Pathogenesis of Experimental Feline Leukemia Virus Infection2

Rojko, Jennifer L.; Hoover, Edward A.; Mathes, Lawrence E.; Olsen, Richard G.; Schaller, Joseph

doi:10.1093/jnci/63.3.759

Cited by 130 publications

(99 citation statements)

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“…De acordo com esses parâmetros, após exposição oronasal, a infecção era classificada como: infecção regressiva -Ocorre a replicação viral nas tonsilas e linfonodos regionais (ROJKO et al, 1979), o animal desenvolve resposta imune efetiva contra o vírus e este é eliminado. Não ocorre disseminação sistêmica e a antigenemia/viremia é indetectável (LUTZ et al, 1980;TORRES et al, 2010).…”

Section: Patogenia Do Felv Com O Emprego De Técnicas Convencionais Deunclassified

“…Se o animal não desenvolve imunidade adequada, o vírus é disseminado sistemicamente por linfócitos e monócitos. A antigenemia/viremia é transiente, pois é detectável por cerca de três a seis semanas, ocorrendo completa eliminação do vírus após esse período (LUTZ et al, 1980;FLYNN et al, 2000;FLYNN et al, 2002); infecção latente -O animal apresenta antigenemia/ viremia por mais de três semanas e ocorre infecção de células da medula óssea (ROJKO et al, 1979;HARTMANN, 2006). Dentro de meses, o animal desenvolve uma resposta imune capaz de eliminar a antigenemia/viremia, mas o DNA proviral está presente nas células precursoras da medula.…”

Section: Patogenia Do Felv Com O Emprego De Técnicas Convencionais Deunclassified

“…Esses mesmos testes eram utilizados para a interpretação e a classificação das diferentes fases da infecção, sendo possível a determinação de três categorias: infecção regressiva e infecção latente pela montagem de uma resposta imune efetiva e infecção progressiva no caso de uma resposta imune deficiente (ROJKO et al, 1979;HARTMANN, 2006). Uma vez que uma resposta imune efetiva dos animais era capaz de eliminar a infecção, ocorreram grandes investimentos para o desenvolvimento da primeira vacina considerada efetiva contra retrovírus (LEWIS, 1981;SPARKES, 1997).…”

Section: Introductionunclassified

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Vírus da leucemia felina: análise da classificação da infecção, das técnicas de diagnóstico e da eficácia da vacinação com o emprego de técnicas sensíveis de detecção viral

Figueiredo

Júnior

2011

Cienc. Rural

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Section: Patogenia Do Felv Com O Emprego De Técnicas Convencionais Deunclassified

Section: Introductionunclassified

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Vírus da leucemia felina: análise da classificação da infecção, das técnicas de diagnóstico e da eficácia da vacinação com o emprego de técnicas sensíveis de detecção viral

Figueiredo

Júnior

2011

Cienc. Rural

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“…While animals in our studies were inoculated through the intraperitoneal route, the most frequent route of exposure to FeLV in nature is thought to be oronasal contact with infectious saliva. Parenteral routes of inoculation used experimentally (e.g., intraperitoneal, intravenous) have been speculated to mimic the natural introduction of FeLV in the course of cat bites during fights or copulation (Rojko and Kociba, 1991). Indeed, a seminal study in which young cats were inoculated through either the oronasal or intraperitoneal route demonstrated a generally similar pattern of spread in vivo (Rojko et al, 1979).…”

Section: The Unique Ltr and Su Gene Sequences Of Felv-945 Act As Detementioning

confidence: 99%

“…Parenteral routes of inoculation used experimentally (e.g., intraperitoneal, intravenous) have been speculated to mimic the natural introduction of FeLV in the course of cat bites during fights or copulation (Rojko and Kociba, 1991). Indeed, a seminal study in which young cats were inoculated through either the oronasal or intraperitoneal route demonstrated a generally similar pattern of spread in vivo (Rojko et al, 1979). It is noteworthy that, in the natural cohort, FeLV-945 was not identified in T-cell tumors.…”

Section: The Unique Ltr and Su Gene Sequences Of Felv-945 Act As Detementioning

confidence: 99%

Advances in understanding molecular determinants in FeLV pathology

Lévy

2008

Veterinary Immunology and Immunopathology

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Feline leukemia virus (FeLV) occurs in nature not as a single genomic species but as a family of closely related viruses. The disease outcome of natural FeLV infection is variable and likely reflects genetic variation both in the virus and the naturally outbreeding host population. A series of studies have been undertaken with the objectives of examining natural FeLV genetic variation, the selective pressures operative in FeLV infection that lead to predominance of natural variants, and the consequences for infection and disease progression. Genetic variation among FeLV isolates was examined in a cohort of naturally infected cats with thymic lymphoma of T-cell origin, non-T-cell multicentric lymphoma, myeloproliferative disorder or anemia. The predominant isolate in the cohort, designated FeLV-945, was identified exclusively in disorders of non-T-cell origin. The FeLV-945 LTR was shown to contain a unique 21-bp repeat element, triplicated in tandem downstream of enhancer. The 21-bp triplication was shown to act as a transcriptional enhancer and to confer a replicative advantage through the assembly of a distinctive transcription factor complex. Oncogene utilization during tumor induction by FeLV-945 was studied using a recombinant Moloney murine leukemia virus containing the FeLV-945 LTR. This approach identified novel loci of common proviral integration in tumors, including the regulatory subunit of PI-3Kgamma. Mutational changes identified in FeLV-945 SU were shown not to alter receptor usage as measured by host range and superinfection interference, but to significantly increase the efficiency of receptor binding. To determine whether the unique sequence elements of FeLV-945 influence the course of infection and disease in vivo, recombinant viruses were constructed in which the FeLV-945 LTR alone, or the FeLV-945 SU gene and LTR were substituted into the prototype isolate FeLV-A/61E. Longitudinal studies of infected animals showed that substitution of the FeLV-945 LTR into FeLV-A/61E resulted in a significantly more rapid disease onset, but did not alter the tumorigenic spectrum. In contrast, substitution of both the FeLV-945 LTR and SU gene changed the disease outcome entirely. Together, these observations indicate that the distinctive LTR and SU gene of FeLV-945 mediate a rapid pathogenesis with distinctive clinical features and oncogenic mechanisms.

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Feline Leukaemia Virus

Jarrett

Neil

2012

Encyclopedia of Life Sciences

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Feline leukaemia virus (FeLV) is a gammaretrovirus that causes a variety of fatal diseases including leukaemia and lymphoma in its host, the domestic cat, and occasionally in large cat species. Many cats become persistently infected and develop disease after an incubation period of several years, during which virus can be transmitted to other cats. Disease is often associated with the generation of FeLV variants with increased pathogenic potential that can arise by mutation of envelope sequences, duplication of transcriptional enhancer elements or recombination with host proto‐oncogene sequences. FeLV can also produce variants by recombination with endogenous proviruses related to FeLV that are found in the domestic cat and its close relatives. The prevalence of FeLV infection has been reduced in many cat populations by isolation of infected carriers and more recently by vaccines that augment the natural ability of most cats to control infection. Key Concepts: The outcome of infection by FeLV depends on the infectious dose, age and immunocompetence of the host. Many cats achieve lifelong control, if not elimination of infection. Cats that become persistently viraemic are at risk of a variety of FeLV‐related diseases after a latent period of up to several years. The common infectious form, FeLV‐A can acquire altered entry receptor specificity by envelope gene mutation (to FeLV‐C) or recombination with endogenous FeLV‐related proviruses (to FeLV‐B). FeLV envelope variants may induce fatal diseases of rapid onset including nonregenerative anaemia (FeLV‐C) or wasting and immunodeficiency (FeLV‐T). The oncogenic potential of FeLV can evolve by duplication of transcriptional enhancer control elements in the long‐terminal repeat or by transduction of host proto‐oncogene sequences. Although the immune parameters of vaccine protection remain unclear, FeLV demonstrates the feasibility of effective immunisation against the gamma retroviruses. Commercial FeLV vaccines in recent or current use include inactivated FeLV, infected cell extracts, recombinant envelope protein and live recombinant poxvirus vaccines.

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Pathogenesis of Experimental Feline Leukemia Virus Infection2

Cited by 130 publications

References 0 publications

Vírus da leucemia felina: análise da classificação da infecção, das técnicas de diagnóstico e da eficácia da vacinação com o emprego de técnicas sensíveis de detecção viral

Vírus da leucemia felina: análise da classificação da infecção, das técnicas de diagnóstico e da eficácia da vacinação com o emprego de técnicas sensíveis de detecção viral

Advances in understanding molecular determinants in FeLV pathology

Feline Leukaemia Virus

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