Literature DB >> 16143990

An immigration-death model to estimate the duration of malaria infection when detectability of the parasite is imperfect.

Wilson Sama1, Seth Owusu-Agyei, Ingrid Felger, Penelope Vounatsou, Tom Smith.   

Abstract

Immigration-death models are proposed to analyse the infection dynamics in longitudinal studies of panels of heavily parasitized human hosts where parasites have been typed at regular intervals by PCR. Immigration refers to the acquisition of a new parasitic genotype, occurring at rate lambda, and death refers to the clearance of a parasitic genotype (with rate mu). The models assume that corresponding to each observed process which is the detection or failure to detect a parasitic genotype, is an underlying true process which is hidden as a result of imperfect detection. We consider: (i) a model in which no distinction is made between the different members of the human population, who collectively represent the habitat of the parasites, and (ii) a model that allows for the accrual of infections with age. The models are fitted to a panel data set of malaria genotype of parasites belonging to the msp2 FC27 and 3D7 allelic families from a study of the dynamics of Plasmodium falciparum in Northern Ghana. Maximum likelihood estimates suggest that on average any individual residing in this holo-endemic area will acquire 16 new infections per year (95 per cent CI, 15-18) (defined by their single locus genotypes) and that infection with any of these genotypes lasts on average 152 days (95 per cent CI, 138-169). We estimate that an average of 47 per cent (95 per cent CI, 42-51) of the parasite types present in the host are detected in a finger-prick blood sample. This model provides a basis for analyses of how these quantities vary with the age, and hence the immune status of the host.

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Year:  2005        PMID: 16143990     DOI: 10.1002/sim.2189

Source DB:  PubMed          Journal:  Stat Med        ISSN: 0277-6715            Impact factor:   2.373


  16 in total

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3.  Novel genotyping tools for investigating transmission dynamics of Plasmodium falciparum.

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4.  Age-specific patterns of DBLα var diversity can explain why residents of high malaria transmission areas remain susceptible to Plasmodium falciparum blood stage infection throughout life.

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Journal:  Int J Parasitol       Date:  2022-01-31       Impact factor: 4.330

5.  Detectability of Plasmodium falciparum clones.

Authors:  Michael T Bretscher; Francesca Valsangiacomo; Seth Owusu-Agyei; Melissa A Penny; Ingrid Felger; Tom Smith
Journal:  Malar J       Date:  2010-08-18       Impact factor: 2.979

6.  Artemisinin-based combination therapy does not measurably reduce human infectiousness to vectors in a setting of intense malaria transmission.

Authors:  Bernadette J Huho; Gerard F Killeen; Heather M Ferguson; Adriana Tami; Christian Lengeler; J Derek Charlwood; Aniset Kihonda; Japhet Kihonda; S Patrick Kachur; Thomas A Smith; Salim Mk Abdulla
Journal:  Malar J       Date:  2012-04-18       Impact factor: 2.979

7.  The dynamics of natural Plasmodium falciparum infections.

Authors:  Ingrid Felger; Martin Maire; Michael T Bretscher; Nicole Falk; André Tiaden; Wilson Sama; Hans-Peter Beck; Seth Owusu-Agyei; Thomas A Smith
Journal:  PLoS One       Date:  2012-09-18       Impact factor: 3.240

8.  How much remains undetected? Probability of molecular detection of human Plasmodia in the field.

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Journal:  PLoS One       Date:  2011-04-28       Impact factor: 3.240

9.  Endemicity response timelines for Plasmodium falciparum elimination.

Authors:  David L Smith; Simon I Hay
Journal:  Malar J       Date:  2009-04-30       Impact factor: 2.979

10.  Asymptomatic Plasmodium falciparum infections may not be shortened by acquired immunity.

Authors:  Michael T Bretscher; Nicolas Maire; Ingrid Felger; Seth Owusu-Agyei; Tom Smith
Journal:  Malar J       Date:  2015-08-04       Impact factor: 2.979

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