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

• Published in: PloS one Vol. 6; no. 1; p. e16034
• Main Authors: Ouwe-Missi-Oukem-Boyer, Odile, Touré Ndouo, Fousseyni S., Ollomo, Benjamin, Mezui-Me-Ndong, Jérome, Noulin, Florian, Lachard, Isabelle, Ndong-Atome, Guy-Roger, Makuwa, Maria, Roques, Pierre, Branger, Michel, Preux, Pierre-Marie, Mazier, Dominique, Bisser, Sylvie
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 10.01.2011; Public Library of Science (PLoS)
• Subjects: Acquired immune deficiency syndrome; Adolescent; Adult; Aged; Aged, 80 and over; AIDS; Analysis; Antigens; Antimalarials; Antimalarials - therapeutic use; Blood; Carriers; Cytokines; Developmental stages; Emergence; Epidemiology; Health aspects; Hepatitis; Hepatitis B; Hepatitis B - complications; Hepatitis B - epidemiology; Hepatitis B virus; Hepatitis C; Hepatitis C - complications; Hepatitis C - epidemiology; Hepatitis C virus; Humans; Infection; Infections; Life Sciences; Liver; Longitudinal Studies; Malaria; Malaria - complications; Malaria - epidemiology; Malaria - virology; Medical research; Medicine; Microscopy; Middle Aged; Molecular modelling; Multivariate analysis; Parasites; Patients; Plasmodium falciparum; Plasmodium falciparum - growth & development; Polymerase chain reaction; Santé publique et épidémiologie; Studies; Time Factors; Vector-borne diseases; Viral infections; Viruses; Volunteers; Young Adult; France; Africa
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0016034

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. 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. 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. 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.