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Paula G. Ferreira - One of the best experts on this subject based on the ideXlab platform.
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Early acute depletion of lymphocytes in Calicivirus-infected adult rabbits
Veterinary Research Communications, 2010Co-Authors: Raquel M. Marques, Artur P. Águas, António Costa-e-silva, Luzia Teixeira, Paula G. FerreiraAbstract:Rabbit Haemorrhagic Disease (RHD) is a lethal Infection caused by Calicivirus that kills 90% of the infected adult rabbits within 3 days. The Calicivirus replicates in the liver and causes a fulminant hepatitis. Most studies on the pathology of RHD have been focused on the fulminant liver disease. This may not be the only mechanism in the pathogenesis of RHD: Calicivirus Infection may also induce leukopenia in the infected adult rabbits. We show now by flow cytometry analysis that the Calicivirus induces an early decrease in B and T cells, in both spleen and liver. The depletion of B and T cells was associated with apoptosis labelled by annexin V. These changes occurred in rabbits before they showed enzymatic evidence of liver damage and persisted after liver transaminase values were very high. We conclude that depletion of lymphocytes caused by the Calicivirus Infection precedes or attends liver damage. The relative contribution of this lymphocyte depletion for the pathogenesis of the fatal Calicivirus Infection of rabbits remains to be investigated.
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A simple and rapid method for isolation of Caliciviruses from liver of infected rabbits.
Research in veterinary science, 2010Co-Authors: Luzia Teixeira, Raquel M. Marques, Artur P. Águas, Paula G. FerreiraAbstract:Abstract Rabbit Haemorrhagic Disease Virus (RHDV), a member of the Caliciviridae family, is the etiologic agent of Rabbit Haemorrhagic Disease (RHD); this viral disease is highly contagious and kills more than 90% of infected adult rabbits. Research on experimental Calicivirus Infection uses inocula obtained from livers of rabbits dying from Calicivirus Infection. This implies that Caliciviruses have to be purified from liver homogenates. Current methods to isolate Caliciviruses from rabbit livers are time consuming. We propose here a new procedure for fast purification of rabbit Caliciviruses from liver homogenates that uses centrifugation through an iodixanol gradient. This method offers in approximately 2 h a sample with a high degree of Calicivirus purity, as shown by its biochemical and immunocytochemistry analysis, which is also able to kill adult rabbits from RHD within 48 h of inoculation.
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Inflammatory response of young rabbits to Calicivirus Infection
Microscopy and Microanalysis, 2009Co-Authors: Raquel M. Marques, Artur P. Águas, A. Costa-e-silva, Paula G. FerreiraAbstract:AbstractCaliciviruses cause rabbit haemorrhagic disease (RHD) that kills more than 90% of the infected adult animals within 1 a 3 days of Infection. The virus replicates in the liver and causes a fulminant hepatitis in adult rabbits leading to RHD. A mystery of the Calicivirus Infection is that young rabbits (less than 8-weeks old) are resistant to the Infection, in spite of undergoing viral replication in the liver and of expressing transient hepatitis. Heterophils were the predominant inflammatory cells seen in hepatic tissue of infected adult rabbits, whereas mononuclear cells dominated the inflammatory infiltrates of the infected young rabbits (4-weeks-old). In order to define the role of inflammation in the pathogenesis of the Calicivirus Infection, we have studied the cellular inflammatory response in young rabbits experimentally infected by Calicivirus. For this, we have used transmission electron microscopy (TEM) and flow cytometry to identify the inflammatory cells that infiltrate the hepatic tissue of young rabbits at 48 hours of Calicivirus Infection. In same infected rabbits, lymphoid organs (spleen and thymus) were used to quantify by flow cytometry the total number of leukocytes seen inside these organs.
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Adult rabbits acquire resistance to lethal Calicivirus Infection by adoptive transfer of sera from infected young rabbits.
Veterinary Immunology and Immunopathology, 2007Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Márcia Dinis, Artur P. ÁguasAbstract:Calicivirus Infection of adult rabbits induces the so-called rabbit haemorrhagic disease (RHD) that kills 90% or more of the infected animals; in contrast, young rabbits (up to 8-week-old animals) are resistant to the same infectious agent. We report that Calicivirus inoculation of young rabbits induced moderate titres of antiviral antibodies. When these rabbits reached adulthood, a second Calicivirus inoculation resulted in resistance to RHD and boosting of antibody titres in half of the rabbits. Adoptive transfer of sera from Calicivirus-infected young rabbits to naive adult rabbits conferred resistance to RHD. We conclude that Calicivirus Infection of young rabbits induces specific anti-Calicivirus antibodies that will protect them from RHD when they reach adulthood.
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Liver disease in young rabbits infected by Calicivirus through nasal and oral routes.
Research in Veterinary Science, 2006Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Artur P. ÁguasAbstract:Calicivirus Infection causes rabbit haemorrhagic disease (RHD) that kills more than 90% of adult animals, whereas young rabbits are naturally resistant to this viral disease. It has been proposed that the different response of adult and young rabbits to Calicivirus Infection is due to absence of viral receptors in respiratory and digestive systems of young animals. We have searched for liver disease in 4-week-old rabbits inoculated with a Calicivirus suspension by intranasal and oral routes. These young rabbits showed cell damage and mononuclear infiltration of the liver. The hepatic lesions were associated with mild to moderate increase in circulating transaminases. We conclude that the previously reported reduction of viral receptors in the epithelium of respiratory and digestive systems of young rabbits does not inhibit Calicivirus from inducing liver disease in these hosts.
Artur P. Águas - One of the best experts on this subject based on the ideXlab platform.
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Early acute depletion of lymphocytes in Calicivirus-infected adult rabbits
Veterinary Research Communications, 2010Co-Authors: Raquel M. Marques, Artur P. Águas, António Costa-e-silva, Luzia Teixeira, Paula G. FerreiraAbstract:Rabbit Haemorrhagic Disease (RHD) is a lethal Infection caused by Calicivirus that kills 90% of the infected adult rabbits within 3 days. The Calicivirus replicates in the liver and causes a fulminant hepatitis. Most studies on the pathology of RHD have been focused on the fulminant liver disease. This may not be the only mechanism in the pathogenesis of RHD: Calicivirus Infection may also induce leukopenia in the infected adult rabbits. We show now by flow cytometry analysis that the Calicivirus induces an early decrease in B and T cells, in both spleen and liver. The depletion of B and T cells was associated with apoptosis labelled by annexin V. These changes occurred in rabbits before they showed enzymatic evidence of liver damage and persisted after liver transaminase values were very high. We conclude that depletion of lymphocytes caused by the Calicivirus Infection precedes or attends liver damage. The relative contribution of this lymphocyte depletion for the pathogenesis of the fatal Calicivirus Infection of rabbits remains to be investigated.
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A simple and rapid method for isolation of Caliciviruses from liver of infected rabbits.
Research in veterinary science, 2010Co-Authors: Luzia Teixeira, Raquel M. Marques, Artur P. Águas, Paula G. FerreiraAbstract:Abstract Rabbit Haemorrhagic Disease Virus (RHDV), a member of the Caliciviridae family, is the etiologic agent of Rabbit Haemorrhagic Disease (RHD); this viral disease is highly contagious and kills more than 90% of infected adult rabbits. Research on experimental Calicivirus Infection uses inocula obtained from livers of rabbits dying from Calicivirus Infection. This implies that Caliciviruses have to be purified from liver homogenates. Current methods to isolate Caliciviruses from rabbit livers are time consuming. We propose here a new procedure for fast purification of rabbit Caliciviruses from liver homogenates that uses centrifugation through an iodixanol gradient. This method offers in approximately 2 h a sample with a high degree of Calicivirus purity, as shown by its biochemical and immunocytochemistry analysis, which is also able to kill adult rabbits from RHD within 48 h of inoculation.
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Inflammatory response of young rabbits to Calicivirus Infection
Microscopy and Microanalysis, 2009Co-Authors: Raquel M. Marques, Artur P. Águas, A. Costa-e-silva, Paula G. FerreiraAbstract:AbstractCaliciviruses cause rabbit haemorrhagic disease (RHD) that kills more than 90% of the infected adult animals within 1 a 3 days of Infection. The virus replicates in the liver and causes a fulminant hepatitis in adult rabbits leading to RHD. A mystery of the Calicivirus Infection is that young rabbits (less than 8-weeks old) are resistant to the Infection, in spite of undergoing viral replication in the liver and of expressing transient hepatitis. Heterophils were the predominant inflammatory cells seen in hepatic tissue of infected adult rabbits, whereas mononuclear cells dominated the inflammatory infiltrates of the infected young rabbits (4-weeks-old). In order to define the role of inflammation in the pathogenesis of the Calicivirus Infection, we have studied the cellular inflammatory response in young rabbits experimentally infected by Calicivirus. For this, we have used transmission electron microscopy (TEM) and flow cytometry to identify the inflammatory cells that infiltrate the hepatic tissue of young rabbits at 48 hours of Calicivirus Infection. In same infected rabbits, lymphoid organs (spleen and thymus) were used to quantify by flow cytometry the total number of leukocytes seen inside these organs.
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Adult rabbits acquire resistance to lethal Calicivirus Infection by adoptive transfer of sera from infected young rabbits.
Veterinary Immunology and Immunopathology, 2007Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Márcia Dinis, Artur P. ÁguasAbstract:Calicivirus Infection of adult rabbits induces the so-called rabbit haemorrhagic disease (RHD) that kills 90% or more of the infected animals; in contrast, young rabbits (up to 8-week-old animals) are resistant to the same infectious agent. We report that Calicivirus inoculation of young rabbits induced moderate titres of antiviral antibodies. When these rabbits reached adulthood, a second Calicivirus inoculation resulted in resistance to RHD and boosting of antibody titres in half of the rabbits. Adoptive transfer of sera from Calicivirus-infected young rabbits to naive adult rabbits conferred resistance to RHD. We conclude that Calicivirus Infection of young rabbits induces specific anti-Calicivirus antibodies that will protect them from RHD when they reach adulthood.
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Liver disease in young rabbits infected by Calicivirus through nasal and oral routes.
Research in Veterinary Science, 2006Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Artur P. ÁguasAbstract:Calicivirus Infection causes rabbit haemorrhagic disease (RHD) that kills more than 90% of adult animals, whereas young rabbits are naturally resistant to this viral disease. It has been proposed that the different response of adult and young rabbits to Calicivirus Infection is due to absence of viral receptors in respiratory and digestive systems of young animals. We have searched for liver disease in 4-week-old rabbits inoculated with a Calicivirus suspension by intranasal and oral routes. These young rabbits showed cell damage and mononuclear infiltration of the liver. The hepatic lesions were associated with mild to moderate increase in circulating transaminases. We conclude that the previously reported reduction of viral receptors in the epithelium of respiratory and digestive systems of young rabbits does not inhibit Calicivirus from inducing liver disease in these hosts.
A. Costa-e-silva - One of the best experts on this subject based on the ideXlab platform.
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Inflammatory response of young rabbits to Calicivirus Infection
Microscopy and Microanalysis, 2009Co-Authors: Raquel M. Marques, Artur P. Águas, A. Costa-e-silva, Paula G. FerreiraAbstract:AbstractCaliciviruses cause rabbit haemorrhagic disease (RHD) that kills more than 90% of the infected adult animals within 1 a 3 days of Infection. The virus replicates in the liver and causes a fulminant hepatitis in adult rabbits leading to RHD. A mystery of the Calicivirus Infection is that young rabbits (less than 8-weeks old) are resistant to the Infection, in spite of undergoing viral replication in the liver and of expressing transient hepatitis. Heterophils were the predominant inflammatory cells seen in hepatic tissue of infected adult rabbits, whereas mononuclear cells dominated the inflammatory infiltrates of the infected young rabbits (4-weeks-old). In order to define the role of inflammation in the pathogenesis of the Calicivirus Infection, we have studied the cellular inflammatory response in young rabbits experimentally infected by Calicivirus. For this, we have used transmission electron microscopy (TEM) and flow cytometry to identify the inflammatory cells that infiltrate the hepatic tissue of young rabbits at 48 hours of Calicivirus Infection. In same infected rabbits, lymphoid organs (spleen and thymus) were used to quantify by flow cytometry the total number of leukocytes seen inside these organs.
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Adult rabbits acquire resistance to lethal Calicivirus Infection by adoptive transfer of sera from infected young rabbits.
Veterinary Immunology and Immunopathology, 2007Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Márcia Dinis, Artur P. ÁguasAbstract:Calicivirus Infection of adult rabbits induces the so-called rabbit haemorrhagic disease (RHD) that kills 90% or more of the infected animals; in contrast, young rabbits (up to 8-week-old animals) are resistant to the same infectious agent. We report that Calicivirus inoculation of young rabbits induced moderate titres of antiviral antibodies. When these rabbits reached adulthood, a second Calicivirus inoculation resulted in resistance to RHD and boosting of antibody titres in half of the rabbits. Adoptive transfer of sera from Calicivirus-infected young rabbits to naive adult rabbits conferred resistance to RHD. We conclude that Calicivirus Infection of young rabbits induces specific anti-Calicivirus antibodies that will protect them from RHD when they reach adulthood.
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Liver Enzymes and Ultrastructure in Rabbit Haemorrhagic Disease (RHD)
Veterinary Research Communications, 2006Co-Authors: P. G. Ferreira, A. Costa-e-silva, E. Monteiro, M. J. R. Oliveira, A P AguasAbstract:Rabbit haemorrhagic disease (RHD) is caused by a Calicivirus Infection that kills most adult rabbits 24–72 h after viral inoculation. Two liver enzymes (AST, aspartate aminotransferase, and ALT, alanine aminotransferase) were monitored in blood samples of Calicivirus-infected rabbits during the short course of RHD. Values of AST were used to differentiate three stages of hepatocellular degeneration in RHD: mild (up to 20-fold increase in AST), moderate (150–200-fold elevation of AST) and severe (more than 1000-fold elevation in AST). Liver samples of rabbits from these three biochemical stages of hepatocellular degeneration of RHD were studied by transmission electron microscopy to define the fine structure of the hepatocytes. In the mild hepatocellular degeneration there was proliferation (microvesiculation) of the smooth endoplasmic reticulum and swelling of mitochondria into spheroid bodies with loss of cristae. In moderate hepatocellular degeneration, vacuolization of cytoplasm and mitochondrial damage continued to be present, and there was also formation of autophagic vesicles. In the severe hepatocellular degeneration of RHD, the altered mitochondria also showed loss of density of their matrix; rupture of cytoplasmic vacuoles led to the formation of large vesicles. Marked depletion of liver glycogen was also found in this late stage of RHD. These data offer a correlation between biochemical and cytological features of the liver during the hepatocellular degeneration of RHD.
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Liver disease in young rabbits infected by Calicivirus through nasal and oral routes.
Research in Veterinary Science, 2006Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Artur P. ÁguasAbstract:Calicivirus Infection causes rabbit haemorrhagic disease (RHD) that kills more than 90% of adult animals, whereas young rabbits are naturally resistant to this viral disease. It has been proposed that the different response of adult and young rabbits to Calicivirus Infection is due to absence of viral receptors in respiratory and digestive systems of young animals. We have searched for liver disease in 4-week-old rabbits inoculated with a Calicivirus suspension by intranasal and oral routes. These young rabbits showed cell damage and mononuclear infiltration of the liver. The hepatic lesions were associated with mild to moderate increase in circulating transaminases. We conclude that the previously reported reduction of viral receptors in the epithelium of respiratory and digestive systems of young rabbits does not inhibit Calicivirus from inducing liver disease in these hosts.
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Leukocyte-hepatocyte interaction in Calicivirus Infection: differences between rabbits that are resistant or susceptible to rabbit haemorrhagic disease (RHD).
Veterinary Immunology and Immunopathology, 2004Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Maria João Oliveira, Eurico Monteiro, Artur P. ÁguasAbstract:Calicivirus Infection is lethal for adult rabbits, whereas young rabbits (less than 8-weeks-old) are resistant to the same infectious agent. The virus replicates in the liver and causes a fulminant hepatitis in adult rabbits leading to rabbit haemorrhagic disease (RHD); this is in contrast with the mild and transient hepatitis observed in infected young rabbits. We have used electron microscopy to compare liver leukocyte infiltrates between young (resistant) and adult (susceptible) rabbits, 36-48 h after inoculation of the animals with Caliciviruses. In adult rabbits, liver infiltrates were made up mostly of heterophils, and they were located near hepatocytes showing severe cellular damage. In contrast, liver leukocyte infiltrates of RHD-resistant young rabbits were dominated by lymphocytes that depicted membrane contacts with the cell surface of undamaged hepatocytes. We conclude that: (i) the cellular inflammatory response of the liver to Calicivirus Infection is different in rabbits that are susceptible (adult) or resistant (young) to RHD; (ii) leukocyte infiltration of the adult liver by heterophils is probably directed at the removal of dead hepatocytes, whereas the liver lymphocytic infiltration of young rabbits suggests the expression of viral antigens on the surface of liver cells of the RHD-resistant animals.
A P Aguas - One of the best experts on this subject based on the ideXlab platform.
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Liver Enzymes and Ultrastructure in Rabbit Haemorrhagic Disease (RHD)
Veterinary Research Communications, 2006Co-Authors: P. G. Ferreira, A. Costa-e-silva, E. Monteiro, M. J. R. Oliveira, A P AguasAbstract:Rabbit haemorrhagic disease (RHD) is caused by a Calicivirus Infection that kills most adult rabbits 24–72 h after viral inoculation. Two liver enzymes (AST, aspartate aminotransferase, and ALT, alanine aminotransferase) were monitored in blood samples of Calicivirus-infected rabbits during the short course of RHD. Values of AST were used to differentiate three stages of hepatocellular degeneration in RHD: mild (up to 20-fold increase in AST), moderate (150–200-fold elevation of AST) and severe (more than 1000-fold elevation in AST). Liver samples of rabbits from these three biochemical stages of hepatocellular degeneration of RHD were studied by transmission electron microscopy to define the fine structure of the hepatocytes. In the mild hepatocellular degeneration there was proliferation (microvesiculation) of the smooth endoplasmic reticulum and swelling of mitochondria into spheroid bodies with loss of cristae. In moderate hepatocellular degeneration, vacuolization of cytoplasm and mitochondrial damage continued to be present, and there was also formation of autophagic vesicles. In the severe hepatocellular degeneration of RHD, the altered mitochondria also showed loss of density of their matrix; rupture of cytoplasmic vacuoles led to the formation of large vesicles. Marked depletion of liver glycogen was also found in this late stage of RHD. These data offer a correlation between biochemical and cytological features of the liver during the hepatocellular degeneration of RHD.
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severe leukopenia and liver biochemistry changes in adult rabbits after Calicivirus Infection
Research in Veterinary Science, 2006Co-Authors: Paula G. Ferreira, Maria João Oliveira, A Costaesilva, Emanuel Monteiro, Elisabete M Cunha, A P AguasAbstract:Abstract Calicivirus Infection is the major cause of the severe decrease in the stocks of wild and farm rabbits that has occurred worldwide during the last two decades. Adult rabbits (10-weeks-old) were experimentally infected with a Calicivirus inoculum that killed all animals by causing rabbit haemorrhagic disease (RHD) within 24–62 h of Infection. The rabbits were used to evaluate blood cell numbers and serum biochemistry every 6 h, starting 12 h after the inoculation of the Caliciviruses. No significant changes in blood parameters were observed in most of the rabbits up to 18 h of Infection. Severe leukopenia was seen 6 h before death of the infected rabbits; both heterophils and lymphocytes contributed to the decrease in circulating white blood cells. Platelets were also severely decreased in number. Marked enhancement in liver enzymes was seen 6–12 h before death of the infected rabbits. There was also evidence both for cholestasis, as expressed by the elevated levels of direct (conjugated) bilirubin, and for hypoglycemia, an alteration that it is likely to contribute for the seizures that rabbits show during the late stages of RHD. Liver ultrastructure of rabbits that died from RHD revealed extensive hepatocyte vacuolization, severe changes in mitochondrial structure, and depletion of glycogen granules. We conclude that: (i) severe leukopenia characterizes the final hours of Calicivirus-induced RHD; (ii) hypoglycemia and cholestasis precede death of rabbits from RHD; (iii) the kinetics of liver enzymes allows an accurate prediction of the time of death of rabbits from Calicivirus-induced RHD.
Maria João Oliveira - One of the best experts on this subject based on the ideXlab platform.
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severe leukopenia and liver biochemistry changes in adult rabbits after Calicivirus Infection
Research in Veterinary Science, 2006Co-Authors: Paula G. Ferreira, Maria João Oliveira, A Costaesilva, Emanuel Monteiro, Elisabete M Cunha, A P AguasAbstract:Abstract Calicivirus Infection is the major cause of the severe decrease in the stocks of wild and farm rabbits that has occurred worldwide during the last two decades. Adult rabbits (10-weeks-old) were experimentally infected with a Calicivirus inoculum that killed all animals by causing rabbit haemorrhagic disease (RHD) within 24–62 h of Infection. The rabbits were used to evaluate blood cell numbers and serum biochemistry every 6 h, starting 12 h after the inoculation of the Caliciviruses. No significant changes in blood parameters were observed in most of the rabbits up to 18 h of Infection. Severe leukopenia was seen 6 h before death of the infected rabbits; both heterophils and lymphocytes contributed to the decrease in circulating white blood cells. Platelets were also severely decreased in number. Marked enhancement in liver enzymes was seen 6–12 h before death of the infected rabbits. There was also evidence both for cholestasis, as expressed by the elevated levels of direct (conjugated) bilirubin, and for hypoglycemia, an alteration that it is likely to contribute for the seizures that rabbits show during the late stages of RHD. Liver ultrastructure of rabbits that died from RHD revealed extensive hepatocyte vacuolization, severe changes in mitochondrial structure, and depletion of glycogen granules. We conclude that: (i) severe leukopenia characterizes the final hours of Calicivirus-induced RHD; (ii) hypoglycemia and cholestasis precede death of rabbits from RHD; (iii) the kinetics of liver enzymes allows an accurate prediction of the time of death of rabbits from Calicivirus-induced RHD.
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Leukocyte-hepatocyte interaction in Calicivirus Infection: differences between rabbits that are resistant or susceptible to rabbit haemorrhagic disease (RHD).
Veterinary Immunology and Immunopathology, 2004Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Maria João Oliveira, Eurico Monteiro, Artur P. ÁguasAbstract:Calicivirus Infection is lethal for adult rabbits, whereas young rabbits (less than 8-weeks-old) are resistant to the same infectious agent. The virus replicates in the liver and causes a fulminant hepatitis in adult rabbits leading to rabbit haemorrhagic disease (RHD); this is in contrast with the mild and transient hepatitis observed in infected young rabbits. We have used electron microscopy to compare liver leukocyte infiltrates between young (resistant) and adult (susceptible) rabbits, 36-48 h after inoculation of the animals with Caliciviruses. In adult rabbits, liver infiltrates were made up mostly of heterophils, and they were located near hepatocytes showing severe cellular damage. In contrast, liver leukocyte infiltrates of RHD-resistant young rabbits were dominated by lymphocytes that depicted membrane contacts with the cell surface of undamaged hepatocytes. We conclude that: (i) the cellular inflammatory response of the liver to Calicivirus Infection is different in rabbits that are susceptible (adult) or resistant (young) to RHD; (ii) leukocyte infiltration of the adult liver by heterophils is probably directed at the removal of dead hepatocytes, whereas the liver lymphocytic infiltration of young rabbits suggests the expression of viral antigens on the surface of liver cells of the RHD-resistant animals.
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Transient decrease in blood heterophils and sustained liver damage caused by Calicivirus Infection of young rabbits that are naturally resistant to rabbit haemorrhagic disease
Research in veterinary science, 2004Co-Authors: Paula G. Ferreira, A. Costa-e-silva, Maria João Oliveira, Emanuel Monteiro, Artur P. ÁguasAbstract:Abstract Young rabbits are naturally resistant to rabbit haemorrhagic disease (RHD) caused by the same Calicivirus that kills, within 3 days, nearly all adult animals. We have investigated changes in blood leukocytes, and in the morphology and biochemistry of the liver (the organ where Caliciviruses replicate) of young rabbits undergoing benign Infection by the RHD virus. Four-week-old rabbits were infected with a Calicivirus inoculum having a titre of 2 12 haemagglutination units either sacrificed 18, 24, 48 and 72 h later, or kept for follow-up studies up to 21 days after inoculation. The Infection caused an acute and transient decrease in blood heterophils, and sustained enhancement in hepatic transaminases. Inflammatory infiltrates of the liver were seen in all animals after 24 h of Infection; they had a predominant midlobular location. Hepatocytes could present different degrees of cell damage, including cell death; these lesions were limited to the liver cells located around the inflammatory infiltrates. Liver transaminases peaked 24–48 h after Calicivirus Infection; this was the same timing when liver infiltration and hepatocyte damage were more evident. No alterations of other parameters of liver biochemistry were observed. We conclude that Calicivirus Infection of young rabbits causes a subclinical disorder characterised by an acute and transient decrease in circulating heterophils, and focal liver damage that is expressed by intralobular infiltration by heterophils, initially, and, later on, by mononuclear cells. Our finding of persistence of increased values of liver transaminases suggests chronicity of the Infection in young rabbits. We propose that, although resistant to RHD, young rabbits infected by Calicivirus may be long-term carriers of the infectious agent and, thus, become a major source of transmission of the virus.
