The immunobiology of sexual behavior: Gender differences in the suppression of sexual activity during illness

Ronit Avitsur, Raz Yirmiya*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

102 Scopus citations


Following infection or injury, sick individuals experience profound psychological and behavioral changes, such as anorexia, depressed activity, and reduced self-care behavior. In the present review, we present evidence for a gender-difference in the behavioral response to sickness. Specifically, following immune activation, sexual activity is suppressed in female, but not in male rats. This gender difference is specific to sexually related responses, because other behaviors, such as locomotion, are equally affected by immune challenges in males and estrous females. The suppression of female sexual behavior, induced by either endotoxin (lipopolysaccharide), or the cytokine interleukin-1 (IL-1), are mediated by central mechanisms that are independent of alterations in ovarian hormone secretion. Furthermore, synergistic effects of the cytokines IL-1 and tumor necrosis factor α (TNFα) are involved in modulating sexual behavior in sick females, and prostaglandins synthesis is required for the effects of IL-1 on female sexual behavior. The gender difference in the behavioral response to immune activation may be related to the findings that at the same doses and timing in which IL-1 suppressed sexual activity in female but not in male rats, females produced more prostaglandin E2 (PGE2) in the brain, and less corticosterone than males. Finally, we are suggesting that the suppressive effect of cytokines on female reproductive behavior may serve as a mechanism to reduce conception during infection, which exposes the mother and the fetus to dangers such as spontaneous abortions, preterm labor and maternal mortality.

Original languageAmerican English
Pages (from-to)787-796
Number of pages10
JournalPharmacology Biochemistry and Behavior
Issue number4
StatePublished - Dec 1999

Bibliographical note

Funding Information:
We thank Edna Cohen, Ohr Barak, Yehuda Pollak, and Joseph Weidenfeld for their help and contribution to specific aspects of this work. IL-1ra was generously provided by Amgen Inc., Boulder, CO. Recombinant rat TNFα was generously provided by Dr. Stephen Poole. RrTNFα was produced within the context of the BIOMED Concert Action “Cytokines in the Brain.” This research was supported by a grant from the German–Israeli Foundation for Scientific Research and Development and by Grant 97-204 from the United-States Israel Binational Foundation.


  • Brain
  • Cytokines
  • Interleukine-1
  • Lipopolysaccharide
  • Rats
  • Sexual behavior
  • Sickness behavior
  • Tumor necrosis factor-α


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