Avian Sarcomas: Immune Responsiveness and Pathology

Wainberg, Mark A.; Halpern, Melissa D.

doi:10.1007/978-1-4613-2059-3_7

Cited by 4 publications

(5 citation statements)

References 59 publications

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“…Conversely, evidence has been found to suggest that endogenous retroviruses may enhance exogenous retroviral infection. Conservation of viral epitopes between endogenous and exogenous retroviruses may prevent the production of antibodies capable of neutralization of the virus, as has been seen in Friend murine leukemia virus infections (61) and avian leukosis virus infections (62,63). Overall, further investigation of endogenous and exogenous interactions is required to determine the influence that endogenous retroviruses have over exogenous retroviral infections.…”

Section: Figmentioning

confidence: 99%

Feline Leukemia Virus (FeLV) Disease Outcomes in a Domestic Cat Breeding Colony: Relationship to Endogenous FeLV and Other Chronic Viral Infections

Powers

Chiu

Kraberger

et al. 2018

J Virol

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Exogenous feline leukemia virus (FeLV) is a feline gammaretrovirus that results in a variety of disease outcomes. Endogenous FeLV (enFeLV) is a replication-defective provirus found in species belonging to the genus, which includes the domestic cat (). There have been few studies examining interaction between enFeLV genotype and FeLV progression. We examined point-in-time enFeLV and FeLV viral loads, as well as occurrence of FeLV/enFeLV recombinants (FeLV-B), to determine factors relating to clinical disease in a closed breeding colony of cats during a natural infection of FeLV. Coinfections with feline foamy virus (FFV), feline gammaherpesvirus 1 (FcaGHV-1), and feline coronavirus (FCoV) were also documented and analyzed for impact on cat health and FeLV disease. Correlation analysis and structural equation modeling techniques were used to measure interactions among disease parameters. Progressive FeLV disease and FeLV-B presence were associated with higher FeLV proviral and plasma viral loads. Female cats were more likely to have progressive disease and FeLV-B. Conversely, enFeLV copy number was higher in male cats and negatively associated with progressive FeLV disease. Males were more likely to have abortive FeLV disease. FFV proviral load was found to correlate positively with higher FeLV proviral and plasma viral load, detection of FeLV-B, and FCoV status. Male cats were much more likely to be infected with FcaGHV-1 than female cats. This analysis provides insights into the interplay between endogenous and exogenous FeLV during naturally occurring disease and reveals striking variation in the infection patterns among four chronic viral infections of domestic cats. Endogenous retroviruses are harbored by many animals, and their interactions with exogenous retroviral infections have not been widely studied. Feline leukemia virus (FeLV) is a relevant model system to examine this question, as endogenous and exogenous forms of the virus exist. In this analysis of a large domestic cat breeding colony naturally infected with FeLV, we documented that enFeLV copy number was higher in males and inversely related to FeLV viral load and associated with better FeLV disease outcomes. Females had lower enFeLV copy numbers and were more likely to have progressive FeLV disease and FeLV-B subtypes. FFV viral load was correlated with FeLV progression. FFV, FcaGHV-1, and FeLV displayed markedly different patterns of infection with respect to host demographics. This investigation revealed complex coinfection outcomes and viral ecology of chronic infections in a closed population.

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Section: Figmentioning

confidence: 99%

Feline Leukemia Virus (FeLV) Disease Outcomes in a Domestic Cat Breeding Colony: Relationship to Endogenous FeLV and Other Chronic Viral Infections

Powers

Chiu

Kraberger

et al. 2018

J Virol

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“…The contribution of the RSV oncogene v-src (Stdhelin et al 1976) to the progressive growth of tumors in chickens is, however, unclear because RSV is replication-competent and the growth of tumors is facilitated by continuous spread of the virus and oncogene to neighboring cells by reinfection (Pont6n 1964). Another complicating factor peculiar to oncogenic retroviruses such as RSV is a high antigenicity of proteins encoded by the viral replication genes, especially the env gene, which is thought to be the main target of the host anti-tumor immunity (for review see Wainberg and Halpern 1986).…”

Section: Imbr~ltk~kmmentioning

confidence: 99%

“…More rapid regression of RSV-induced than v-src-induced tumors was observed in the resistant CB (B12/B 12) line. This could be explained by a lack of the most immunogenic target, the env-encoded glycoprotein (for review see Wainberg and Halpern 1986), on non-virus-producing tumors. Thus, CB (regressor) and CC (progressor) congenic lines may differ in both src-specific and virus-specific cell-mediated immunity.…”

Section: Iltsojs_~!onmentioning

confidence: 99%

src-specific immunity in inbred chickens bearing v-src DNA- and RSV-induced tumors

et al. 1994

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The growth pattern (progression/regression) of v-src DNA- and Rous sarcoma virus (RSV)-induced tumors was analogous on a panel of inbred chicken lines. The decisive role of the major histocompatibility complex [Mhc(B)] alleles in resistance to the progression of these tumors was formally proved in segregating backcross populations. The immune mechanism of tumor regression was demonstrated by both in vivo and in vitro assays. A protective effect of v-src-specific immunity against RSV challenge was shown in Rous sarcoma regressor, line CB (B12/B12). Immune cells from regressors of v-src DNA-induced tumors can protect syngeneic hosts from the development of tumor after challenge with both v-src DNA and RSV. Suppression of RSV-induced tumor cell growth in vitro was also achieved by the use of cocultivation with spleen cells from chickens in which v-src DNA-induced tumors had regressed. This in vitro sarcoma-specific response was Mhc(B)-restricted. Chickens of the congenic Rous sarcoma progressor line CC (B4/B4) are sometimes able to regress v-src DNA-induced tumors, but immune cells can only slow the growth of v-src DNA-induced tumors in syngeneic hosts. This suggests that the primary reason for the susceptibility of CC chickens is a weak v-src-specific immune response. Furthermore, some of the v-src DNA-induced tumors were transplantable across the Mhc(B) barrier. The growth of tumor allografts was able to be facilitated when immunological tolerance to the B-F/L region antigens (class I and class II) had been established. This demonstrated that a high tumorigenicity of the transplantable tumor was not due to the lack of Mhc(B) antigens on tumor cells.

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“…However, CMI is an important aspect of the immune response against RSVinduced tumors and related avian sarcomas; the available literature has recently been reviewed (Schat, 1987a;Wainberg and Halpern, 1987). The present review will focus on the more recent information on antiviral and antitumor responses in REV and Marek's disease.…”

Section: Introductionmentioning

confidence: 97%

Importance of Cell-Mediated Immunity in Marek's Disease and Other Viral Tumor Diseases

Schat

1991

Poultry Science

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Cell-mediated immune (CMI) responses to viral tumor diseases are often used as examples of the importance of antiviral and antitumor immunity in chickens. Especially, reticuloendotheliosis virus (REV) and Marek's disease herpesvirus (MDV) are used as models to study the development of cytotoxic T-lymphocytes against viral and tumor antigens and activation of natural killer (NK) cells. Major histocompatibility complex Class I-restricted, antiviral cytotoxic T-lymphocytes expressing CD4-/CD8+ markers are induced after infection with REV. Thus far, this is the only example of Class I-restricted cytotoxic T-lymphocytes in chickens. Antiviral cytotoxic T-lymphocytes may be induced by infection with MDV or by vaccination, but conclusive evidence has not yet been provided. Antitumor responses have not been demonstrated against REV-induced tumors. Although Marek's disease is often used as an example for the importance of antitumor immunity, there is a lack of convincing data demonstrating antitumor immunity mediated by cytotoxic T-lymphocytes. Activation of NK cells by MDV infection or vaccination is probably an important part of CMI responses against Marek's disease viral antigens but not against tumor antigens.

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Avian Sarcomas: Immune Responsiveness and Pathology

Cited by 4 publications

References 59 publications

Feline Leukemia Virus (FeLV) Disease Outcomes in a Domestic Cat Breeding Colony: Relationship to Endogenous FeLV and Other Chronic Viral Infections

Feline Leukemia Virus (FeLV) Disease Outcomes in a Domestic Cat Breeding Colony: Relationship to Endogenous FeLV and Other Chronic Viral Infections

src-specific immunity in inbred chickens bearing v-src DNA- and RSV-induced tumors

Importance of Cell-Mediated Immunity in Marek's Disease and Other Viral Tumor Diseases

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