Generally, males have lower immunity than females. 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.
http://www.newswise.com/articles/2001/10/VIRUSES.PH2.html
19-Oct-01
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
These researchers first set out to
determine if manipulating sex steroids in adult rodents would impact the
response to inoculation with the Seoul virus (a Hantavirus that naturally
occurs in Norway rats). The researchers found that in the male rats, the
production of antibodies increased, enhanced Th1 responses (inflammatory
responses) against infection occurred, and shed or released the virus into
the environment for a longer time period than comparable females in the
study. Accordingly, hormone manipulation in female and male adult rodents
had no effect on their normal response to virus infection.
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.
Conclusions
Altering the immune response to infection
occurs at a neonatal stage, as evidenced by the lowering levels of testosterone
in male mice. However, manipulating testosterone levels in female mice
had no impact on the immune system. These results suggest that the preponderance
of gender-related immunological diseases must be related to mechanisms
other than sex steroids alone, possibly genetic differences between the
sexes.
The American Physiological Society
(APS) was founded in 1887 to foster basic and applied science, much of
it relating to human health. The Bethesda, MD-based Society has more than
10,000 members and publishes 3,800 articles in its 14 peer-reviewed journals
every year.
Editor's Note: To set up an interview
with Dr. Klein, please contact Donna Krupa in the APS newsroom @ 412.281.3700
(the Crawford Room). After newsroom hours, contact 703.967.275l (cell),
703.527.7357 (office) or djkrupa1@aol.com (email).
Contact: Donna Krupa at: 703.527.7357
(office)
OR AT THE APS Newsroom @ The Westin
Convention Center/Pittsburgh, PA
© 1995-2001 Newswise
American Physiological Society (APS)
or Cell: 703.967.2751 or djkrupa1@aol.com
(email)
October 17-20, 2001
Tel: 412.281.3700 (The Crawford
Room)