from eleven symptomatic cats, four in-contact cats and 27 cats with no contact with symptomatic cats were collected and tested for FCV, feline herpesvirus-1 (FHV-1), feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV). Phylogenetic analyses based on the capsid (VP1) gene of FCV and virus neutralization with antisera raised against four FCV vaccine strains were performed. Nine kittens and two adult cats in two shelters and two veterinary clinics in four geographically distinct locations in Switzerland and Liechtenstein were affected. The cats showed fever, tongue and skin ulceration, head and paw edema, and occasionally jaundice, generalized edema and dyspnea. All symptomatic cats tested FCV-positive but were negative for FHV-1, FeLV and FIV, with the exception of one FIV-positive kitten. All kittens of one litter and both adult cats died. The disease did not spread to cats in the environment. Cats in the environment displayed phylogenetically distinct, but related, FCV strains. Virus neutralization patterns suggested that some cases might have been potentially prevented by vaccination with the optimal vaccine strain. In conclusion, clinicians should be aware of severe, non-epizootic forms of FCV infections with initial clinical presentations similar to VSD