I am thankful to the people who have been helpful to me throughout for completing my research study and without these people by my side it would have been impossible for me to complete this dissertation. Particularly, I am grateful to my friends, family and facilitator for their helpful and extensive comments on the earlier drafts that were submitted. I am also thankful to the authors who preceded me and shared my interests. The works of other authors have provided me with a bunch of information to learn and build from and they also served as examples to imitate.
DECLARATION
I [type your full first names & surname here], declare that the following dissertation/thesis and its entire content has been an individual, unaided effort and has not been submitted or published before. Furthermore, it reflects my opinion and take on the topic and is does not represent the opinion of the University.
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TABLE OF CONTENTS
ACKNOWLEDGEMENT2
DECLARATION3
CHAPTER 01: INTRODUCTION5
Aims and Objectives6
Research Questions6
Layout of the Dissertation7
Literature Sources9
Titles and Abstracts10
Ethical Considerations10
CHAPTER 03: DATA TO SUPPORT THE RESEARCH12
Testosterone Physiology12
Testosterone Biosynthesis, Transport, and Metabolism13
Testosterone Action on Target Cells14
Basic Mammalian Immune Responses15
Endocrine-Immune System Interplay17
Parasite-Immune System Interplay18
Transmission versus Susceptibility19
CHAPTER 04: CONCLUSION21
REFERENCES24
APPENDIX27
CASP Model27
CHAPTER 01: INTRODUCTION
Testosterone has emerged as an important mechanism linking variation in male reproductive behaviour to parasite infection in vertebrates, and there are numerous pathways by which testosterone can influence infection risk, particularly in free-living animals. Parasitism is considered to be a key factor that can influence and be influenced by host behaviour (Cohn, 1979a). Nevertheless, significant gaps remain in our understanding of the mechanisms that link host behaviour to variation in parasite infection. In male vertebrates, androgens, particularly testosterone, play a central role in shaping behavioural, morphological and physiological variation associated with alternative mating tactics, social status, dominance and ultimately reproductive success (Cohen and Sadun, 1976).
Testosterone is also widely considered to come with fitness costs in terms of increased male mortality, due in part to a combination of direct and indirect effects of testosterone on immune function and parasite exposure. As such, testosterone provides a functional link between male mating behaviour and parasite infection and represents an important starting point for unravelling the pathways by which reproductive behaviour may influence infectious disease risk. A number of pathways could theoretically link testosterone to behaviour-associated variation in parasite infection. One of the most widely considered paths is summarized by the immuno-competence handicap hypothesis (ICHH), which posits that testosterone, by positively affecting secondary sexual characters on the one hand, and simultaneously depressing immunity on the other, creates a physiological trade-off between the intensity of sexual signals and risk of parasite infection (Christensen and Dobson, 1979).
By extension, if signal intensity influences male behaviour and intersexual selection, then reproductive behaviour and social status should be closely linked with parasitism. While a large number of studies have tested predictions of the ICHH, a meta-analysis exploring the weight of evidence in favour of its two main assumptions, that testosterone: (i) reduces immuno-competence and (ii) increases parasitism, found limited support ...