Skip to main content Accessibility help
×
Hostname: page-component-78c5997874-94fs2 Total loading time: 0 Render date: 2024-11-19T13:20:45.779Z Has data issue: false hasContentIssue false

Invited Discussion

Published online by Cambridge University Press:  04 August 2010

Valerie Isham
Affiliation:
University College London
Graham Medley
Affiliation:
University of Warwick
Get access

Summary

There was fascinating dichotomy presented this morning by the papers of Nowak and Taylor. This dichotomy has been given several names during this meeting, and my favourite is the distinction between thought experiments to understand the processes that generate observed patterns, and the analysis of real experimental data. These two papers are essentially addressing the same subject: the pattern of CD4 counts over time, and it appears to me that both approaches would benefit from consideration of the other. On one hand, Taylor explains much of the variability in the observed counts as being derived from an underlying stochastic process, whereas it may well be due to a highly non-linear process changing on a time-scale faster than the sampling interval. On the other hand, Nowak does not use his model to produce predictions of CD4 numbers which may actually be testable by comparison with such data.

There is general problem here with the use of deterministic models, i.e. those that produce a single value or set of single value results for each time point without any measure of variability. Differential equations are an invaluable tool for mathematical descriptions of disease processes, but suffer from the fact that data-derived estimates are required for the processes embedded in the equation system, for example density dependent transmission. There are methods available for fitting equations directly to observations of the system over time, but these tend to regard the variability in data as some form of random error, and the fitting involves simple reduction of the average difference between observation and model.

Type
Chapter
Information
Models for Infectious Human Diseases
Their Structure and Relation to Data
, pp. 189 - 190
Publisher: Cambridge University Press
Print publication year: 1996

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×