Why are women underrepresented in many areas of science, technol- ogy, engineering, and mathematics (STEM)? This is a question with no easy answers. In science, as in many areas of life, bias against
women exists (1), but researchers disagree
on how much bias matters: Some suggest
that the effects of bias accumulate over time
to shape careers (2), whereas others argue
that gender differences in preferences are
much more important (3). However, it is
likely impossible to disentangle the effects
of societal bias and individual preferences,
because people’s understanding of gender
differences shape their preferences (4). Research suggests differences in innate ability
are unlikely to play a major role (3), but one
route to more equal representation across
academic fields might be convincing both
women and men that this is true. On page
262 of this issue, Leslie et al. (5) show that
how ability is viewed within a field plays a
key role in how well women are represented.
Two puzzles complicate typical explanations of women’s underrepresentation in
science. First, race and gender interact in
ways that are problematic for one-size-fits-all approaches. In the United States, for
example, although Asian women choose
physical science majors at lower rates than
Asian men, they do so at similar rates to
white men, and at nearly twice the rate of
white women. Of U.S. Asians who earned
Bachelor’s degrees in 2011, 1.9% of women
and 2.4% of men majored in the physical
sciences, compared to 2.1% of white men
and 1.0% of white women (6). Second, gender representation varies considerably both
within STEM and within non-STEM fields.
As noted by Leslie et al., in 2011 women received 54% of U.S. Ph.D.’s in molecular biology, compared with 18% in physics, 72% in
psychology, and 31% in philosophy.
Leslie et al. offer a novel framework for
understanding this second puzzle by show-
ing that how ability is viewed in different
fields correlates with the degree to which
By Andrew M. Penner
How should a better gender
balance be achieved?
SOCIAL SCIENCE in IFNαβR-deficient mice. Administration
of IFN-λ to mice with persistent norovirus
infection reduced virus shedding below
detectable amounts (see the figure). Moreover, injection of exogenous IFN-λ cleared
the virus from mice devoid of an adaptive
immune system (thus, eliminating the possibility that the animals invoked norovirus
antigen–specific targeting by T and B cells
of the adaptive immune system). Similarly,
the administration of exogenous IFN-λ also
ablated acute rotavirus infection in vivo
(2). Consequently, this finding may have
far-reaching implications regarding “
sterilizing” innate immunity against enteric
Wild-type mice should be able to induce
IFN-λ, so why did they fail to clear persistent norovirus infection? Baldridge et al.
provide a possible link between the host’s
microbiota and the antiviral response governed by λ IFNs. The authors found that
ablation of the gut microbiota by antibiotic
treatment results in clearance of persistent
murine norovirus infection; restoring gut
microbiota with that from untreated mice
(through fecal transplant) rescued virus
replication. This result has been separately
confirmed in both antibiotic-treated (7)
and germ-free animals (8). By stark contrast, antibiotic-treated mice lacking IFN-λ
signaling were unable to clear viral infection. Thus, IFN-λ is required to clear the virus, but its antiviral activity is diminished
in the presence of the gut microbiota. This
raises the possibility that the microbiota
may directly or indirectly benefit the virus
by inhibiting virally induced IFN-λ signaling. Indeed, another murine virus, mouse
mammary tumor virus, exploits the host’s
gut microbiota by cloaking itself in bacterial lipopolysaccharide, a constituent of
the outer membrane of Gram-negative bacteria (9). Virus-bound lipopolysaccharide
triggers the pattern recognition receptor
Toll-like receptor 4, which blocks the antivirus immune response by eliciting the
production of IL-10, an immunosuppres-sive cytokine.
Enteric viruses, including reoviruses
(10, 11), norovirus (4, 7, 8), and poliovirus
(10, 12), are known now to require the gut
microbiota for successful replication and
transmission. The mechanisms through
which the microbiota facilitates propagation of these viruses are not yet clear. In
the case of murine norovirus, it may be
that viral infection of B cells requires the
presence of glycans, resembling histo-blood group antigens synthesized by specific types of enteric bacteria (7). Another
possibility, suggested by the study of Baldridge et al., is that the gut microbiota may
interfere with antiviral innate immunity,
quenching IFN-λ signaling by an as-yet-undiscovered mechanism.
The findings of Nice et al. and Baldridge
et al. prompt many questions. For example,
it is unclear how MNV and other viruses
elicit IFN-λ production, and what cell
types sense this cytokine in the gut. Another question is why type I IFN production, which is triggered by MNV (8), does
not contribute to the antivirus response in
the gastrointestinal tract. One possibility
is that the virus blocks the effects of both
type I and type III IFNs with the help of the
microbiota. It is also possible that a specific hierarchy exists through which IFNs
control the virus, with IFN-λ providing superior protection in the gut whereas type I
IFNs mainly protect systemic organs. That
type III IFNs induce an antiviral response
identical to that of type I IFNs and that
their cognate receptor primarily lies within
the intestinal epithelium can explain their
essential role in the control of acute intestinal infections.
It appears that all orally transmitted viruses studied thus far exploit the gut microbiota for efficient transmission. However,
many viruses enter the host through other
surfaces, which also harbor commensal
bacteria. Exploring the interaction between
viruses and the surrounding microbial community should reveal how commensals contribute to the transmission of an array of
viruses, not only enteric pathogens. ■
1. J.Angel, M.A.Franco, H.B.Greenberg, D.Bass, J.
Interferon Cytokine Res. 19, 655 (1999).
2. J. Pott et al ., Proc. Natl. Acad. Sci. U.S.A. 108, 7944 (2011).
3. T.J.Nice et al., Science 347, 269(2015).
4. M. T.Baldridge et al., Science 347, 266(2015).
5. S. V. Kotenko et al ., Nat. Immunol. 4, 69 (2003).
6. P. Sheppard et al ., Nat. Immunol. 4, 63 (2003).
7. M. K. Jones et al ., Science 346, 755 (2014).
8. E. Kernbauer, Y. Ding, K. Cadwell, Nature 516, 94 (2014).
9. M. Kane et al ., Science 334, 245 (2011).
10. S. K. Kuss et al ., Science 334, 249 (2011).
11. R.Uchiyama, B.Chassaing,B.Zhang,A. T.Gewirtz, J.
Infect. Dis. 210, 171 (2014).
12. C.M.Robinson, P.R.Jesudhasan, J.K.Pfeiffer, Cell Host
Microbe 15, 36 (2014).
“Exploring the interaction
between viruses and the
community should reveal
how commensals contribute
to the transmission of an
array of viruses…”