The aim of the study was to demonstrate a link between uncomplicated Babesia canis infection in dogs and blood concentrations of zinc and copper and erythrocytic antioxidant defence – activities of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT). The study was based on 15 naturally occurring cases of canine babesiosis with anorexia, pyrexia, depression, pale mucous membrane, splenomegaly and dark red urine. Microscopic examination of Giemsa-stained peripheral blood smears and the results of PCR confirmed B. canis infection. Seven apparently healthy dogs brought in for either a check-up or vaccination were used for comparison. The levels of the erythrocytic antioxidant enzymes - SOD and CAT - were significantly higher in the infected dogs than in cytologically negative dogs. The levels of blood micronutrients were significantly lower in the infected dogs (0.478 μg of zinc per mL vs 1.241 μg/mL and 0.722 μg of copper per mL vs 1.392 μg/mL). Oxidative stress can be posited as one of the mechanisms leading to anaemia in dogs with babesiosis, and therefore antioxidant biomarker and copper and zinc concentrations could be used as indicators of disease severity and prognostic markers.

The aim of the study was to demonstrate a link between uncomplicated Babesia canis infection in dogs and blood concentrations of zinc and copper and erythrocytic antioxidant defence – activities of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT).

Porcine epidemic diarrhoea virus (PEDV) infection causes watery diarrhoea, vomiting, anorexia, and weight loss, especially among neonatal piglets, inflicting on them morbidity and mortality potentially reaching 90%–100%. Despite it being known that certain mammalian cell phases are arrested by PEDV, the mechanisms have not been elucidated, and PEDV pathogenesis is poorly understood. This study determined the effect of an epidemic PEDV strain on cell cycle progression. We observed the effect of the PEDV SHpd/2012 strain on an infected Vero cell cycle through flow cytometry and Western blot, investigating the interrelationships of cell-cycle arrest, the DNA damage–signalling pathway caused by PEDV and the phosphorylation levels of the key molecules Chk.2 and H2A.X involved upstream and downstream in this pathway. PEDV induced Vero cell-cycle arrest at the G1/G0 phase. The phosphorylation levels of Chk.2 and H2A.X increased with the prolongation of PEDV infection, and no significant cell-cycle arrest was observed after treatment with ATM or Chk.2 inhibitors. The proliferation of PEDV was also inhibited by treatment with ATM or Chk.2 inhibitors. PEDV-induced cell-cycle arrest is associated with activation of DNA damage–signalling pathways. Our findings elucidate the molecular basis of PEDV replication and provide evidence to support further evaluation of PEDV pathogenesis.

Porcine epidemic diarrhoea virus (PEDV) infection causes watery diarrhoea, vomiting, anorexia, and weight loss, especially among neonatal piglets, inflicting on them morbidity and mortality potentially reaching 90%–100%. Despite it being known that certain mammalian cell phases are arrested by PEDV, the mechanisms have not been elucidated, and PEDV pathogenesis is poorly understood. This study determined the effect of an epidemic PEDV strain on cell cycle progression.

African swine fever virus (ASFV) is a large, double-stranded DNA virus and the sole member of the Asfarviridae family. ASFV infects domestic pigs, wild boars, warthogs, and bush pigs, as well as soft ticks (Ornithodoros erraticus), which likely act as a vector. The major target is swine monocyte-macrophage cells. The virus can cause high fever, haemorrhagic lesions, cyanosis, anorexia, and even fatalities in domestic pigs. Currently, there is no vaccine and effective disease control strategies against its spread are culling infected pigs and maintaining high biosecurity standards. African swine fever (ASF) spread to Europe from Africa in the middle of the 20ᵗʰ century, and later also to South America and the Caribbean. Since then, ASF has spread more widely and thus is still a great challenge for swine breeding. The genome of ASFV ranges in length from about 170 to 193 kbp depending on the isolate and contains between 150 and 167 open reading frames (ORFs). The ASFV genome encodes 150 to 200 proteins, around 50 of them structural. The roles of virus structural proteins in viral infection have been described. These proteins, such as pp220, pp62, p72, p54, p30, and CD2v, serve as the major component of virus particles and have roles in attachment, entry, and replication. All studies on ASFV proteins lay a good foundation upon which to clarify the infection mechanism and develop vaccines and diagnosis methods. In this paper, the roles of ASFV structural proteins in viral infection are reviewed.

African swine fever virus (ASFV) is a large, double-stranded DNA virus and the sole member of the Asfarviridae family. ASFV infects domestic pigs, wild boars, warthogs, and bush pigs, as well as soft ticks (Ornithodoros erraticus), which likely act as a vector. The major target is swine monocyte-macrophage cells. The virus can cause high fever, haemorrhagic lesions, cyanosis, anorexia, and even fatalities in domestic pigs. Currently, there is no vaccine and effective disease control strategies against its spread are culling infected pigs and maintaining high biosecurity standards. African swine fever (ASF) spread to Europe from Africa in the middle of the 20th century, and later also to South America and the Caribbean. Since then, ASF has spread more widely and thus is still a great challenge for swine breeding. The genome of ASFV ranges in length from about 170 to 193 kbp depending on the isolate and contains between 150 and 167 open reading frames (ORFs). The ASFV genome encodes 150 to 200 proteins, around 50 of them structural. The roles of virus structural proteins in viral infection have been described. These proteins, such as pp220, pp62, p72, p54, p30, and CD2v, serve as the major component of virus particles and have roles in attachment, entry, and replication. All studies on ASFV proteins lay a good foundation upon which to clarify the infection mechanism and develop vaccines and diagnosis methods. In this paper, the roles of ASFV structural proteins in viral infection are reviewed.

Fowl adenovirus can cause important diseases in chickens such as inclusion body hepatitis, hepatitis hydropericardium syndrome, and gizzard erosion and ulceration. Inclusion body hepatitis has been regularly reported from many countries. This is the first case report from Turkey, describing an outbreak of inclusion body hepatitis in broiler farms due to fowl adenovirus-8b (FAdV-8b). Broiler flocks with mortality about 10% were visited in Turkey, and necropsy was performed on dead birds. Samples were subjected to PCR assay to detect FAdV and other viral pathogens. After sequencing, phylogenetic analysis was performed and the nucleotide sequences of hexon genes were compared with the FAdV sequences data available in GenBank. Clinical signs such as anorexia, depression, ruffled feathers, huddling, and greenish diarrhoea were observed. Mortality started at the 8ᵗʰ day of age and ranged from 10% to 14%. Necropsy showed severe hepatitis, jaundice, and pancreatitis. The main necropsy findings included a pale, enlarged, haemorrhagic, and friable liver along with swollen and haemorrhagic kidneys and spleen. PCR and sequence analysis revealed the presence of fowl adenovirus serotype 8b (FAdV-E). This is the first report on characterisation and the pathological lesions associated with FAdV in broilers in Turkey. Our findings suggest that FAdV strains could be an emerging pathogen in Turkish broilers and could actively contribute to hepatitis and immunosuppression.

Fowl adenovirus can cause important diseases in chickens such as inclusion body hepatitis, hepatitis hydropericardium syndrome, and gizzard erosion and ulceration. Inclusion body hepatitis has been regularly reported from many countries. This is the first case report from Turkey, describing an outbreak of inclusion body hepatitis in broiler farms due to fowl adenovirus-8b (FAdV-8b).

Accurate measurements of serum aminotransferase (ALT) activity in dogs relies on the endogenous pro-enzyme pyridoxal 5-phosphate (P5P). The purpose of this study was to determine whether the exclusion of P5P from the analytical method causes an underestimation of serum ALT activity in dogs suffering from babesiosis and in those manifesting evidence of hepatocellular damage, and to determine if anorexia causes sufficient P5P depletion to affect in vitro serum ALT activity. One-hundred-and-twenty healthy control dogs and 105 Babesia-infected dogs were included in the study. Two methods for ALT measurement were used: Method 1 included P5P, and Method 2 excluded P5P from the reaction mixture. Higher serum ALT activity was measured with Method 1 in the Babesia-infected dogs (P < 0.001), as well as in 14 dogs with suspected hepatocellular damage (P = 0.03). Duration of anorexia had no effect, irrespective of the method used. Although inclusion of P5P to the reaction mixture consistently resulted in higher measured serum ALT activity, the differences were too small to have led to incorrect diagnoses in the Babesia-infected dogs suspected of liver disease.

Accurate measurements of serum aminotransferase (ALT) activity in dogs relies on the endogenous pro-enzyme pyridoxal 5-phosphate (P5P). The purpose of this study was to determine whether the exclusion of P5P from the analytical method causes an underestimation of serum ALT activity in dogs suffering from babesiosis and in those manifesting evidence of hepatocellular damage, and to determine if anorexia causes sufficient P5P depletion to affect in vitro serum ALT activity. One-hundred-and-twenty healthy control dogs and 105 Babesia-infected dogs were included in the study. Two methods for ALT measurement were used: Method 1 included P5P, and Method 2 excluded P5P from the reaction mixture. Higher serum ALT activity was measured with Method 1 in the Babesia-infected dogs (P < 0.001), as well as in 14 dogs with suspected hepatocellular damage (P = 0.03). Duration of anorexia had no effect, irrespective of the method used. Although inclusion of P5P to the reaction mixture consistently resulted in higher measured serum ALT activity, the differences were too small to have led to incorrect diagnoses in the Babesia-infected dogs suspected of liver disease.