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Abstract Background The city of Doha in Qatar has a high density of feral cats and there is a high risk of toxoplasmosis for the resident human population. No data currently exist for the prevalence of infection with Toxoplasma gondii in the city. Methods We analysed the serological response to Toxoplasma gondii of 1625 subjects referred for routine hospital based serological tests in Doha, Qatar. Prevalence of current/recent infection was assessed through an enzyme-linked immunosorbent assay (ELISA) for the presence of specific anti-T. gondii IgM antibodies, and previous history of infection through IgG. Results Overall prevalence of IgG responses was 29.8% and this did not differ between the sexes nor between the three years of the study although there was a marked age effect. Among children less than 1 year old prevalence was 22.9%, but then dropped to in utero from immune mothers. Prevalence then increased steadily to peak at 41.2% among the oldest age class (>45 years). The prevalence of IgG antibody also varied significantly with region of origin, with higher rates for subjects from Africa, followed by those from the Eastern Mediterranean or Asia and lowest rates for subjects from the Arabian Peninsula. No IgM antibodies were detected in any subjects younger than 19 years, but prevalence increased to plateau at 7 – 9% in subjects aged over 20 years, and also varied with region of origin. In this case prevalence was highest among subjects from the Arabian Peninsula and least among those from Asia. Prevalence of IgM was higher among male subjects but did not vary between the three years of the study. Conclusion Although these data are based on a selected subset of the population, they nevertheless provide the first evidence that toxoplasmosis is endemic in Qatar in the human population, and that both age and region of origin play a role in the epidemiology of the infection. Concerns relating to the role of high density of feral cats in sustaining the infection were highlighted.

Caliciviruses are important pathogens of man and animals; feline calicivirus (FCV) is responsible for an acute upper respiratory tract disease in cats. To date, little is known about the mechanism of cell damage induced by these viruses. We set out to determine if apoptosis played any role in cell death in FCV infection of cultured cells. We demonstrate that caspase-2, -3, and -7 were activated during FCV infection, as evidenced by pro-form processing and an increase in acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin cleavage activity, as well as cleavage of poly(ADP-ribose)polymerase. Caspase activation coincided with the condensation of chromatin. At about 8 h post infection we also detected cleavage of the FCV capsid protein; this was prevented by caspase inhibitors. Taken together these results suggest that FCV triggers apoptosis within infected cells and that caspases are involved in the cleavage of the capsid protein.

Feline calicivirus (FCV) is responsible for an acute upper respiratory tract disease in cats. The FCV capsid protein is synthesized as a precursor (76 kDa) that is post-translationally processed into the mature 62 kDa capsid protein by removal of the N-terminal 124 amino acids. Our previous studies have also detected a 40 kDa protein, related to the FCV capsid protein, produced during infection. Here we demonstrate that cleavage of the FCV capsid protein, during infection of cells in culture, was prevented by caspase inhibitors. In addition, caspase-2, -3 and -7 were activated during FCV infection, as shown by pro-form processing, an increase in N-acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin cleavage activity and in situ poly(ADP-ribose) polymerase cleavage. Caspase activation coincided with the induction of apoptosis and capsid cleavage to the 40 kDa fragment. An in vitro cleavage assay, using recombinant human caspases and in vitro-derived FCV capsid protein, revealed that caspase-2, and to a lesser extent caspase-6, cleaved the capsid protein to generate a 40 kDa fragment. Taken together, these results suggest that FCV triggers apoptosis within infected cells and that caspase-induced capsid cleavage occurs concomitantly with apoptosis. The possible role of capsid cleavage in the pathogenesis of FCV infection is discussed.