Immune function often differs between sexes in vertebrates, i.e. immunity shows a sexual dimorphism with females most often being more immunocompetent than males (Rolff, 2002, Zuk and Stoehr, 2002, Nunn et al., 2009, Vincent and Sharp, 2014, Gipson and Hall, 2016). Sex differences in immunological capability lead to the higher susceptibility of males to infection compared to females and thus greater infection-related pathology in males (Rolff, 2002, Zuk and Stoehr, 2002, Nunn et al., 2009, Vincent and Sharp, 2014, Gipson and Hall, 2016, Klein and Flanagan, 2016, Takahashi and Iwasaki, 2021). In most human societies, women are also more resilient against infectious diseases (Boyle and Ferlay, 2004, Ayabina et al. 2021). For instance, male patients are more likely to experience severe COVID-19 than female patients, and male patients with COVID-19 are twice more likely to require ICU admission and also are 30% more likely to die due to this disease when compared to female patients (Marina and Piemonti, 2020, Chen et al., 2020, Guan et al., 2020, Pan et al., 2020, Scully et al., 2020, Islam et al., 2021, Jacobsen and Klein, 2021). Therefore, biological sex differences in immune function likely underlie male bias for certain infectious diseases (Takahashi and Iwasaki, 2021).
However, the presence of higher female immunocompetence is not restricted to humans, and in many species, males show higher intensity of infection than females (Poulin, 1996, Zuk and McKean, 1996, Moore and Wilson, 2002, Sheridan et al., 2000, Martínez-Guijosa et al., 2015, Calero-Riestra and García, 2016, Oliver-Guimerá et al., 2017, Schalk and Forbes, 1997). These intersexual differences in immune responses have been mostly attributed to sex-specific host characteristics, such as the endocrine-immune interactions (Grossman, 1985). Some hypotheses assume that testosterone suppresses immune function in males, yet consistent support for this assumption could not been reported (Folstad and Karter, 1992, Roberts et al., 2004). For instance, many insect species show a female-biased sexual dimorphism in immune function, yet insects are devoid of sex-specific hormones (Kurtz et al., 2000, Joop et al., 2006). However, the differences in immunocompetence is not a single factor contributing to the intersexual differences in infection rates. Differential exposure of animals to parasites based on differences in mating behaviour or foraging can also influence sexually dimorphic patterns of infection by parasites (Skorping and Jensen, 2004, Nunn and Altizer, 2006). In many species, behaviour and life histories show significant differences between males and females, and this is likely to be reflected in physiological traits such as immune function (Zuk and Stoehr, 2002). Females invest more into reproduction compared to males, and although males maximize fitness via mating rate, females maximize it via longevity, and ultimately, this would select for relatively higher investment in immune function in females (Zuk and Stoehr, 2002, Rolff, 2002).
Studies on sex differences in terms of infection intensities in birds are limited. One study in birds showed that testosterone treatment exacerbates hemoparasitic infection in free-ranging male dark-eyed juncos (Deviche and Parris, 2006). Another study found that the males from a wild population of Tawny pipits were more likely to be infected by avian malaria parasites (Haemoproteus and Plasmodium) than the females, and this sex-bias parasitism was evident in nestlings in addition to adults, highlighting the influence of host sex on parasite prevalence (Calero-Riestra and García, 2016). To better understand the sex differences in birds in terms of infection intensity by parasites, we compared the infection intensities by three different parasite lineages belonging to the morphological species Haemoproteus majoris, a widespread blood parasite of birds (namely PARUS1, PHSIB1 and WW2), betweens sexes in 14 different bird species present in a natural bird commmunity (Huang et al., 2018a, Huang et al., 2018b). We found that the infection intensity of a H. majoris lineage, WW2, but not of other two lineages (PARUS1 and PHSIB1), is higher in male birds than in female birds. Furthermore, we showed that total infection intensities of these three H. majoris lineages (PARUS1 (%) + PHSIB1 (%) + WW2 (%)) is higher in male birds compared to female birds, at the community level. Our study supports previous reports showing that male birds may be more susceptible to infection by certain parasites than female birds. We propose that sexual dimorphism in immune responses in birds might be more common than previously thought, similar to that observed in other animals, influencing host population dynamics in the case of infections by certain parasites such as haemosporidian parasites.