RESUMO
The Kilham rat virus (KRV) is a parvovirus originally isolated from a rat sarcoma in the late 1950s. The clinical signs associated with a natural KRV infection include foetal resorption in dams, runting, ataxia, cerebellar hypoplasia and jaundice in suckling rats, and sudden death, scrotal cyanosis, abdominal swelling and dehydration in juvenile rats. The ability of this virus to produce persistent infections has resulted in a high frequency of contamination of cell cultures and transplantable-tumor system. In addition, the virus may interfere with research in other ways. The remarkable resistance to environmental conditions determines the importance of the detection and control of this agent, especially in the laboratory animal production. This study determines the seroprevalence of Kilham antibodies from sera of adult rats from conventional facilities, using the haemagglutination inhibition test. The seroprevalence varied between 27.8% and 75%. This result confirms that the virus is circulating in Argentinean conventional facilities and might be interfering with research. The recognized Kilham virus may be prevented from supply sources by implementing a health monitoring schedule including a regular serological surveillance, and by keeping the animals under barrier systems.
Assuntos
Animais de Laboratório/imunologia , Anticorpos Antivirais/sangue , Infecções por Parvoviridae/veterinária , Parvovirus/imunologia , Ratos/imunologia , Doenças dos Roedores/epidemiologia , Animais , Anticorpos Antivirais/imunologia , Argentina/epidemiologia , Testes de Inibição da Hemaglutinação , Infecções por Parvoviridae/epidemiologia , Infecções por Parvoviridae/imunologia , Infecções por Parvoviridae/virologia , Doenças dos Roedores/imunologia , Doenças dos Roedores/virologia , Estudos Soroepidemiológicos , Organismos Livres de Patógenos EspecíficosRESUMO
There is growing evidence that necrosis, instead of apoptosis, could act as a natural adjuvant, which could activate an immune response. In this work we have investigated if induction of tumor necrosis could trigger the affluence of inflammatory cells at the tumor site, and thus induce an immune response. For this purpose, a liquid N2 spray was applied on human melanoma (IIB-MEL-J cell line) xenografted in nude mice and 24 h later some mice received intratumorally a single 500 U dose of recombinant murine granulocyte macrophage-colony-stimulating factor. 77-100% of the tumor mass underwent necrosis. Congestion, edema, and endothelial cell activation were the first noticeable events. A quick infiltrative response of polymorphonuclear leukocytes around the tumor was detected 24 h after liquid N2 application, peaking at day 3. Massive macrophage recruitment was observed since day 3. An early intratumoral infiltration with inflammatory cells was only detected in the group that received recombinant murine granulocyte macrophage- colony-stimulating factor after necrosis induction by liquid N2. Coexisting DEC 205- and F4/80-positive cells increased in number, and their localization was predominantly peritumoral after necrosis. Antibody response was only detected in the groups with tumor-induced necrosis. Our results suggest that cryosurgery-induced necrosis could be a useful model to analyze the interaction among necrosis, inflammation, and the generation of an immune response.