Infection with Toxoplasma gondii can promote chronic liver diseases in HIV-infected individuals.

Liver pathologies and infection with Toxoplasma gondii (Nicolle et Manceaux, 1908) are widespread among HIV-infected patients. However, a possible contribution of toxoplasmosis to the development of various forms of liver diseases in HIV-infected individuals has not yet been determined. This research is a retrospective cohort study. Medical cards of 907 HIV-positive patients, including 119 individuals who died, were studied. The patients were divided into two groups: 531 patients were seropositive to T. gondii and 376 seronegative. General liver pathology was more widespread among patients seropositive to T. gondii than in seronegative patients (63.1 ± 2.1% and 51.9 ± 2.6%, respectively, p < 0.001). The association of seropositive to T. gondii with general liver pathology is weak both in the whole cohort (Pearson's contingency coefficient C = 0.112), and among the deceased patients (C = 0.228). Chronic HBV-HCV coinfection was more common in the seropositive than in seronegative individuals as it was found both in entire cohorts (26.0 ± 1.9% and 18.6 ± 2.0%, respectively, p = 0.010) and in died patients (31.0 ± 5.5% and 14.6 ± 5.1%, respectively, p = 0.041). Toxoplasma gondii had a weak role in distributing of HBV-HCV coinfection between cohorts (C = 0.187). In both cohorts in patients with chronic hepatitis, regardless of its etiology, there was no significant difference in alanine transaminase activity (ALT). Cirrhosis of the liver occurred 4.5 times more often in deceased seropositive patients than in the entire seropositive cohort (23.9 ± 5.1 and 5.3 ± 2.0, respectively, p = 0.0006) whereas it no significantly increased in seronegative cohort (10.4 ± 4.4 against 4.8 ± 1.1, p > 0.05). In them T. gondii is weakly involved in cirrhosis formation (C = 0.168). Thus, in HIV-infected patients, T. gondii is a weak nonspecific adjunct that supports chronic liver inflammation and progression of cirrhosis, regardless of etiology, but does not influence the degree of hepatitis activity. The increased prevalence of HBV-HCV coinfection in patients seropositive for T. gondii may be related to their risk factor behaviour associated with uncontrolled blood contacts.