Hormonal Changes During Physiological Development Can Alter Immune Response to Viruses and Infections
Researchers release results of new study, sex differences in hantavirus infection: interactions among hormones, genes and immunity
The American Physiological Society
PITTSBURGH, Pa. -- It is generally recognized among immunologists that males of all species have lower immunity than females. Men are more susceptible to a variety of infections, such as dysentery, gonorrhea, and malaria; and to certain cancers. Females are at greater risk of illnesses caused by an overactive immune system, such as systemic lupus erythematosus, diabetes, ulcerative colitis, and arthritis.
Why men and women respond differently to infections caused by viruses or other parasites remains a mystery. How the immune system adopts certain strategies towards particular illnesses has not been determined. Examining gender characteristics, hormones and genes, and how they interact with immunology could provide answers to these questions. This was the goal of a team of Johns Hopkins researchers as they set out to determine how differences in sex are expressed in rats' response to hantaviruses (sex differences in hantaviruses represent an ecologically and clinically relevant model for studies of sex-based differences in infection).
Researchers Sabra L. Klein, Ph.D., A.L. Scott, and G.E. Glass, Ph.D., all from the Department of Molecular Microbiology and Immunology, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md., have conducted a study on "Sex Differences in Hantavirus Infection: Interactions Among Hormones, Genes, and Immunity." Their findings are to be presented at the conference, Genomes and Hormones: An Integrative Approach to Gender Differences in Physiology, being sponsored by the American Physiological Society (APS) October 17-20, 2001, at the Westin Convention Center, Pittsburgh, Pa.
Methodology and Results
In all animals (including humans), sex steroid hormones affect gender-specific development at two distinct times. During perinatal (i.e., during prenatal and early postnatal) development, sex steroids cause permanent, hard-wired differences in the organization of central and peripheral physiology (i.e., organizational effects). After puberty, exposure to sex steroids serves to transiently activate pre-existing hormonal circuits (i.e., activational effects). In mammals, masculine development is induced by early exposure to testosterone, whereas feminine development occurs in the absence of testosterone. Because manipulation of hormones in adult animals had no effect on responses to viral infection, these researchers hypothesized that hormones may hard-wire gender-specific immune responses earlier during development.
Therefore, the next step in the study was to determine if neonatal manipulation of sex hormones organized adult responses to the hantavirus administered to rats. After two to four days of age, male rats were castrated and females were injected with testosterone. All animals were inoculated with the Seoul virus as adults; antibody responses and viral prevalence were assessed in both sexes.
Castrated males displayed female-type responses, i.e. lower concentrations of anti-virus responses with less virus shed than in the control male population. On the other hand, injecting testosterone into female neonatal mice had no impact on that group's response to infection.
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