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A mechanistic underpinning for sigmoid dose-dependent infection
by
Jani Anttila
, Lauri Mikonranta
, Jouni Laakso
, Veijo Kaitala
, Lasse Ruokolainen
, Tarmo Ketola
in
Disease transmission
/ Diseases
/ Dosage
/ dose response
/ Environment models
/ Experimental data
/ Immune response
/ Infections
/ Infectious diseases
/ Infectivity
/ inoculum
/ mechanistic models
/ Mortality
/ pathogenicity
/ Pathogens
/ Sound
2017
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A mechanistic underpinning for sigmoid dose-dependent infection
by
Jani Anttila
, Lauri Mikonranta
, Jouni Laakso
, Veijo Kaitala
, Lasse Ruokolainen
, Tarmo Ketola
in
Disease transmission
/ Diseases
/ Dosage
/ dose response
/ Environment models
/ Experimental data
/ Immune response
/ Infections
/ Infectious diseases
/ Infectivity
/ inoculum
/ mechanistic models
/ Mortality
/ pathogenicity
/ Pathogens
/ Sound
2017
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Do you wish to request the book?
A mechanistic underpinning for sigmoid dose-dependent infection
by
Jani Anttila
, Lauri Mikonranta
, Jouni Laakso
, Veijo Kaitala
, Lasse Ruokolainen
, Tarmo Ketola
in
Disease transmission
/ Diseases
/ Dosage
/ dose response
/ Environment models
/ Experimental data
/ Immune response
/ Infections
/ Infectious diseases
/ Infectivity
/ inoculum
/ mechanistic models
/ Mortality
/ pathogenicity
/ Pathogens
/ Sound
2017
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A mechanistic underpinning for sigmoid dose-dependent infection
Journal Article
A mechanistic underpinning for sigmoid dose-dependent infection
2017
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Overview
Theoretical models of environmentally transmitted diseases often assume that transmission is a constant process, which scales linearly with pathogen dose. Here we question the applicability of such an assumption and propose a sigmoidal form for the pathogens infectivity response. In our formulation, this response arises under two assumptions: 1) multiple invasion events are required for a successful pathogen infection and 2) the host invasion state is reversible. The first assumption reduces pathogen infection rates at low pathogen doses, while the second assumption, due to host immune function, leads to a saturating infection rate at high doses. The derived pathogen dose:infection rate relationship was tested against an experimental data on host mortality rates across different pathogen doses. Compared to two simpler alternatives, the sigmoidal function gave a better fit to patterns in host mortality rate (process), as well as host mortality (endpoint). Combining these alternative approaches made us more confident to conclude that the proposed model for disease transmission is theoretically sound, provides a good description of the data at hand, and is likely to be useful in developing more reliable models for infectious diseases.
Publisher
Nordic Society Oikos,Blackwell Publishing Ltd
Subject
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