Hepatitis C Virus Infection May Lead to Slower Emergence of P. falciparum in Blood

International audienceBACKGROUND: Areas endemic for Plasmodium falciparum, hepatitis B virus (HBV) and hepatitis C virus (HCV) overlap in many parts of sub-Saharan Africa. HBV and HCV infections develop in the liver, where takes place the first development stage of P. falciparum before its further spread in blood. The complex mechanisms involved in the development of hepatitis may potentially influence the development of the liver stage of malaria parasites. Understanding the molecular mechanisms of these interactions could provide new pathophysiological insights for treatment strategies in Malaria. METHODOLOGY: We studied a cohort of 319 individuals living in a village where the three infections are prevalent. The patients were initially given a curative antimalarial treatment and were then monitored for the emergence of asexual P. falciparum forms in blood, fortnightly for one year, by microscopy and polymerase chain reaction. PRINCIPAL FINDINGS: At inclusion, 65 (20.4%) subjects had detectable malaria parasites in blood, 36 (11.3%) were HBV chronic carriers, and 61 (18.9%) were HCV chronic carriers. During follow-up, asexual P. falciparum forms were detected in the blood of 203 patients. The median time to P. falciparum emergence in blood was respectively 140 and 120 days in HBV- and HBV+ individuals, and 135 and 224 days in HCV- and HCV+ individuals. HCV carriage was associated with delayed emergence of asexual P. falciparum forms in blood relative to patients without HCV infection. CONCLUSIONS: This pilot study represents first tentative evidence of a potential epidemiological interaction between HBV, HCV and P. falciparum infections. Age is an important confounding factor in this setting however multivariate analysis points to an interaction between P. falciparum and HCV at the hepatic level with a slower emergence of P. falciparum in HCV chronic carriers. More in depth analysis are necessary to unravel the basis of hepatic interactions between these two pathogens, which could help in identifying new therapeutic approaches against malaria

Relation entre hépatite C ou B et infection à P. falciparum dans une zone hyperendémique de transmission palustre au Gabon.

International audienc

Kaplan-Meier Survival Curves for the Patients According to (A) Age or (B) Hepatitis C Virus serostatus.

<p>(A) in blue fraction of patients ≤36 years old free of infection, in red patients ≥36 years old free of infection. (B) in blue fraction of patient HCV negatives free of infection, in red fraction of patient HCV positive free of infection.</p

Cox proportional hazard model.

<p>Legend: HR: hazard ratio; CI: confidence interval; P: P value.</p

Age distribution according to infection status.

<p>* <i>P</i>≤0.0001. # <i>P</i><10⁻⁵. $ <i>P</i> = 0.001. £ <i>P</i><0.002. NS, not significant.</p

Characteristics of the whole cohort and of participants according to HBV and HCV serostatus.

<p><i>P</i> = 0.0004</p><p>£ two persons not tested.</p

Parasite density distribution according to hepatitis virus serostatus.

<p>Parasite density distribution in the 203 patients in whom <i>P. falciparum</i> blood forms emerged after the last day of initial curative treatment, according to HBV serostatus (▴, 25 positive; , 178 negative) and HCV serostatus (♦, 28 positive; , 175 negative). The median parasite density in the 203 subjects (160 p/µL) is indicated by a horizontal dashed line. The dotted line at 5000 p/µL corresponds to the threshold of clinical malaria.</p