i have hypothesized that mammalian offspring sex ratios (proportions male at birth) are partially controlled by the hormone levels of both parents around the time of conception. recently data have been published (privately) which impugn suggestions of mine (based on that hypothesis) relating to the offspring sex ratios of people who are carriers of hepatitis B virus; and (publicly) to hormone profiles of women who are infected with the protozoan parasite Toxoplasma gondii. Here these data are reviewed in the light of data on offspring sex ratios of people infected with hepatitis c, and cytomegalovirus and T. gondii; and of mice with T. gondii and the trichostrongyline nematode Heligmosomoides polygyrus. three proposals are made viz: 1. Women infected with T. gondii may have high oestrogen levels. this would potentially explain reports of their high offspring sex ratios, long gestations and (perhaps) behavioural traits. 2. some of these infective organisms may 'prefer' a particular endocrine environment in their host (in the sense that it facilitates replication or transmission or both). 3. some of these organisms apparently cause changes in that endocrine environment as a consequence of their presence. if both the latter two proposals were correct, it could explain recent puzzling data on the offspring sex ratios of hepatitis B carriers. and if this solution turns out to be correct, it would suggest new endocrine means of combating hepatitis B infection. Keywords: cytomegalovirus cMV, Heligmosomoides polygyrus, hepatitis B virus HBV, hepatitis c virus HcV, sex ratio at birth, Toxoplasma gondii 115 to be low in cMV-seropositive women: hence ex hypothesi, their low offspring sex ratio. i know no evidence on whether the virus, once present, alters oestrogen levels in women, nor on whether offspring sex ratio alters with duration of infection.
Hepatitis C virus (HCV)i know only one published set of data on the sexes of offspring born to women infected with hepatitis c. the European Paediatric Hepatitis c Virus Network (2005) reported 802 boys and 668 girls born to infected women. this sex ratio (proportion male) of 0.546 yields a chisquared value of 6.2, with 1 df, p < 0.02, tested against an expected contemporary European live birth sex ratio of 0.513 (Parazzini et al. 1998). the difference between these two sex ratios (0.033) is small but typical of much established human sex ratio variation. the evidence is weak, but one might speculate that this unusual offspring sex ratio has an endocrine basis (as would be suggested by my hypothesis). analogously, Blumberg (2006) noted sex differences in morbidity and mortality from hepatitis B which he suggested might have endocrine bases. other evidence is that hepatitis c (like hepatitis B) is a powerful risk factor for hepatocellular cancer (Hcc) (Kumada et al. 2009). Moreover, men who are destined to develop HCC have significantly higher T levels than controls (Yuan et al. 1995, Yu et al. 2001). so it is suggested here that (at least at the time infection is in...